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Health Effects of Artificial Light

5. What are the effects on people who have conditions that make them sensitive to light?

  • 5.1 Skin diseases
  • 5.2 Eye conditions
  • 5.3 Other conditions linked to light flicker

5.1 Skin diseases

The SCENIHR opinion states:

3.6. Adverse health effects in persons with pathological conditions

3.6.1. The Photosensitive skin diseases

In contrast to light effects on the skin of the normal population, there are two patient groups (Table 4) who react abnormally to sunlight. Those whose disease is induced by ultraviolet/visible/infrared; and others who have a pre-existing skin disease which can be photo-aggravated. Essentially, skin photo-testing is abnormal in the true photosensitivity disease group and normal in the photo-aggravated group. The wavelength dependency, where known, is described in Table 5. The majority of patients are aware of the relationship to sunlight exposure, but skin disease activity following incidental artificial light exposure is much less commonly described. The photodermatoses

Photosensitive diseases induced by light are sub-divided into endogenous and exogenous groups (Table 4). They represent a wide range of diseases which, for space reasons, are succinctly described below.

Table 4. "Light related" skin diseases

Table 5. Wavelength dependency in photosensitive diseases

A. The Endogenous photodermatoses

This group is sub-divided into the idiopathic and genophotodermatoses.

i) Idiopathic photodermatoses

Although the exact mechanism is unknown, this group of conditions is believed to be immunologically based. Little prevalence data exists. These diseases have been extensively reviewed (Ferguson and Dover 2006, Honigsmann and Hojyo-Tomoka 2007).

This group of light induced disorders have good clinical evidence for a UV induction role as seen in photoprovocation testing conducted with solar simulator, monochromator and broadband sources.

With the exception of Xeroderma pigmentosum and Lupus erythematosus, animal models do not yet exist for this group of diseases. This undoubtedly has held up understanding of individual diseases.

What is clear from the clinic is that there is a wide range of individual disease severity with differing amounts of UV being required to provoke lesions in patients. It is also evident in this particularly susceptible group that the main concern with the change from the use of incandescent to low energy light sources relates to the UV content of CFLs. Newer LED illumination lamps do not emit in the UV region and are therefore not such an issue for these UV sensitive patients. This explains the CFL emphasis of this section.

Polymorphic light eruption (PLE) or polymorphous light eruption (PMLE) PLE which is the most common of all the photodermatoses, usually affects females and presents in spring/early summer (or when taking a sunshine holiday) with an itchy red spotty rash on sunlight exposed areas. It usually develops on exposure to between half to a few hours of sunlight, with symptoms often appearing several hours later. The condition settles in one to two weeks without scarring. Although the prevalence is often stated to increase with the distance from the equator (Pao et al. 1994), a recent multicentre European study reported a high overall prevalence of 18% (Rhodes et al. 2010a) without variation between mainly fair skinned populations at different latitudes. The range of severity and wavelength dependency varies greatly between individuals. Many have a relatively minor disease triggered by UVA whereas a minority have a severe, disabling problem triggered by UVB/A extending into the visible wavebands (Bilsland et al. 1993, Frain-Bell 1985, Lindmaier and Neumann 1991). Although there are no written reports of PLE induced by artificial lighting other than sunbeds, an occasional PLE patient will comment on a possible role.

Low dose ambient sunlight exposure may be associated with improvement via a hardening process of skin thickening and pigmentation. For this reason some patients are free of activity on the face and hands.


Although in the majority of patients it is unlikely that artificial light sources will induce this skin disease (activity during winter months being rarely reported), there may be a small number of patients in whom UV and/or visible light emitting artificial sources could produce the eruption. It is also possible in others that low dose chronic UV radiation could contribute to a hardening process and thereby produce a degree of protection.

In the absence of clinical data, it is reasonable to assume that in a small minority of individuals, provocation of PLE may follow artificial light UV exposure. Chronic actinic dermatitis (CAD) This uncommon condition which may be incapacitating, particularly affects males over the age of 50 years (Hawk and Lim 2007). It has a prevalence which has only been studied in Scotland where 16.5:100,000 (Dawe 2009) were affected. The skin is sensitive to multiple contact allergens as well as UVA and UVB and in 50% of patients also visible light (Dawe and Ferguson 2003, Ferguson 1990). Another type of uncommon chronic actinic dermatitis (CAD) (prevalence unknown) has been identified in atopic dermatitis sufferers (Russell et al. 1998). It appears that these young patients in their teens and early 20s have CAD with a breadth and severity which varies greatly between patients. A role for fluorescent lighting has been commented upon within the literature (Hawk and Lim 2007). The problem is perennial in about 50% (of the elderly male type), which suggests a role for artificial lighting. An open study has revealed some patients to have the potential of CFL induced skin flares (Eadie et al. 2009). No similar work with unfiltered halogen sources is reported. It seems likely that they too would be capable of the same problem.


Severe and perhaps even moderately affected individuals with this condition may, when exposed to artificial UV or visible light, experience induction of CAD.

Actinic prurigo (AP)

This is an uncommon scarring condition that particularly affects American Indians and less frequently Caucasian and Asian populations (Honigsmann and Hojyo-Tomoka 2007). With an age of onset usually in the first decade it predominantly affects females. Patients complain of a perennial problem with deterioration during spring and summer. Pruritic, oedematous erythema with papules is evident following exposure to sunlight (Ross et al. 2008). Repetitive UVA provocation testing is capable of lesion induction. Management of AP is more difficult than that of PLE. Some cases benefit from a UV desensitisation course early in spring (Gambichler et al. 2005). Its prevalence is estimated at 3.3:100,000 of the Scottish population (Dawe 2009).

No formal provocation study with low energy CFL or other lamps has been conducted.


Severe cases may potentially be at risk from CFL or other UV emitting sources (Eadie et al. 2009).

Solar urticaria

This is an uncommon potentially serious skin disorder that affects males and females (Horio and Holzle 2007). It may arise in any age group but is particularly common in the first four decades of life. The condition is of long duration with about one third of patients failing to respond to anti-histamine and other treatments. It has a wavelength dependency most commonly in the UVA region extending into the visible and occasionally also affecting the UVB region. The life threatening risk is of generalised urticaria with anaphylactic shock. The prevalence in Scotland has been estimated to be 3.1:100,000 (Beattie et al. 2003). Provocation of the lesions is relatively straightforward in the most sensitive group. Light in the visible region (green) in some patients may inhibit eruption induction. Patients with severe UVA visible light sensitivity have reported indoor lighting triggered disease activity (Harber et al. 1985, Horio and Holzle 2007).


Severely affected patients may be at risk from CFL and unfiltered halogen sources producing UV/visible radiation. It should be noted that incandescent light sources also cause problems in some patients.

Hydroa vaccineforme

This condition is rare, arising in 1:300,000 of the Scottish population (Dawe 2009). It is a blistering eruption of sun exposed skin affecting both sexes which heals with characteristic scarring (Gupta et al. 2000, Honigsmann and Hojyo-Tomoka 2007). Occasionally, the eyes can be affected with photophobia and conjunctival inflammation and scarring. Some patients spontaneously resolve in childhood, others continue into adulthood. It appears that UVA wavelengths are particularly effective when used repetitively to induce the characteristic skin lesions (Eramo et al. 1986).


It is possible that some severely affected patients may be provoked by UVA emitting low energy artificial light sources. Lupus erythematosus (LE) Lupus erythematosus is an uncommon clinically significant group of closely related auto immune diseases that involve the skin. They affect all age groups in both sexes and are made up of four recognised sub types:

1. Systemic lupus erythematosus (SLE) is the most serious and potentially lethal form which affects both the skin and systemic organs.

2. Subacute cutaneous lupus erythematosus (SCLE).

3. Chronic discoid lupus erythematosus (CDLE).

4. Lupuserythematosus tumidus (LET).

There is no doubt that UV exposure plays an important induction or aggravation role in all LE sub types. This field has been extensively reviewed (Hasan et al. 1997, Kuhn et al. 2006, Millard et al. 2000). Many LE patients may not be aware of their photosensitivity. This lack of correlation with experimental UV induction of skin lesions is thought to be due to the need for chronic UV exposure and a delayed time interval of up to a week between exposure and development of the skin lesions. In SLE, there is evidence that UV exposure induced skin flares arise in 72-85% of patients (Dubois and Tuffanelli 1964) and can be accompanied by a flare of potentially serious internal organ disease e.g. kidney, lung and joint involvement (Léone et al. 1997, Wysenbeek et al. 1989). In the less serious sub-types, UV damage seems localised to the skin, producing disfigurement which is particularly important as the face and hands are affected with both acute erythema and a scarring potential. Incidence and sex distribution of LE varies with sub type. SLE, the most studied, has a prevalence in Europe (per 100,000) of 12.5 to 39. It is more common in the Afro-Caribbean population.

The mechanism of action of UV radiation relates to the believed pathogenesis of this autoimmune group of diseases. Current thinking is that LE arises in a group of individuals who have an antibody response directed against nuclear components of their own cell breakdown products. Cell death may be induced by a number of external factors including UV exposure and well described lupus inducing drugs (Wu et al. 2007).

Early skin provocation work suggested UVB wavelengths to be mainly responsible (Baer and Harber 1965, Cripps and Rankin 1973, Freeman et al. 1969). Further murine work suggested the waveband extended into the UVA region (Bruze et al. 1985, Gilliam and Sontheimer 1982, Golan and Borel 1984, Wollina et al. 1988). Later attempts to reproduce the skin lesions with artificial UV revealed an abnormal response to both UVB and UVA with 93% of a large group of LE sub types having a positive photoprovocation test. Importantly, it was reported that in patients, multiple doses to relatively large areas of skin coupled with extended readings were required to maximise the positivity of this test (Sanders et al. 2003). In other published work (Hasan et al. 1997) a positive provocation test with artificial UV was achieved in 100% of SCLE patients, 70% of those with SLE and 64% with discoid lupus erythematosus (DLE). The skin of non LE controls did not react. Again, the wavelengths involved were UVB and UVA. In these studies it was noted that the dose for induction varied between patients and was considerably slower in evolution with longer persistence after induction than photo induced lesions of the other photodermatoses (Table 3).

In contrast to the shorter UV wavelengths (UVB/UVA) having a definite role in the induction of lupus, there is unexpected evidence that longer UVA wavelengths i.e. UVA1 (340-400 nm) may have a favourable effect on LE activity. This reasonably robust evidence has been reviewed by Pavel (2006). Some clinical data exists commenting on the role of artificial lighting inducing skin LE. In one study, SLE flares due to fluorescent lighting were reported (Rihner and McGrath 1992). Thirteen of 30 sun sensitive SLE patients described an increase in skin disease activity following exposure to an unshielded fluorescent lighting source, while the same light source with UV filtering had no effect in the same patients. Consequently it was recommended that patients with SLE and other photosensitive conditions should avoid unfiltered fluorescent lamps.


It seems reasonable to assume that at least some LE patients, and particularly those with SLE, are at risk from chronic UV exposure from some low energy emitting lamps such as CFLs and unfiltered halogen bulbs. In this context it is noted that LE support groups are already advising the use of double rather than single envelope CFLs.


This group of mixed inherited and environmentally induced photosensitivity skin diseases (Elder 1998, Murphy and Anderson 2007) relate to an accumulation of a photosensitive porphyrin within the skin. A disease example is erythropoietic protoporphyria, the main feature of which is burning or prickling pain in the sunlight exposed skin. A few minutes of intense visible light are usually enough to elicit symptoms causing the individual to try to escape from the light source and seek relief, for example, using cold water compresses. Erythropoietic protoporphyria develops in childhood, or even during infancy. It should be noted that cutaneous porphyrias are particularly sensitive to the blue light region so there would be an argument that fluorescent lighting would be a greater problem when compared with tungsten bulbs (which have less blue light). Porphyrias are rare disorders. For example, the prevalence of congenital erythropoietic porphyria (Günther’s disease) in the UK is approximately 2 per 3,000,000 live births. Erythropoietic protoporphyria prevalence is 1 to 2 per 100,000 inhabitants (Burns et al. 2004, Marco et al. 2007). Although an unusual event, theatre and other visible light sources can produce phototoxic burns in those patients with particularly high levels of porphyrins (Meerman et al. 1994).


Artificial, visible light sources which would include incandescent bulbs may produce skin reactions in the most sensitive patients.

ii) Genophotodermatoses

The diverse group of inherited photosensitive skin diseases given in Table 3 include Xeroderma pigmentosum (XP), Cockayne’s, Bloom’s, trichothiodystrophy, Rothmund- Thomson Syndrome and the Smith-Lemli-Opitz syndrome, which are all rare (Berneburg and Kraemer 2007, Ferguson and Dover 2006).

Xeroderma pigmentosum, as an example of this group, is reported to have a prevalence of 1:250,000 in Europe and the USA (Robbins et al. 1974). XP in its classical excision repair form has marked photosensitivity to UVB/A wavelengths. The development of skin cancer in early childhood makes photoprotection against these mutagenic wavelengths an essential part of management. This disease is associated with a significantly shortened life span. The other diseases which are rarer than Xeroderma pigmentosum vary in their wavelength susceptibility and degree of abnormal photosensitivity.


UV radiation from artificial light sources is associated with an increased skin cancer risk in XP. Patients are currently advised to avoid all sources emitting UVB/A wavelengths. These would include CFLs and unfiltered halogen bulbs. B. The Exogenous photodermatoses i) Drug/chemical induced photosensitivity Many drugs are known to be capable of inducing photosensitivity (Moore 2002, Selvaag 1997). However, many drugs listed as photosensitizers are infrequent causes of the problem and likely to have an idiosyncratic mechanism (Shields 2004). They do so by a variety of mechanisms, most commonly phototoxicity, which indicates that any individual exposed to a sufficient quantity of a drug and appropriate irradiation will be affected. Other mechanisms result in a small number of individuals being affected. Examples of photosensitizing drugs are listed below. Much less commonly seen is the mechanism of drug-induced photoallergy, which involves a sensitised immune system, which follows topical exposure to a photoallergic drug or chemical (usually sunscreens).

Generally, such reactions are UVA dependent with some drugs extending into the UVB and visible range (Ferguson 1998).


Amiodarone is a cardiac anti-dysrhythmic agent that causes sunlight induced burning, and a prickling sensation with erythema in approximately 50% of individuals on a high dose. The wavelengths responsible are UVA and visible light. Unsightly slate-grey skin pigmentation may also develop on photoexposed sites (Ferguson et al. 1985).


Phenothiazine-derivative drugs have an antipsychotic action, thought to act by blocking dopaminergic transmission within the brain. They produce skin discomfort, erythema and blistering elicited by exposure to UVA. Unsightly skin discolouration may also follow.

Fluoroquinolone antibiotics

This is a large group of drugs that exhibit variable degrees of phototoxicity. Symptoms include erythema and blistering; wavelengths responsible are mainly in the UVA region (Ferguson 2003).

ii) Photofrin and other anti-cancer photodynamic therapy (PDT) agents Photofrin and Foscan are potent intentional visible wavelength dependent photosensitizers used in photodynamic therapy of internal cancers. These drugs can elicit skin phototoxic responses when exposed to visible radiation from artificial light sources (Hettiaratchy et al. 2000, Moriwaki et al. 2001).


The majority of drugs known to have a phototoxic potential would not be expected to have the problem induced by CFL and unfiltered halogen light sources. However, skin flares whilst taking intentional photosensitizers, as during PDT, would be expected following artificial visible light exposure.

With photofrin, photosensitivity might be expected to occur with CFL and LED sources to a greater extent than that currently seen with incandescent lighting. This is due to a combination of greater sensitivity of porphyrins to blue light (soret band), coupled with an enhanced blue light emission of these sources. However, such patients are aware of their extreme photosensitivity which needs careful management.

iii) Photoallergic Contact Dermatitis

Photoallergic contact dermatitis is an uncommon delayed-type hypersensitivity reaction elicited by low doses of UVA radiation in susceptible individuals. The main groups of photocontact allergens current in the environment are organic sunscreen chemicals, and topical non-steroidal anti-inflammatory drugs. When the diagnosis is made, patients can quickly stop the responsible agent and avoid the provoking wavelengths, usually in the UVA region.


Except in the most photoallergic individuals, UVR artificial light sources are unlikely to be a significant factor in this group of patients. Photoaggravated dermatoses

This diverse group of diseases (Werth and Honigsmann 2007) differs from the true photo dermatoses in that they also arise without UV/visible light exposure. Only a small proportion report that their problem is sunlight exacerbated. Phototesting reveals normal responses to UV and visible radiation. Atopic dermatitis (AD) is an example of this large group. About 10% of people with atopic dermatitis are aware of light triggered exacerbations. The other 90% have a perennial problem with no evidence of sunlight induction and even may have a tendency to flare in the wintertime. The mechanism and wavelength dependency are unknown as these patients have a normal phototest skin response. In fact, many of these patients respond well to UVB phototherapy. In some patients a coincidental true photodermatoses may be the explanation. In such cases, induction by light will vary with the wavelength dependency and degree of sensitivity of the true dermatoses.


As can be seen from Table 3, the number of diseases within the potential photoaggravated group is extensive. As the precise role of artificial light sources is unknown, it is perhaps unlikely that they play a significant role. Conclusions on photosensitive skin diseases

There is strong evidence based on phototesting that UV and, in some patients, visible light, induces the skin lesions of the true photodermatoses. Although sunlight is reported by some patients as the main source of disease activity, occasionally severely affected patients over the range of endogenous (and exogenous) diseases do exhibit or suspect a role for artificial lighting. For this group of patients, artificial light sources with a considerable UV emission would be best avoided. Therefore, the previous SCENIHR opinion recommended that if using CFLs, a double envelope type is preferable. This is supported in the current opinion. Although a second envelope undoubtledly reduces the UV emissions, the currently available data show a high variability of UV and blue light emission due to different internal design parameters even for the same externally visible architecture, i.e. also in presence of a second envelope. While some compact fluorescent lamps are in the same category, retrofit LED lighting, which does not emit UVR on the physical grounds of the light generation therein, would provide potentially an even better option for such patients. The UV/blue light irradiation from halogen lamps is also highly dependent on the lamp type. Here attention needs to be given to the proper installation of those lamps which are sold by the manufacturer to be installed at larger distance or in conjunction with special luminaires or filters against e.g. UV or IR irradiation or to prevent other hazards like fires. While it is unlikely that there would be a significant UV risk from halogen lamps for the general public, provided that protective measures are complied with, the UV content of these lamps can rise to levels which are of concern for patients with light-associated skin disorders at close operating distances and long exposure times. This, however, is not a very common use pattern for this lamp type. Unfortunately, due to limited study, there is a lack of controlled skin provocation data using the range of artificial lighting sources. Where some work has been conducted in particularly severely affected individuals, as in the photodermatoses, lupus erythematosus, chronic actinic dermatitis and solar urticaria, there is good evidence of induction of skin disease by single envelope fluorescent light sources. Such work needs to be confirmed and extended using the range of energy saving lamp types over the different diseases with controlled study methods in greater numbers of patients. Until such data exist, it seems reasonable to assume that the UVR component of artificial lighting in an as yet undefined number of patients, may contribute to induction of their skin disease and in the case of lupus erythematosus possibly also their systemic disease.

Source & ©: , Health effects of artificial light, 19 March 2012,
 3.6.1 The photosensitive skin diseases, pp. 61-68.

5.2 Eye conditions

The SCENIHR opinion states:

3.6.2. Photosensitive eye conditions

Inherited retinal degeneration affects about 1.5 million individuals worldwide. The disorders may be inherited in any one of the recognised patterns, and fall within a spectrum ranging from Retinitis pigmentosa (RP) to macular dystrophies. In RP the initial symptom is loss of night vision and subsequently loss of lateral vision. In late-stage disease, vision is restricted to a narrow central cone but detailed vision remains good. There is also an intermediate group which is characterized by progressive loss of side and central vision equally. In macular diseases, central vision is lost but side vision remains good. Several hundred disorders exist within this family of diseases that vary in their age of onset, speed of progression and final vision capacity. In severe cases of disease, there may be loss of all useful vision in early life, whilst others may be unaware of the presence of disease even in late life.

Light can accelerate degeneration through non-specific toxicity to photoreceptors already stressed by the effects of a mutation, or through a specific interaction with mutant rhodopsin. Experiments with cultured photoreceptors have suggested that activation of mislocalised rhodopsin could kill rods by stimulating inappropriate signaling pathways (Alfinito et al. 2002).

In two specific human forms of regional (macular) RP, i.e. Ogushi disease and Stargardt disease, light has been recognized as aggravating and light protection as protective. Indeed, mutations of proteins involved in rhodopsin deactivation after light exposure (i.e. rhodopsin kinase, arrestin), induce prolonged insensitivity of rod vision following light exposure and different forms of retinal degeneration ranging from stationary blindness to true RP (Ogushi disease) (Chen et al. 1999, Paskowitz et al. 2006). In Stargardt disease, a hereditary macular dystrophy whose features often include progressive loss of central vision with onset during the first or second decade of life, macular atrophy and fundus flecks, massive accumulation of lipofuscin and extensive A2E accumulation is seen in RPE cells. The disease shows autosomal recessive inheritance and is caused by mutations in ABCA4, a transporter localised to the rims of photoreceptor outer segment discs. ABCA4 mutations have also been identified in fundus flavimaculatus, autosomal recessive RP and cone-rod dystrophy. A possible link with age- related macular degeneration has been proposed but remains poorly documented. Due to the very high content of A2E in RPE cells, blue light is considered to be an aggravating factor for Stargardt disease (Maeda et al. 2009, Mata et al. 2001). Since in most patients presenting with RP symptoms, the causative mutation is not known, it may be prudent to avoid unnecessary exposure to bright light in patients presenting RP, particularly the regional RP (affecting mostly the macula).

Conclusions on photosensitive eye conditions

The effect of light is variable depending on the genetic alterations that are causing retinal degeneration. In specific conditions like Stargart disease, accumulation of lipofuscin early in life renders the RPE cells particularly sensitive to type II photochemical damage. In other retinal dystrophies, light does not exert any aggravating effect. However, since the causative mutation is seldom known to the patient or their family, and because there is no clear correlation between genotype and phenotype, it is recommended for all patients with retinal dystrophy to be protected from light by wearing special protective eyeware that filter the shorter and intermediate wavelengths.

Source & ©: , Health effects of artificial light, 19 March 2012,
 3.6.2 Photosensitive eye conditions, pp. 68-69.

5.3 Other conditions linked to light flicker

The SCENIHR opinion states:

3.6.3. Flicker, other conditions

Flicker, modulation of light intensity which can be perceived by the human visual system, has been implicated in certain pathologic conditions, most notably epilepsy. The criticial flicker frequency (CFF; where it is not possible to discern single events) is around 50 Hz for luminance, whereas it is considerably lower, ca. 25 Hz, for chromaticity (Shady et al. 2004; Carmel et al. 2006). Flicker of higher frequencies is invisible to humans since the visual system is averaging over 20 ms or more. Through stroboscopic effects, however, modulated light of higher frequency may be observable if the observer and a patterned object are in relative motion and are illuminated by modulated light. Even if the flicker frequency is well above the CFF, non-perceived may have effects on visual performance (Veitch and McColl 2001; Shady et al. 2004)). The possible influence of flicker from CFLs on various conditions was discussed in the previous SCENIHR opinion (2008). It was also noted that modulation of light from CFLs at 100 Hz was measured and this may be perceived under certain conditions (Khazova and O’Hagan 2008).

Flicker perception generally depends on the time dependence of the light emitted by a light source and on the circumstances of observation (motion, attention, saccadic eyeball motion, field of view, geometry of the incident light etc. ). Flicker has been been reduced considerably for fluorescent lighting with the implementation of 'flicker free' high frequency (kHz) ballasts operating at higher frequency (see also previous SCENIHR opinion). A residual modulation of the light intensity, however, with twice the power line frequency, can still occur if AC components of the supply voltage are insufficiently filtered by the power supply circuitry or by time averaging mechanisms inherent to the light generation. The frequency characteristics of the emitted light depends so strongly on specific engineering parameters, that general conclusions can not be drawn on one versus the other technology. There are lighting technologies available and installed (sodium lamps with ferromagnetic ballasts in street lighting) however, which emit considerably modulated light. This suggests that quality standards for lamps may be considered to set minimal requirements for light quality (intensity modulation, colour rendering, and other parameters in addition to energy efficiency). Regarding other lighting technologies, it was recently reported (IEEE 2010) that LED- generated light, for example, may undergo periodic fluctuations, flicker, with large amplitude (see also ANSES 2010). This light flicker is mainly due to the electronic power supply (driver) of the LED. It is always periodic and its fundamental frequency is similar to the power frequency fluctuation (which is twice the current variation frequency). Usually, LED drivers convert mains to DC current that supplies the LED. Good quality drivers (applicable to any lighting technology) use Power Factor Correctors (PFC, filters) that limit residual current fluctuation after AC/DC conversion to less than 10% of the root mean square current value. This residual power ripple can induce light flickering at a frequency that is two times higher than the mains (50 or 60 Hz depending on the country, inducing flicker of 100 or 120 Hz). Low quality LED drivers with passive power factor correction stages can be subject to higher fluctuation rates especially at low dimming levels and produce perceivable flicker (lamp switch on/off periodically). Furthermore a large proportion of LED drivers on the market use Power Wave Modulation (PWM) architecture in order to dim the light output. PWM uses short pulses at high frequency (several kHz) with variable duty cycle. Under these conditions, light fluctuation is expected at high frequency (twice the pulse frequency). Generally it is not expected that the end-user will observe any flicker, except for low quality products in very deep dimming situations. However, ambient flicker at imperceptibly high frequencies can penetrate the neural site for flicker adaptation, which is presumed to be in the primary visual cortex (Movshon and Lennie 1979). Indeed, earlier physiological studies have demonstrated activity in the human visual cortex in response to imperceptibleflicker frequencies (Regan 1968, Van der Tweel 1964), but these studies suggested no impact on perception as a result of this cortical activity. The IEEE work mentioned above (IEEE 2010) states that high frequency flicker can induce risks including headaches and eye- strain. The sources of high frequency flicker associated with headache include lighting (formerly principally lighting from gas discharge lamps) and computer screens (formerly cathode ray tube displays, now LED back-lights and lamps).

Various non-skin conditions (Irlen-Meares syndrome, myalgic encephalomyelitis, fibromyalgia, dyspraxia, autism, HIV), which are not otherwise considered in this opinion, were discussed in the SCENIHR opinion from 2008 (SCENIHR 2008). No additional data regarding the effects of CFLs on these conditions have been published since then. There is no scientific evidence linking these conditions to other lighting technologies. There is a need for additional experimental and epidemiological studies before final conclusions can be drawn regarding several of these conditions.


The previous SCENIHR opinion on Light Sensitivity stated that modern CFLs are basically flicker-free due to their electronic ballasts. However, it was also noted that studies indicated that hardly noticeable residual flicker can occur during certain conditions in both CFLs and incandescent bulbs. No further information has become available regarding CFLs and incandescent bulbs since then. Also LEDs are normally flicker-free, although it has been mentioned that some low quality products can produce perceivable flicker. Possibly, flicker of higher frequencies can influence the human visual cortex, although data on this are old and difficult to evaluate. More research on possible flicker emissions and subsequent health effects from CFLs, incandescent bulbs and LEDs seems thus to be warranted.

There is no scientific evidence available to evaluate if conditions such as Irlen-Meares syndrome, myalgic encephalomyelitis, fibromyalgia, dyspraxia, autism, and HIV are influenced by the lighting technologies considered in this opinion.

Source & ©: , Health effects of artificial light, 19 March 2012,
 3.6.3 Flicker, other conditions, pp. 69-71.

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