DOI: 10.1111/exd.
12393
www.wileyonlinelibrary.com/journal/EXD
The maximal cumulative solar UVB dose allowed to maintain
healthy and young skin and prevent premature photoaging
Masamitsu Ichihashi1,2 and Hideya Ando3
1
Sun Care Institute, Osaka, Japan; 2Saiseimirai Clinic Kobe, Kobe, Japan; 3Department of Applied Chemistry and Biotechnology, Okayama
University of Science, Okayama, Japan
Correspondence: Masamitsu Ichihashi, Saiseimirai Clinic Kobe, Kobe Commerce, Industry and Trade Center Building 23F, 5-1-14 Hamabedori
Chuo-ku, Kobe 651-0083, Japan, Tel.: 81-78-862-1101, Fax: 81-78-862-1102, e-mail: mm_ichihashi@hotmail.com
Abstract: The young facial skin of children with a smooth healthy
appearance changes over time to photoaged skin having mottled
pigmentation, solar lentigines, wrinkles, dry and rough skin,
leathery texture, and benign and malignant tumors after exposure
to chronic, repeated solar radiation. The first sign of photoaging
in Japanese subjects is usually solar lentigines appearing around
20 years of age on the face. Fine wrinkles can then appear after
30 years of age, and benign skin tumors, seborrhoeic keratoses,
can occur after 35 years of age in sun-exposed skin. We
theoretically calculated the maximal daily exposure time to solar
radiation, which could prevent the development of photoaged
skin until 60 and 80 years of age, based on published data of
personal solar UVB doses in sun-exposed skin. One MED
(minimal erythema dose) was determined to be 20 mJ/cm2, and
200 MED was used as the average yearly dose of Japanese
children. Further, we hypothesized that the annual dose of
Japanese adults is the same as that of the children. The cumulative
UVB dose at 20 years of age was thus calculated to be 4000 MED,
and 22 MED was used as the maximal daily UVB dose based on
data measured in Kobe, located in the central area of Japan. We
used the solar UVB dose from 10:00 a.m. to 14:00 p.m. which
Introduction
The ageing of human skin is caused by genetic and environmental
factors, which disturb the functions and structure of epidermal and
dermal cells and extracellular matrix components. Among environ-
mental factors, solar ultraviolet (UV) B radiation (290–320 nm)
and UVA radiation (320–400 nm) are the most harmful ones, as
chronic exposure to solar radiation is known to induce skin photo-
aging. Skin photoaging is characterized by the development of pig-
mentary disorders, such as solar lentigines, as well as and wrinkles
and benign, premalignant and malignant skin tumors on sun-
exposed skin (1–6). These skin alterations due to repeated chronic
solar UV exposure are mostly caused by solar UV-induced DNA
damage of epidermal cells in each exposure. Most DNA damage is
repaired by functional repair systems of cells, but only about 50% of
cyclobutane pyrimidine dimers produced by a single UVB irradia-
tion is repaired during the first 24 h (7). Therefore, the mutation
rate may increase in some cells after repeated exposure to high doses
of UV, possibly due to ‘The rule of A’ operating in DNA synthesis at
the sites where DNA damage remains unrepaired (8).
Life-span is extending steadily in developed countries, and aged
individuals over 70 years of age now occupy 20–30% of the popu-
ª 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
Experimental Dermatology, 2014, 23 (Suppl.1), 43–46
Review
occupies 60% of the total daily UV dose, to obtain the maximal
UVB per hour in a day, and calculated the maximal daily UV
exposure time that would delay the onset of solar lentigines until
60 or 80 years of age. The mean daily sun exposure time to
maintain healthy skin until 80 years of age in the summer was
calculated to be 2.54 min (0.14 MED) for unprotected skin and
127 min with the use of a sunscreen of SPF (sun protection
factor) of 50. In this study, we did not evaluate the photoaging
effect of UVA radiation, but findings of the adverse effects of
UVA radiation on the skin have accumulated in the last decade.
Therefore, it will be important to estimate the maximal dose of
solar UV radiation to retard the onset of photoaging based on an
evaluation of both solar UVB and UVA in the future. Finally, we
expect that this study may contribute to keeping Japanese and
other types of skin young and healthy by limiting the exposure of
the skin to solar radiation outdoors during the day.
Key words: cumulative dose – minimal erythema dose – photoaging –
solar lentigine – solar ultraviolet light – ultraviolet light protection
Accepted for publication 24 March 2014
lation in many countries. It is ideal for aged persons to work
healthily and actively among young people with young skin and
contribute to the public as active citizens as long as possible. The
first sign of photoaging of the skin develops around 20 years of
age in Japanese, with a slight earlier trend of photoaging skin in
people who live in southern parts where annual sunlight is higher
than in northern parts of Japan (9). The first signs of photoaging
in Japanese are usually pigmented spots, particularly in Asians
having moderate melanin contents in the epidermis. Secondly,
fine wrinkles appear after 30 years of age. Benign skin tumors,
seborrhoeic keratosis, usually occur after 35 years of age among
Japanese.
We aimed to theoretically calculate the maximal daily and
yearly solar UVB dose acceptable that would prevent and retard
the onset of photoaging until 60 and 80 years of age, based on
published data reporting the daily and yearly solar UV doses, mea-
sured for a limited term or calculated from the outdoor activity
information, to which children, teenagers and adults are exposed
(10). We calculated the daily and yearly cumulative dose as mini-
mal erythema dose (MED). Further, we propose a maximal expo-
sure time per day and per year to solar radiation, with and
43

Ichihashi and Ando
without the use of high SPF- and PA-sunscreens to retard the first
sign of photoaging until the age of 80.
Determination of one MED, and cumulative solar
UV dose until the first onset of photoaging
In the beginning, we calculated the lifetime cumulative solar UV
dose of Japanese subjects, based on the results reported by Ono
et al. (10), because it is well recognized that the personal solar UV
exposure dose directly measured by chemical, physical or biologi-
cal procedures is the best way to evaluate UV effects on human
skin in relevance to dose response. We determined 200 MED to
be the average yearly dose of Japanese, based on the results of
Ono et al. Further, we used 20 mJ/cm2 as one MED, based on a
few reasons: firstly, one MED of Japanese is distributed from 20
to 60 mJ/cm2 (15–50 min exposure at midday in the summer)
depending on the Japanese skin phototype (11); secondly, Ono
et al. estimated one MED for Japanese, based on their measure-
ment, to be 20 mJ/cm2.
Ono et al. (10). measured the solar UVB dose of Japanese chil-
dren aged 11 and 12 years using UV colouring labels attached on
their shirts at the upper arm in the morning for the entire day for
seven consecutive days at each of the four seasons. They then esti-
mated the yearly UV dose using outdoor activity records of chil-
dren and UV irradiance at monitoring stations. Further, we used a
report by Thieden et al. (12). showing that there are no significant
differences in UV dose among the age groups of children, teenag-
ers and adults in Danish volunteers. There is a high variation of
annual UV radiation between Japan and Holland, and the daily
life style of Japanese adults exposing their skin to sunlight may
not be exactly the same as that of Danish people. We hypothesized
that Japanese adults receive an annual solar UV dose at the same
rate throughout their lifetime, and calculated the cumulative dose
until 20, 60 and 80 years of age. Based on these assumptions, a
cumulative solar UVB dose estimated at 20 years of age when the
first solar lentigine usually develops was as follows; 200 MED/
year 9 20 years = 4000 MED.
Further, we determined the maximal cumulative solar UVB
dose needed to maintain young skin until an older age based on
two hypotheses as follows: A linear regression line obtained in an
epidemiological study on the effect of solar radiation on the
development of photoaging, pigmented spots and wrinkles, which
was seen on the face of females who live in Kagoshima city
(located in the southern part of Japan) and Akita city (located in
the northern part of Japan) where annual solar radiation is
around 60% that of Kagoshima city, indicated that pigmented
spots usually first appear around 20 years of age in both cities.
Pigmented spots seem to develop earlier in Kagoshima, but a
detailed analysis of the age of first appearance of pigmented spots
was not carried out in that study (2). Further, based on our clini-
cal observations of patients who visited our clinic with a com-
plaint of pigmentary disorders, we speculated that the first sign of
photoaging is solar lentigines that appear around 20 years of age
in Japanese females.
Determination of maximal daily UV dose
Next, we determined the maximal daily UVB dose based on data
measured among four locations in Japan from 1996 to 2009 by
the Japan Meteorological Agency (13). The maximal daily dose
was 7 KJ/m2 recorded in Kagoshima in June, 1996, which is calcu-
lated as 35 MED/day and 5.25 MED/h from 10:00 a.m. to 14:00
44
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p.m. These were extremely high compared with other data in each
year of the same term at different Japanese locations. The maximal
MED/day in Tsukuba (located nearest to Tokyo among the four
stations) was 30.83 KJ/m2, equal to 15.4 MED, recorded in July
2001. Further, the maximal daily UVB dose measured in Kobe
between 1991 and 2001, using a Burger Meter was 22.0 MED in
July, 1994. Considering these data, we used 22 MED as the maxi-
mal daily UVB dose in this study as Kobe is located nearly in the
central area of Japan.
Proposal of recommended maximal yearly and
daily UVB dose to retard the onset of photoaging
Recommended maximal yearly doses to retard the onset of solar
lentigines until 60 and 80 years of age were calculated as follows:
4000 MED  60 years = 66.7 MED (until 60 years of age) and
4000 MED  80 years = 50 MED (until 80 years of age).
The maximal daily MED to keep young and healthy skin with-
out solar lentigines until 60 and 80 years of age was then calcu-
lated as follows:
66.7 MED/year  365 days = 0.18 MED for 60 years, and 50
MED/year  365 days = 0.14 MED for 80 years of age.
Next, the MED was converted to the daily exposure time subjects
were allowed to spend outdoors in midday in clear summer radiat-
ing the strongest solar UVB flux. As around 60% of the daily maxi-
mal dose of 22 MED is delivered during the 4 h from 10:00 to 14:00,
we can calculate the UVB dose/ hr as follows; 22 MED 9 0.6 
4 = 3.3 MED. Therefore, the outdoor life time (9) allowed (OLTA)
during a day near noon in the summer is calculated as follows: 3.3
MED: 0.18 MED = 60 min: 9, 9 = 3.27 min (60 years of age) and
3.3 MED: 0.14 MED = 60 min: 9, 9 = 2.54 min (80 years of age).
In the spring (March and April) and autumn (October and Novem-
ber) season, the daily maximal dose is fixed as 1/2 of the summer
season; therefore, the OLTA during a day is calculated to be
3.3 min 9 2 = 6.6 min (60 years) and 2.54 9 2 = 5.8 min
(80 years), and in the winter season (December, January, February),
the OLTA per day is calculated to be 3.27 min 9 5 = 16.3 min
(60 years) and 2.54 min 9 5 = 12.7 min (80 years) (Table 1).
Sunscreen can change our outdoor lifestyle in
sunny midday
The mean daily sun exposure time allowed to keep young skin
until 80 years was calculated to be from 2.54 min in the summer
and 12.7 min in the winter, which is too short to spend a com-
fortable outdoor life even in the winter. Therefore, we estimated
the time for outdoor life when people use a sunscreen with a
high SPF. When people use a sunscreen with an SPF of 50, they
will be able to work and play outdoors for nearly 2 h, even in
the middle of clear summer days near noon, as shown in the
following:
The maximal UV exposure time/day is 3.27 min for keeping
young skin until 60 years of age, is extended to 163 min/day
(3.27 min 9 50 = 163 min), and for people who want to delay
the onset of solar lentigines until 80 years of age, the 2.54 min is
extended to 127 min/day (2.54 MED 9 50 = 127 min). 163 and
127 min exposure may be long enough for Japanese outdoor
sports, such as football or beach volleyball, even though these are
times allowed at the time of the strongest UVB flux. Therefore,
our results suggest that we are able to spend more than 2 or 3 h
outdoors even on clear days in the summer in Japan with the use
of sunscreens having a high SPF.
ª 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
Experimental Dermatology, 2014, 23 (Suppl. 1), 43–46

Table 1. Recommended daily solar UVB dose and time delay to the onset of solar lentigine with age
Solar UVB dose/year
Onset of solar
lentigine
2 2
(year of age) J/m MED
20 40 000 200
60 13 333 66.7
80 5000 50
Daily time recommended for keeping skin without solar lentigines, the first sign of photoaging of the skin among Japanese females, was calculated based on the 200
MED and solar UVB dose of 40 000 J/m2 which were accumulated till 20 years of age when the first solar lentigine appears. 200 MED and 40 000 J/m2 were used as
the minimal dose to produce solar lentigines, and the daily allowed exposure time till 60 and 80 years of age between 10:00 a.m. and 14:00 p.m. was calculated and is
2.54 and 3.27 min, respectively.
Importance of anti-ageing on the appearance of
facial and other sun-exposed skin
The average lifespan of Japanese is 86.39 years of age for females
and 79.64 years of age for males, according to a national survey in
2012, and is expected to extend to an older age in the near future,
possibly due to the ideal health insurance system of Japan that
covers the entire Japanese population. The aged are expected to
live by themselves without any help from others, as long as possi-
ble, but at present, they need some help from others during the
last 7 years before their death, due to their inability to conduct
their own activities required for their daily lives, including cook-
ing, washing, cleaning and visiting hospitals for their medical care.
Anti-ageing medicine is well recognized in Japan to be essential to
allow the aged population to live healthily and happily as active
members of society. Anti-ageing medicine also aims to make peo-
ple keep young and healthy skin without photoaging until they
are older (14). In this study, we propose a maximal exposure time
allowed for outdoor life per day and per year to keep young and
healthy skin without pigmented spots, wrinkles and skin tumors
until 60 and 80 years of age, based on assumptions and data
reported by other research groups and our own data. The time
allowed for exposure per day to retard the onset of the first
photoaging skin sign, solar lentigines, until 80 years of age is
2.54 min around noon, in the summer, which is extremely short
for comfortable outdoor life and sports. However, we are able to
extend the time that can be spent outdoors playing sports and
working more than one hr, even around noon time in the middle
of the summer by simply applying a sunscreen with a high SPF.
In the winter, as average daily UV dose decreases roughly to 1/4–
1/5 that of the summer, so people are able to spend several hr
outside in the sunshine if they use a proper sunscreen. Even in
the summer, we can spend a few hours under sunlight before 10
a.m. and after 2 p.m., when the UV flux is low compared with the
time in the middle of the day.
Future study: determination of maximal daily
exposure time to solar radiation evaluating the
UVA and infrared radiation effects on photoaging
In this study, we did not evaluate the role of solar UVA radiation
in photoaging, but UVA has been shown to induce human skin
darkening by polymerization of monomer melanin, such as di-
hydroxy-indole carboxylic acid (DHICA), by H2O2 produced
within 24 h after exposure to UVA (15). Further, UVA has been
reported to induce reactive oxygen species in human keratinocytes
by the activation of NADPH (nicotinamide adenine dinucleotide
ª 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
Experimental Dermatology, 2014, 23 (Suppl. 1), 43–46
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Maximal cumulative UVB dose to prevent photoaging
Solar UVB dose/day Time/day around noon (min)
With
Without sunscreen
J/m MED sunscreen of SPF 50
109.6 0.55 10.16 508
36 0.18 3.27 163.5
28 0.14 2.54 127
phosphate) oxidase, which stimulates PGE2 (prostaglandin E2)
synthesis, leading to skin inflammation (16). UVA occupies more
than 90% of solar UV radiation that reaches the surface of the
earth and has been shown to produce DNA damage in the form
of cyclobutane pyrimidine dimers (CPD) and oxidized bases,
which may also contribute to the development of pigment spots
and skin tumors (17,18). In addition, UVA is thought to be highly
immunosuppressive and has been shown to have interactive effects
on the immune system with UVB radiation (19,20), because the
UVA dose at the surface of the earth is 20–50 times higher than
that of UVB, and it penetrates window glass and skin, even if a
high SPF sunscreen is applied. In addition, melanin bound with
lipid peroxides becomes darker, and keratinocytes with melanin-
oxidized lipid complexes are reported to detach more slowly from
the basal layer, leading to delayed epidermal turnover, which
results in increased levels of melanin pigment formation. There-
fore, the maximal dose of solar radiation necessary to retard the
onset of photoaging and skin cancer development based on the
detailed evaluation of both UVB and UVA needs to be determined
in the future.
Wrinkle formation is understood to be caused by the acceler-
ated degradation and resulting decrease in collagen and elastic
fibres due to increased protease activities of matrix metallopro-
teinases (MMPs), which are triggered by reactive oxygen species
produced by solar UVB and UVA radiation (21,22). DNA damage
is reported to be involved in the upregulation of MMP mRNA
levels (23), but the precise role of DNA damage in the control of
MMPs is not yet clear.
Recently, infrared A radiation was shown to be one factor that
induces wrinkles by increasing mRNA and protein levels of MMPs
following the generation of reactive oxygen species (24,25). In the
future, the role of infrared A radiation on the development of
solar lentigines has to evaluated, because it occupies more than
59% of the solar radiation that reaches the earth’s surface.
Proposal of the mechanism of solar lentigine
development
We propose that pigmented spots are possibly caused by gene
mutations related to melanogenesis, as patients with xeroderma
pigmentosum (XP) (14) who have mutations in genes essential to
repair CPD, the most common type of DNA damage produced by
UV, develop solar lentigines around 5 months of age after a few
sunburns caused by exposing the skin only several min for each
sunbathing, and benign tumors develop on the face around 1 year
of age, but no wrinkles develop during childhood (Fig. 1). In
45
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Ichihashi and Ando

KC of normal UVB KC of solar lentigine

ET-1
ET-1
N N
Keratinocyte
SCF Keratinocyte
SCF
KGF/KGFR
αMSH

Melanocyte

Figure 2. Mechanisms of solar lentigine formation in skin chronically exposed to

Figure 1. A 6-month-old baby with xeroderma pigmentosum (XP) having a
number of pigmented spots on the face after a few sunbathing exposures. The
patient was diagnosed clinically with XP, as the baby developed a severe sunburn
each time after a short sun exposure, and was confirmed to have a mutation in his
XPA gene.
healthy subjects, on the other hand, solar lentigines develop
around 20 years of age as mentioned previously (9). Aoki et al.
(26) showed the upregulation of tyrosinase related protein-1
(TRP-1) at the basal layer of solar lentigo skin of healthy Japanese,
but they did not clarify the mechanism of the continued hyper-
melanosis in solar lentigines due to TRP-1 upregulation. Further,
to prove our hypothesis that solar lentigines are caused by gene
mutations of keratinocytes and /or melanocytes, we must demon-
strate mutations of genes relevant to melanogenesis in cells, possi-
bly keratinocytes, which are located in the pigmented spots
(Fig. 2).
Contribution of DNA damage during childhood to
photoaging
In addition, high dose exposure to sunlight during childhood
under 10 years of age has been shown to increase the incidence of
skin cancer in Caucasians (27). Further, the rate of gene mutations
in cells undergoing DNA synthesis is shown to increase by the rule
of ‘A’, substitution of C to T, after two divisions (8). The rule of
‘A’ must take place more frequently in cells of children in whom
DNA synthesis occurs more frequently than in adult cells, since
about 0.3 billion cells, the total cell number of a baby at birth
solar radiation. A stem cell of epidermal keratinocytes may have a mutation in the
promoter regions of genes that affect melanogenesis, such as stem cell factor
(SCF), endothelin-1 (ET-1) and a-MSH (a-melanocyte stimulating factor), after
chronic solar UV exposure. This may result in a cell that produces an increased
level of one or more of these factors even after a single solar UV radiation. The
mutated stem cell proliferates and produces transit amplifying cells, which have the
same mutation as the stem cell, and may induce abnormally high levels of gene
expression, stimulating melanocytes to produce abundant amounts of melanin,
resulting in large amounts of melanosome transfer to surrounding keratinocytes,
making pigmented spots called solar lentigines.
(including the skin) continues to increase in number to about
6 billion cells in an adult.
In the present study, we did not evaluate the effects of UVB
and UVA in photoaging during childhood, particularly in children
under 10 years of age, as we have no reliable data of the daily and
yearly sun exposure dose of Japanese children under 10 years of
age.
Conclusions
Finally, we expect that the present study, which proposes a maxi-
mal exposure dose and time to solar radiation per day and per
year, may contribute to Japanese and other types of skin having a
similar melanogenic activity to provide information to public edu-
cation campaigns to try to change behaviour and reduce exposure
to UV to maintain young and healthy skin as we age.
Conflict of interest
The authors have no conflicts of interest that are directly relevant to the
content of this article.

References
1 Monestier S, Gaudy C, Gouvernet J et al. Br J
Dermatol 2006: 154: 438–444.
2 Akiba S, Shinkura R, Miyamoto K et al. J
Epidemiol 1999: 9 (Suppl.): S136–S142.
3 Ueda M, Matsunaga T, Bito T et al. Photoderma-
tol Photoimmunol Photomed 1996: 12: 22–26.
4 Warren R, Gartstein V, Kligman A M et al. J Am
Acad Dermatol 1991: 25: 751–760.
5 Fisher G J, Wang Z Q, Datta S C et al. N Engl J
Med 1997: 337: 1419–1428.
6 Ichihashi M, Ueda M, Budiyanto A et al. Toxicol-
ogy 2003: 189: 21–39.
7 Young A R, Orchard G E, Harrison G I et al. J
Invest Dermatol 2007: 127: 975–978.
8 Taylor J S. Mutat Res 2002: 510: 55–70.
9 Hillebrand G G, Miyamoto K, Schnell B et al. J
Dermatol Sci 2001: 27 (Suppl. 1): S42–S52.
10 Ono M, Munakata N, Watanabe S. Photochem
Photobiol 2005: 81: 437–445.
11 Kawada A. Photodermatol 1986: 3: 327–333.
12 Thieden E, Philipsen P A, Standy-Moller J et al. J
Invest Dermatol 2004: 123: 1147–1150.
13 Annual Report of Ozone Layer Monitoring.
2008. Japan Meteorological Agency March
2009. Maximal daily cumulative UVB dose and
monthly mean daily UVB dose at Sapporo, Tsu-
kuba, Kagoshima, Naha and Syowa Station,
Antarctica.
14 Ichihashi M, Ando H, Yoshida M et al. Anti-
Aging Med 2009: 6: 46–59.
15 Maeda K, Hatao M. J Invest Dermatol 2004:
122: 503–509.
16 Valencia A, Kochevar I E. J Invest Dermatol
2008: 128: 214–222.
17 Rochette P J, Therrien J P, Drouin R et al.
Nucleic Acids Res 2003: 31: 2786–2794.
18 Ikehata H, Kawai K, Komura J I, et al. J Invest
Dermatol 2008: 128: 2289–2296.
19 Stapelburg M P F, Williams R B H, Byrne S N
et al. J Invest Dermatol 2009: 129: 2694–2701.
20 Poon T S, Barnetson R S, Halliday G M. J Invest
Dermatol 2005: 125: 840–846.
21 Kang S, Fisher G J, Voorhees J J. Clin Geriatr
Med 2001: 17: 643–659.
22 Fisher G J, Kang S, Varani J et al. Arch Dermatol
2002: 138: 1462–1470.
23 Dong K K, Damaghi N, Picart S D et al. Exp
Dermatol 2008: 17: 1037–1044.
24 Kim M S, Kim Y K, Cho K H et al. Mech Ageing
Dev 2006: 127: 875–882.
25 Schroeder P, Lademann J, Darvin M E et al. J
Invest Dermatol 2008: 128: 2491–2497.
26 Aoki H, Moro O, Tagami H et al. Br J Dermatol
2007: 156: 1214–1223.
27 Kricker A, Armstrong B K, English D R. Cancer
Causes Control 1994: 5: 367–392.

ª 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
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