Blinding light: are fluorescent lamps
safe for your children’s eyes?

2010 by H. Peter Aleff, 2097 Cottonwood Drive, Vineland, NJ 08361
email: prevent@retinopathyofprematurity.org

Replacing the energy-guzzling incandescent light bulbs in your house with more efficient compact fluorescent lamps, or CFLs, is currently being promoted as one of the most immediate actions you can take to help save our planet from global warming.  Many countries and states around the world have passed laws to fade out the old bulbs or are considering to do so, and you can rarely find an article on green building or green living that does not advise you to switch to those CFLs.  The concerns of some critics about the poisonous mercury in all fluorescent lamps are usually countered by assurances that their lower electricity consumption keeps more mercury emissions from coal-fired generating plants out of the air.

Maybe so, depending on who computes those emissions and how close to you they are emitted when a CFL breaks in your living room.  However, potentially brain-damaging air pollution from the improper disposal of fluorescent lamps and the toxic mercury vapors they release when broken is not the only threat from the mercury in them.  While these lamps are working normally, those same mercury vapors dominate the spectrum of virtually all fluorescent light with their so-called mercury emission lines.  These are very sharp and intense spikes of radiation energy, concentrated in several specific wavelengths.  The strongest one among these mercury lines shines precisely in the most retina-damaging region of the visible spectrum, at a wavelength of 435.8 nanometer, which is in the blue-violet region. 

Connect the dots:

A series of circumstantial clues suggests that retinal damage from early and frequent exposure to this most intense among the mercury lines appears likely to be a factor in the current epidemic of accelerated blinding by age-related macular degeneration, or AMD:

·       AMD now damages the vision of people earlier in their lives than prior to about 1990 when it was still called senile macular degeneration[1] because it affected mostly seniors in their seventies and eighties or even later;

·       macular degeneration has often been linked to the lifelong accumulation of debris from light-damaged photoreceptors in the retina of those affected (the macula is the most light-sensitive part of the retina, at its center);

·       virtually all fluorescent lamps concentrate much of their radiation energy at a wavelength of 435.8 nanometers; this is precisely in the most retina-damaging blue-violet wavelength region to which the Occupational Safety literature attributes the highest “blue-light-hazard” values;

·       fluorescent lamps were commercially introduced at the New York World Fair of 1938/39, and the people who now lose their sight clarity to AMD in their sixties and fifties or even sooner are the first generation who grew up under fluorescent lamps in their classrooms;

·       children’s eyes are not yet as yellowed with age as those of adults and do therefore not yet have the adults’ slowly acquired protection from those harsh and retina-damaging blue-violet energy spikes;

·       exposing children not only in school but now even at home to fluorescent light from CFLs seems likely to worsen this early retinal damage and thereby to further accelerate the appearance of their future AMD, even beyond what the time spent in fluorescent-lit classrooms may have done to their parents.

When you connect these dots, the current rush towards an easy but potentially risky technological fix for the energy-wasting of the traditional light bulbs shows a pattern that looks all too familiar.  Examples of this uncritical attitude abound, so keep connecting more dots to fit the above ones into their larger pattern:

·       the former fervor for spraying mosquitoes with DDT to rid the world of malaria -- before the long-term and wide-ranging toxic effects of this insecticide became hard to deny, or

·       the decades-long enthusiasm for chlorofluorocarbon gases as ideal coolants for refrigerators and air conditioners and as convenient propellants for spray cans -- until their ozone-depleting properties and resulting environmental dangers were confirmed beyond any rational doubt, or

·       the once equally strong appeal of asbestos for insulating everything from walls and ceilings to ductwork -- until the cancers it caused became to numerous to ignore, or

·       the lead pigments used to improve wall paints (although Caesar’s architect Vitruvius and others before him had already warned about the poisonous effects of lead on the human body[2]), and the lead anti-knock compounds for gasoline that kept cars running smoothly but poisoned the air with noxious exhausts -- until the brain damage and other harm from both became so clear that both had to be outlawed.

The list goes on and keeps repeating the pattern that some enthusiastically embraced but poorly investigated technologies tend to bite us back until we belatedly discover their long-term effects and serious hazards to our health and/or environment.  This group of bright technologies with dark flip sides appears to include fluorescent light which can severely damage your eyes and even blind you with excess exposure.

Accelerated age-related macular degeneration
and life-long accumulation of light damage

As noted above, AMD was long known in the clinical literature as "Senile Macular Degeneration" because it deteriorated the center of the retina, or macula, of predominantly very old people.  It used to be one of the unfortunate but common facts of life that our vision was likely to blur as we reached an advanced age.  This vision decline used to become noticeable sometimes at age 60, and more typically at 70 or even much later[3].  However, shortly before about 1990, people began to suffer from this reduction in their sight clarity much earlier, so the name of this condition, initially coined for the typical dimming of nonagenarian vision, became today’s “Age-related macular degeneration”, partly perhaps to avoid offending middle-aged patients with the derogatory label “senile”, but also clearly to reflect this gradually emerging new reality.  

There are many clinical articles about AMD, but the mainstream media mostly ignored the recent evolution of this disease towards affecting younger cohorts until Henry Grunwald, a writer for The New Yorker, began suffering from it and investigated in 1996 why he had to bear this traditional burden of old age already in his still prime years.  He found to his surprise that this apparent abnormality had by then become quite common and wrote in his article “Losing Sight”:

"(...) a great many people -- exact figures are hard to come by, but in the United States the number may be as high as fifteen million -- are afflicted with this disease. It is formally known as age-related macular degeneration, or AMD, because most sufferers are over fifty. It is the most common cause of irreversible vision loss in the Western world. Yet it is one of the least commonly known eye problems; until recently, it was rarely written about in the popular press, or even discussed."[4]

Grunwald’s reporting triggered some related coverage in the media echo chamber.  A few days later, the ABC News medical editor, Dr. Timothy Johnson, introduced his audience to this disease. He called it "Macular Degeneration" and said it mostly strikes people 60 years or older:

" (...) this devastating eye disease now affects about 13 million Americans, more than all other eye diseases combined. Every week, one in three seniors is diagnosed with MD, and scientists predict a huge wave of Americans, the baby boomer generation, will soon be facing MD. A staggering 30 million boomers may be facing blindness. Despite these mind numbing numbers, little research is devoted to the cause of or cure for macular degeneration. (...) Scientists don't know what causes macular degeneration, but they have identified some risk factors such as smoking, a high fat diet, and the sun's ultraviolet rays."[5]

One of Dr. Johnson's guests, a Dr. David Seftel, added that between 55 and 64 years of age, a total of 14 per cent of all people will get macular degeneration. Above that, he said, it goes up to 19 per cent, and AMD is becoming the epidemic of the 21st century.

Unfortunately, after this short burst of coverage the media went back to chasing other stories, and AMD disappeared again from the public radar.  The National Eye Institute studied how many free radicals can dance on the pin-like head of a photoreceptor and tested in nearly 100 clinical centers the “AREDs” (age-related eye diseases) formula of a few common anti-oxidant vitamins plus zinc.  This formula is designed to counteract those free radicals.  It caused 7.5 per cent of the test subjects to be hospitalized for urinary tract problems, yet it does not prevent AMD but can only reduce its risk of progressing to the advanced stage by about 25 per cent for at least six years[6].  This may fit the now common medical approach of rather trying to treat a condition with a drug than to prevent it, but it does nothing to stop the epidemic.

The first step in studying an epidemic is usually the acquiring of data about its distribution and incidence as well as any other factors that might be relevant to its causation and reveal a pattern for understanding it. But there is still no national reporting system to collect this information about AMD, and the various state-based blindness registries “have not successfully documented the prevalence, risk factors, and trends in vision loss”[7]. The authors of  The Eye Diseases Prevalence Research Group at the National Eye Institute stated therefore in their estimates of “Age-Related Eye Diseases: An Emerging Challenge for Health Professionals”  that

“the recent estimates provides by (our group) highlight the lack of sufficient information about the prevalence of age-related eye diseases”[8]. 

The numbers of AMD victims mentioned in the above media quotes must therefore be understood in the context of this incertitude, just as a more recent and more conservative series of estimates for specific stages of the disease which was posted in 2004 by the National Eye Institute.  These estimates were based on a meta-analysis of recent population-based studies in the United States, Australia, and Europe.  They proposed that more than seven million individuals 40 years and older in the U.S. had the early stages of AMD and were at risk of developing the more severe forms whereas 1.75 million US citizens had already suffered vision loss from AMD.  They also predicted that this number of severe cases will increase to three million by 2020[9].  

These newer numbers do not mean that fewer people are now suffering from AMD than in the above earlier estimates but simply appear to confirm Grunwald’s observation that exact figures are hard to come by. Still, even these more recent guesses suggest that the numbers of people affected are high and rising, and it is significant that the cut-off date for the group affected by AMD is here down to 40 years which is clearly much younger than the previous “senile” age for the beginning manifestations of this disease. 

Accelerated aging of the retina

Epidemiological studies and other research have linked cumulative life-time retinal damage from light in mostly short blue wavelengths as a contributing factor to Macular Degeneration. For instance, a study of 838 watermen on the Chesapeake Bay estimated their exposures to different wavelengths of visible light and concluded that the established sufferers from AMD, but not the milder cases, “had significantly higher exposures to both blue and [other] visible light over the preceding 20 years. There was no difference in exposure at younger ages.  These data suggest that high levels of exposure to blue and [other] visible light late in life may be important in causing AMD”[10].

Those authors’ inclusion of [other] visible light is due to the fact that the sunlight reflected on the Bay contains both blue and other visible wavelengths which cannot be separated out for such an analysis.  And their conclusion that such exposures even late in life can cause AMD should be a warning that the yellowing of our lenses offers no total protection against adding further damage from excess irradiation, and that the blue light from CFLs can also increase the AMD risk of adults.

Besides aging, other unpreventable risk factors commonly associated with AMD are Caucasian race, female gender, far sightedness, and genetic predisposition. Among the more preventable ones are smoking, a high-animal-fat diet, hypertension, high cholesterol, and obesity.  Like excess irradiation with short-wavelength light, these latter factors are all generators of oxidizing free radicals that can damage the photoreceptors, and this is probably why certain antioxidant vitamins and other nutrients have shown some success in delaying the further progress of the retinal damage. The Eye Digest published by the University of Illinois’ Eye and Ear Infirmary further mentions as the first in its list of possible risk factors

“Exposure to sunlight especially blue light”[11]. 

Typical adult eyes filter out most of the ultra-violet which is by definition invisible and does therefore not reach our retina in noticeable amounts.  From about our early twenties on, the gradual yellowing of our lenses also greatly reduces not only their transparency to ultraviolet radiation but also the amount of blue and visible violet light that does get through to the retina[12]^,[13].  We saw above that even this protection of adult eyes is not complete, but until this at least partial filtering kicks in, our retinae have no shielding at all from concentrated blue-light-hazard wavelengths.  The portion of this hazardous light that arrives on the retina slowly destroys some of the photo-receptors there and transforms them into lipid-rich waste deposits that accumulate in the retinal pigment epithelium which is the layer just below the rod and cone cells of the photoreceptors.  This debris builds up at the foot of the stems of the remaining photoreceptors at a rate that seems to be proportional to the retina's cumulative exposure to light in retina-damaging short wavelengths.

Speeding up the buildup of this debris accelerates the normal aging of the exposed eyes. When the level of debris in the retinal pigment epithelium reaches the danger limit, the spare renewal capacity of too many photoreceptors is used up, and vision declines.[14]  Similar comments in the clinical literature include, for instance:

"Free radicals are produced by metabolic processes that involve the absorption of light and the reduction of molecular oxygen. (...) [The retina's] capacity to absorb light and its need for oxygen enhance the probability that damage to membranous structures of the retina will occur from photochemical effects and associated free radicals. (...) [The protective] mechanisms could become less efficient with age. They can also lose efficiency if they are overwhelmed by an overly abundant or sustained production of free radicals -- for example, with excessive or prolonged exposure to hazardous light. If this happens, damage to ocular cells, such as those in the retina or lens, could occur."[15]
 

"The aging of the eye and the senile regression in visual perception cannot be studied in isolation from the lifelong cumulative effects of optical radiation. (...) The pigment epithelium is a closed system and with increasing age there is a net loss of cells from this layer with a resulting increase in size of those remaining. (...) Senile macular degeneration results from the metabolic disadvantage from the abnormal accumulation of debris between the pigment epithelium and the choroidal blood supply."[16]

Some doctors have claimed there is no damage to the retina as long as the electroretinograms are normal.  However, these ERGs do not show up early damage to the light receptors and will signal a reduced amplitude only after massive destruction of retinal tissue. Diabetics, for instance, can have most of their retina coagulated by laser surgery, but they still retain a normal ERG.[17]  To use a metaphor, imagine the light receptor's ability to react to light is like your ability to breathe: it remains undiminished whether you stand on dry land or in water up to your chin, but once the water rises to your mouth and your nose, your breathing becomes more difficult and then stops. In this image, the ERG measures your breathing rate, not the water level.

The above facts and arguments suggest that this decline of photoreceptor renewal, and therefore of vision, must be expected to begin earlier after a history of abundant and unprotected exposure to retina-damaging blue-violet light.  The combination of the strong “blue-light-hazard” component in fluorescent light with the relative transparency of young eyes to that blue-violet light assures increases in this exposure as more and more households switch from traditional light bulbs to CFLs.

According to the U.S. National Institutes of Health, adult vision loss at its current level costs the country about $51.4 billion a year[18].  This already high cost seems likely to rise significantly if children’s early exposure to retina-damaging radiation during their most vulnerable years becomes even more frequent and thereby damages their vision even earlier in their adult lives than the generation of their parents.

The blue-light hazard to the retina

As Murphy’s Law about things going wrong whenever they can will have it, all common types of fluorescent tubes emit their most intense energy spike at a wavelength of 435.8 nanometers, right in the peak light-hazard region for all animal and human retinae studied.  This narrow spike in the area of maximum eye damage typically accounts for about eight to ten per cent of all the energy emission from the entire lamp and varies only slightly from one type of fluorescent tube to the next, whether they are called “daylight” or “deluxe” or are engineered to provide different color temperatures.

The graph below shows the spectrum of a typical “Deluxe cool-white” fluorescent tube. This particular model was made by Sylvania but looks very similar to the spectra from the same lamp type offered by its other manufacturers.

The five rectangular bars that stick out above the smooth curve of the broadband spectrum average the mercury emission lines as columns ten nanometers wide because the graph would otherwise become to tall.  They are really very narrow spikes, a great many times taller and thinner than on this graph, and they are virtually the same for most types of fluorescent tubes.  The major difference between those types is in the shape of the broadband curve which can be shifted somewhat by using different phosphor mixtures, but the main emission lines are not much affected by these manipulations.

Compact fluorescent lamps exhibit greater variations in the relative proportions of these spikes than the fluorescent tubes.  You can find a collection of spectra from some of  the different models at http://ledmuseum.home.att.net/ledleft.htm^[20].   These range from having the tallest mercury emission line at 435.8 nanometers, as tall or even taller than in the fluorescent tube spectra, in models such as “Dollar Store” Sunbrite “warm white” 3000^oK 18W and Trisonic “soft white” 6500^oK 30W, to third tallest in such CFL models as Osram 2700^oK 9W, TCP 2700^oK 23W, Philips 4100^oK  and 5000^oK 13W, Commercial Electric 14W, and N:Vision “Daylight” 5500^oK 9W.  However, the presence of even taller spikes in longer wavelengths does not render the emission lines at 435.8 nm harmless since any excess exposure to this wavelength has been shown again and again to cause retinal damage.  

These mercury emission spikes are inherent in the way how fluorescent light is produced.  The inside of the lamp glass, whether it is a long straight tube or the more recently developed compact spiral, contains a thin mixture of mercury vapor and some noble gases. Electromagnetic fields in the lamp accelerate ions from metal plates in the ends of the lamp body to high speeds and energy levels. When such fast ions hit the mercury atoms, these absorb them and emit high-energy streams of photons, mostly in two wavelengths in the ultraviolet region that correspond to discrete energy levels of the electrons around the nucleus of the mercury atom.

To convert these ultraviolet photons into the longer wavelengths of visible light, the inside of the fluorescent lamp tube is coated with a layer of phosphor which is Greek for "light bringer".   That phosphor absorbs light and then reemits this radiation spontaneously in a different wavelength. The photon bombardment of the phosphor coating by the excited mercury atoms inside the tube greatly multiplies and accelerates this reradiating glow. The photons emitted from the mercury enter the phosphor atoms and exit at a longer wavelength, using the phosphor atoms like so many launch-pads up into visibility.

It seems fitting that the light-bringing phosphor translates in Latin to the mythical “Lucifer”, the name the early Christian Church fathers had given to the devil, because this beguiling tempter and devious author of all evil appears to have played a major role in bringing us the fluorescent light that lures us with its seductive brightness but then sneakily irradiates our retinae with the wavelength that harms us the most.

Damage-weighted retinal irradiance

The hazards from specific types of light to peoples’ eyes began to be investigated in the early 1960s when lasers started to become common tools in some industrial processes.  Researchers concerned with the industrial safety aspects of such concentrated light studied methodically the effects of different wavelengths and exposure conditions on animals from mice to monkeys, and also on people who had accidentally stared without eye protection at bright lights like the sun or welding arcs.  They found that the most damaging wavelengths for all the mammalian retinae in their tests were in a narrow band of the blue-violet range, between 435 and 440 nanometers (nm), and that this held true not only for the coherent frequency-and-phase-locked light of lasers but as well for the incoherent wavelength-jumble of regular light[21]^,[22].  In other words, when a given number of photons in a given wavelength hit the retina they create the same damage there regardless whether they arrive in ordered ranks or as messy mobs.

In 1974, the U.S. National Institute of Occupational Safety and Health, NIOSH, sponsored a Symposium on Illumination which warned that high lighting levels in that blue-violet region of the spectrum could cause much damage to the eye, particularly retinal and macular degeneration. Three years later, the Public Health Service published its "Guide to the Recognition of Occupational Diseases" with the then recently developed “action spectrum” that lists the “blue-light hazard”, or variations in retinal sensitivity as a function of wavelength. You can examine the relative values of this blue-light-hazard and the damage-weighted impact on the retina for each ten-nanometer-wide band of the visible spectrum listed on my web page http://www.retinopathyofprematurity.org/Babyblindinglights03.htm[23].

That "Guide to the Recognition of Occupational Diseases" also proposed that the retinal damage resulting from exposure times greater than ten seconds was due to a photochemical process, as in the exposure and development of photographic film, rather than to a thermal mechanism of burning the retina with shorter exposures of higher intensities, also in usually higher wavelengths such as infrared[24]. 

Combined with calculations of what portion of each wavelength actually reaches the retina, the so-called “damage-weighted retinal irradiance” derived from this action spectrum is the basis of detailed wavelength-specific exposure limits for adult industrial workers which are published annually by the American Conference of Governmental Industrial Hygienists in A Guide for Control of Laser Hazards[25] and by the Laser Institute of America in their Laser Safety Guide[26].

The earliest version of these industrial exposure limits was established in 1969.  They had to be lowered in 1976 and again in 1981 because of growing evidence that the most eye-damaging types of light harm the retina at doses much lower than previously suspected.  Despite these adjustments of the danger thresholds, the current exposure limits still offer only partial protection, even to the relatively robust adults for whom they were designed.  Instead of including a supposedly hundredfold safety factor as in other exposure limits, the current version for light exposure allows up to 1/27, instead of 1/100, of the lowest damage-weighted retinal irradiance which in animal experiments had caused noticeable damage observed after relatively short latency times[27].

People vary greatly in their sensitivity to light, as tanning and sunburn reactions easily demonstrate, and some damage from low-intensity light, particularly in the shorter wavelengths, becomes noticeable only after longer latency times than those used in most of these experiments[28]. The above arbitrary “safety” factor is therefore not necessarily safe enough for all people.  For instance, people suffering from lupus often try to avoid all fluorescent light because it causes them migraines or other severe bad reactions; their cases are just some of the extremes in a continuum of light damage caused by some components of this highly unnatural illumination.

Children’s lack of protection against excess blue light

A refinement of Murphy’s Law decrees that the things which can go wrong will do so at the worst possible moment.  In the case at hand, this means the exposure of children and adolescents to fluorescent light because their eyes have not yet undergone the gradual yellowing of the lens which protects adult eyes to some degree from the most eye-damaging wavelengths.

When we are born, our eyes are much more transparent to more wavelengths than after our first two decades or so of exposure to light. The harsh violet and blue irradiation which enters our lens causes there chemical oxidation reactions that gradually turn the mass of the lens yellow, just as varnish exposed to sunlight gradually turns yellow, and for the same reason: the oxidation of free radicals[29]. Our so age-yellowed lens filters out a large part of the blue and violet light which would be most harmful to our retinae and so offers us at least some protection.

For comparison, the retinae of babies receive about 90% of the visible light above 400 nm plus 80 to 85% of the ultraviolet light down to about 320 or even 300 nm.  The age-yellowed lens of a 25-year-old lets through only 46 to 50% of the visible light, and next to nothing in the ultraviolet range.

This gradual change in the transparency of our lenses has been documented for decades in such clinical articles as, for instance, “Spectral transmission of the eye to ultraviolet radiations”  (1948)[30], or “The variation with age of the spectral transmissibility of the living human crystalline lens (1959)[31], or “An experimental and clinical evaluation of lens transparency and aging” (1983)[32].  

The yellowing of our lenses is good for adults because the high-energy light it mostly filters out would otherwise severely harm our retinae.  The visible violet wavelengths next to ultraviolet are almost as energetic as those invisible ones and would destroy our light receptors over the years if we had not evolved that adaptive protection for living under a generally blue sky.

Unfortunately, children have not yet built up this protective barrier. The yellowing is very gradual and offers us an effective protection against intensive blue-violet light only from about our late teen years or early twenties on.  Until then, our eyes are largely transparent to those most eye-damaging wavelengths which can wreak their havoc unhindered on the retinae of children and there build up debris that remains unnoticed but uses up much of the spare photoreceptor renewal capacity[33].  The hazard value of the violet and blue spectrum region is therefore much higher for children than the blue-light hazard function for adults in the Action Spectrum Table mentioned above. It is closer to the values shown there for “aphake” eyes that do not have a lens, or only a fully transparent one.  

The damage this “blue-light-hazard” irradiation inflicts on the retina is hard to observe immediately because, like some equally elusive cancers or slow lung contamination diseases, it has a long latency time and often manifests its harm only decades later.  Still, this blue-light damage is the most logical suspect as a major contributing factor to the recently started epidemic of sooner-than-usual age-related macular degeneration. 

The uncritically embraced practice of exposing children and adolescents to fluorescent light seems to be like a demographical time bomb with a once long fuse that has now burned to its end. The sudden explosion of the macular degeneration epidemic would have been easy to predict from the above circumstantial evidence[34] if that explosion had not already begun.  The increased use of fluorescent lamps now even in homes suggests that the epidemic of macular degeneration will get even worse if we continue to ignore the dangers from their light to unprotected eyes.

Reactions to dangers from light

The introduction of electric light provided a welcome break in the discouraging pattern of ignoring the downsides of new technologies because alert professionals quickly addressed one of its dangers. A mere eight years after Edison strung up his first commercial light bulbs in New York, the oculists of London petitioned parliament in 1898 to pass laws against the use of unshaded lights, and consequently research was instituted on various types of shades and reflectors[35]. Or else we might still be squinting at bare bulbs.

Unfortunately, the successors of those oculists were and are less vigilant and less concerned.  When fluorescent tubes were commercially introduced at the New York World Fair of 1938 and 1939, none of the experts raised publicly any concerns about their unnaturally cold and harsh light, or noticed that this innovation in lighting coincided also with the appearance, from 1940 on in the U.S., of a new form of blinding eye damage among premature babies which is now called retinopathy of prematurity. They did not even notice the exact repetition of that clear timing coincidence after World War 2 when fluorescent lamps became also available in other industrial countries and the same there previously unknown baby-blinding epidemic suddenly appeared in those countries, too[36].  To the contrary, the medical community welcomed the new lamps for the appearance of cleanliness their bright blueish light gave to hospital rooms, and for the reputed germicidal properties of the ultraviolet component in their radiation which many of the early fluorescent lamps did not yet filter out as well as most later models do. 

And even now, almost seventy years after fluorescent lamps began to take over most of this country's public buildings, and over forty years since laser researchers discovered and described the retinal hazard from the strong blue-violet component of their light, doctors continue to ignore and downplay this hazard. Indeed, neither the ophthalmologic community, nor even the American Academy of Pediatrics which the U.S. Congress had specifically charged with the task of watching over the health of the nation's children, have done anything to warn the public against those well documented dangers.

Indeed, there are no clinical studies to prove this suggested connection between early exposure to fluorescent light and early-onset macular degeneration. For obvious reasons, there has not been and will not be any double-blind clinical trial of people whom researchers kept all their lives under various controlled conditions of potentially harmful exposures.  The coincidence that the people whose maculae degenerate now so much earlier than in former times are the first generation that grew up under fluorescent lamps in their school rooms could be just that – a mere  coincidence -- and does not by itself prove any causation.  

However, if you follow the logic of fitting the puzzle together and connect this timing with the well established knowledge about the damaging effects of the main mercury emission line’s retinal irradiation, plus the natural delay of our retinal protection against it, then the weight and seamless fit of this circumstantial evidence suggests to cautious parents the prudent motto "better safe than sorry".

Waiting for yet more medical research to establish the detailed dose-response curves of early retinal light damage for medical textbooks would be a modern variation on the French playwright Molière’s observation that the purpose of medical science is not to cure patients but only to name their illness in Latin. Common sense calls for first protecting the children's eyes from hazardous radiation, instead of letting medical scientists formally prove the details of the expected long-term harm from exposing those children systematically to various levels of eye-damaging light as they have already done with countless animals. 

Or can you blindly trust in the never established long-term safety of that unnatural fluorescent irradiation and its devilish mercury emission lines, the strongest of which is well known to damage retinae?  Knowing the clues you know now and can easily verify, can you bet the future of your children's eyes on that alleged and hoped-for but never confirmed safety of compact fluorescent lamps?