6. How and where are people exposed to artificial light?
The SCENIHR opinion states:
3.7. Exposure and health risk scenarios
3.7.1. Exposure situations in various indoor lighting settings
A proper risk assessment would include knowledge of the hazards involved, as well as knowledge about actual exposure. There are at present very few data available regarding personal exposures, with a few exceptions regarding occupational exposures to UV, which are also included in the discussion of the scenario presented in section 3.7.2, where a detailed “worst case scenario” of SCC incidence as a function of UV exposure from fluorescent lamps is presented. Due to the lack of knowledge regarding exposure, it has not been possible to perform any proper risk assessment of various environments with different types of lighting sources. Furthermore, in many cases, we also do not have data regarding disease incidence on the European or even the national level. Taken together, it was considered unrealistic to present further risk assessment scenarios. Based on available data, we here present a number of exposure situations, where the strength of some physical parameters is estimated according to their potential to trigger health impacts.
These exposure situations were chosen because at least one of the present parameters could pose a risk. For instance, most exposure situations in a household setting were ignored as they typically involve an illumination level of 50 lux, a level so low that exposure to potentially problematic radiation is considered negligible. Two types of health situations are included in Table 6 below; the global skin and eye exposure to the ambient light, and the direct eye exposure to blue light coming from a light source in the line of sight. These situations were chosen since they are realistic situations that are included in the health hazards considered in Standard EN 62471.
3.7.2. Worst case scenario of UV exposure of general population from indoor lighting in offices and schools
UV radiation from indoor lighting can potentially increase the risk and incidence of skin cancer. As reviewed in section 22.214.171.124, sunburns appear to contribute markedly to the risk of melanoma, and also to that of basal cell carcinoma. Although sunburns from ambient solar exposure are quite common, healthy individuals will not incur sunburns from exposures to indoor lighting, especially not with lamps in the exempt risk category (RG0). In combination with a UV-related risk from exposures limited to childhood years, melanoma risk is not likely to be notably affected by indoor lighting. This excludes any discernable impact on the mortality from skin cancer which is largely attributable to melanoma. Because the UV-related skin carcinomas are well treatable, any impact on skin carcinomas will mainly concern an increase in morbidity and add to the already increasing load on public health care from these skin cancers. Although accumulated doses from low level UV exposure may contribute to the risk of BCC, the data on risk and incidence of BCC need to be corrected for contributions from sunburn, e.g. by exclusion of BCCs occurring in intermittently exposed skin areas. Selection and analyses of data for a proper correction for sunburn is beyond the scope of this report, and we therefore refrain from including BCC, the most common skin cancer, in a risk assessment of the impact of UV radiation from indoor lighting. Here, we limit ourselves to a simplified straightforward risk analysis for the second most common skin cancer, squamous cell carcinomas (SCCs), in order to generate quantitative information on the potential worst case long-term impact of UV exposure from indoor lighting. Importantly, this scenario is based on the assumption that the risk over the short life- span of an experimental animal (mouse) can be used to extrapolate to 80 years in a human. It furthermore involves extrapolation from the dose levels in experimental studies to real human exposures, assuming a linear dose-response without a threshold e.g. due to the DNA repair pathways. A constant risk coefficient is applied, assumed to represent the entire population, without variability between individuals The accumulated solar UV exposure is the main exogenous determinant of the risk of SCCs of the skin. Although UV exposure rates from indoor lighting will be far lower than those from the summer sun, the steady low level daily exposures may add notably to the annually accumulated UV dose, especially exposures in well lit offices, schools, and public places such as malls etc. Modern lamps emit UV radiation at widely different levels. Although these levels commonly fall well below the emission limit of 2 mW actinic UV per klm (defining the Risk Group 0, "exempt from risk"), preventing acute effects, extensive exposures to some of these lamps may contribute significantly to the annual UV dose. Such exposures may result from lamps in open fixtures or luminaires with reflector and louvers. Glass covers will in general lower effective (erythemal) UV exposures to negligible levels. The risk model for SCC is basically simple, and is based on the average number of tumors that has occurred per individual at risk in a birth cohort of age “a” in absence of death. This number of tumors is referred to as the (tumor) yield, YLD(a), or cumulative hazard function. The yield can be written as a function of the accumulated effective UV exposure, total dose TD(a), and the age:
YLD(a) = (TD(a)/TD0)p1.(a/a0)p2 (1)
where TD0, a0, p1 and p2 are constants (de Gruijl and van der Leun 1991, de Gruijl and van der Leun 2002, Slaper et al. 1996), and on average p1 = 2.3 and p2 = 3.8 (NRPB 2002). As pointed out in the previous section 126.96.36.199, we can take the UV exposure spectrally weighted according to erythemal (sunburn) effectiveness (using the CIE erythemal action spectrum) as a proxy of the carcinogenic UV dose. If the first appearing SCCs occur independently of each other (valid in mice; de Gruijl and van der Leun 1991), the chance for a person of age “a” to have contracted an SCC is:
P(a) = 1 – e-YLD(a) (2)
And if the risk is small (YLD(a)<<1),
P(a) = YLD(a) (3)
For the age-specific incidence (the number of new cases per year per individual at risk of age “a”) we write
I(a) = d YLD(a)/da (4)
The overall incidence in a population (number of cases per year) over all age groups then becomes
I = ∫ I(a) n(a) da (5)
where n(a) is the age distribution in a population, for which we take the European standard population (http://eu-cancer.iarc.fr/5-glossary.html
; accessed 1 April 2011);
∫ n(a) da = 1.
For the following assessment we make the assumption that the contribution from indoor lighting to the risk has been negligible thus far. We then hypothetically add to existing solar UV exposures a regimen of maximum UV exposure from certain types of fluorescent lamps to assess a worst case impact. Considering the low level illumination and sparseness of direct exposure to fluorescent lamps in the homes, we restrict these additional UV exposures from fluorescent lighting to school days (6 h/day, 5 days/week and 40 weeks/year from 5 till 20 years of age) and working days as adults (8 h/day, 5 days/week and 48 weeks/year from 20 till 65 years of age). The fluorescent lamps can be either single-capped (such as single-ended tubes without integrated ballast) or double-capped (e.g. TL tubes). Based on this basic scenario, we can calculate what the increase in risk and incidence will be as a result of a certain increase in annual UV doses; see Table 7 below. One could simplify the calculations of increases in SCC incidences by assuming that the annual dose for everyone is increased by the same percentage (4th column of Table 6; a good approximationstratospheric ozone depletion, Madronich and de Gruijl 1993, Slaper et al. 1996). However, this does not appear to be a valid assumption for added annual doses of UV radiation from indoor lighting on school and working days. A more plausible approximation is that everyone receives about the same additional annual UV dose on top, and irrespective of, whatever annual dose they receive from sunpopulation. Here we assume that everybody persists in their sun exposure behaviour throughout life with a log normal distribution in annual personal solar UV doses close to the distribution observed in a Danish study (Thieden et al. 2004); with 95% in the range 3.3-fold over and unmedian (for the calculations the distributionuncocoionscoco
Table 7. Percent increase in SCC incidence and risk at 80 years of age due to certain added UV doses (from indoor lighting) to the annual UV dose in school and working years (added UV dose given as % of the annual solar UV dose)
Evidently, an increase of a few tenths of a percent in a small personal risk (0.02 for males, 0.013 for females) as presented in Table 6 is not very alarming for an individual. However, if such an exposure regimen occurs population-wide, the increase in incidence can result in a substantial number of additional cases per year. To this end, we consider the incidence (see legend of Table 8) in the Danish population of 5.8 million people, and find that it comes down to 900 new cases of SCC per year. Outdoor workers contribute to this incidence, but do not appear to run an increased risk in Denmark (Kenborg et al. 2010). As a simplification, we make no correction for outdoor workers. Hence, increases in incidence in the range of 0.9 to 19.0 percent from indoor exposure as given in the last column of Table 6 will add 8.7 to 170 additional cases of SCC per year in Denmark (this would add from 9 up to 190 additional cases annually for every 1,000 new cases that are diagnosed in Northwestern Europe).
As a next step, we want to consider the potential impact of commercially available fluorescent lamps on the number of cases of SCC. We had access to measurements on 17 double-capped and 61 single-capped fluorescent lamps (Schulmeister et al. 2011). In a conservative approach we assume light levels of 500 lux (common in well-lit offices) from double- or single-capped fluorescent lamps in ceiling-mounted open luminaires (i.e. no filters inserted) and the corresponding levels of erythemally effective UV exposures (expressed in mW/m2 and SED/h) for 6 h/day on school days and 8 h/day on working days as an adult (“full exposure”). However, these exposure levels pertain to a flat surface at desk top level; exposure to the backs of the hands will probably vary between 50 and 100% of this “full exposure” level, and to the face between 30 and 50% (except for designers and people performing fine assembly or repair work for whom levels may be closer to 1,000 lux and the source closer to hand and face). Moreover, the reflectors in luminaires commonly lower the ratio between UV and visible radiations (personal communication Dr. K. Schulmeister, Lytle et al. 1992-1993); we choose a reduction down to 60%. Combining the effects of reflectors and geometry of exposure we introduce a reduction to 30% of the ”full exposure” as a more realistic maximum level of exposure (“30% exposure” in Table 8). Thus, we computed the increased risks at 65 years of age, the increases in incidences and additional number of SCC cases per year in Denmark for double- and single-capped fluorescent lamps with high, median and low levels of UV output: see Table 8.
From Table 8 we conclude that a conjectural fluorescent lamp at the upper UV limit of the CIE/IEC exempt risk category (RG0) yields >342 additional SCC cases per year under these worst case scenarios. Fluorescent lamps on the market commonly fall well below this limit, but even these lamps well within the exempt category (RG0) with the highest UV output and TL tubes of median UV output still yield substantial numbers of additional cases (47 - 126126). The double-capped TL tubes lamps in general tend to have higher UV outputs at 500 lux than the single-capped ones. Based on these computations a restriction to a maximum increase in SCC incidence of 1% among indoor workers would amount to a maximum erythemal UV output of about 0.18 mW per klx (i.e. roughly corresponding with 0.05 mW actinic UV per klx; one fortieth of the upper limit of RG0). On the other hand, it should be realized that a nice sunny Mediterranean vacation of a week can add as a median some 50 SEDs to an annual dose, which under the present worst case scenario is equivalent to the estimated annual exposure in the office from a fluorescent lamp with 4.8 mW erythemal UV per klx (roughly 1.4 mW actinic UV per klx, just below the upper limit of RG0). The difference is, of course, that in the “vacation case” people deliberately expose themselves, whereas people are not aware of any UV exposure indoors, and may even assume themselves to be completely free from exposure to UV radiation. Moreover, not every indoor worker will acquire such added UV dosages from sunny holidays, whereas most indoor workers are inescapably subjected to the indoor lighting at work; i.e. the latter regimen is imposed on a large portion of the population, but it can be controlled to a large extent through limits on the UV emissions of the lamps.
In actual practice, exposure to fluorescent lamps will be lower than in the worst case scenarios presented here. To improve on these scenario studies we need actual data on indoor personal exposures. Nevertheless, these worst case scenario studies serve to indicate the potential impacts of these lamps on SCC numbers if these lamps dominated indoor lighting outside the home.
Note: Scenario with UV exposure from the fluorescent lamps during school years, 6 h/d, 5d/wk, 40 wks/y from 5 till 20 years of age, and during working days as an adult, 8 h/d, 5d/wk, 48 wk/y from 20 till 65 years of age; numbers in columns 2–5 pertain to full exposure to the lamps at 500 lux; annual dose in SEDs stated under “30% exposure” is a more realistic maximum exposure from working days than at full exposure; the first row under “sources” represents a hypothetical fluorescent lamp at the upper UV limit of the exempt risk category, RG0, according to CIE/IEC standardization. # Overall risk at 65 yrs of age scales to 0.0057 for males and to 0.0036 for females in Denmark, and equals 0.26 for males and 0.17 for females in Australia in 2002 (Staples et al. 2006).
**Not calculated for median solar exposure, but risk estimated from actual cumulative (age- specific) incidence in the white Caucasian population of Australia (Staples et al. 2006).
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