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The Journal of Clinical Endocrinology & Metabolism 87(11):4952– 4956
Copyright © 2002 by The Endocrine Society
doi: 10.1210/jc.2002-020636
Effects of Above Average Summer Sun Exposure on
Serum 25-Hydroxyvitamin D and Calcium Absorption
M. JANET BARGER-LUX
AND
ROBERT P. HEANEY
Creighton University, Omaha, Nebraska 68131
The purpose of this study was to examine the effects of summer sun exposure on serum 25-hydroxyvitamin D [25(OH)D],
calcium absorption fraction, and urinary calcium excretion.
Subjects were 30 healthy men who had just completed a summer season of extended outdoor activity (e.g. landscaping,
construction work, farming, or recreation). Twenty-six subjects completed both visits: after summer sun exposure and
again approximately 175 d later, after winter sun deprivation.
We characterized each subject’s sun exposure by locale,
schedule, and usual attire. At both visits we measured serum
25(OH)D, fasting urinary calcium to creatinine ratio, and calcium absorption fraction. Median serum 25(OH)D decreased
from 122 nmol/liter in late summer to 74 nmol/liter in late
I
T HAS BEEN recognized for some time that at temperate
latitudes serum 25-hydroxyvitamin D [25(OH)D] exhibits an annual cyclic variation, with a peak in late summer and
a nadir in late winter. This variation is generally considered
to be due to a corresponding variation in the amount of UV-B
radiation reaching the skin in summer and winter months.
Webb et al. (1) have reported that at latitudes above 40° (north
or south), photoconversion of 7-dehydrocholesterol to previtamin D does not occur in winter months, and that as
latitude rises, even summer synthesis is blunted. A single
session of solar radiation to the whole body, just sufficient to
produce erythema, yields about 10,000 IU (250 ␮g) vitamin
D3 (2, 3). What is not known is the quantitative total input of
vitamin D from the skin on a daily basis at any time of year,
but particularly during the summer.
Seasonal variation in 25-hydroxyvitamin D [25(OH)D] has
been associated with an opposite cycle of serum PTH and a
directly parallel annual cycle of lumbar spine bone mineral
density in healthy young adults (4). In healthy older women,
similar seasonal patterns for 25(OH)D and PTH have been
reported (5) as well as seasonal fluctuations in bone mineral
density at both spine and hip (6). However, not all who have
looked for such effects have found them.
Reid et al. (7) measured the urinary calcium to creatinine
ratio, strontium (a surrogate for calcium) absorption, and
other variables in frail elderly nursing home residents before
and after 4 wk of limited sun exposure. To our knowledge,
however, no one has reported seasonal differences in the
classical vitamin D functions in healthy, nonelderly adults.
The purposes of the study reported here were 1) to estimate the magnitude of seasonal difference in 25(OH)D
among subjects with above average summer sun exposure,
Abbreviations: BSA, Body surface area; 25(OH)D, 25-hydroxyvitamin D.
winter. The median seasonal difference of 49 nmol/liter (interquartile range, 29 – 67) was highly significant (P < 0.0001).
However, we found only a trivial, nonsignificant seasonal difference in calcium absorption fraction and no change in fasting urinary calcium to creatinine ratio. Findings from earlier
work indicate that our subjects’ sun exposure was equivalent
in 25(OH)D production to extended oral dosing with 70 ␮g/d
vitamin D3 (interquartile range, 41–96) or, equivalently, 2800
IU/d (interquartile range, 1640 –3840). Despite this input, at
the late winter visit, 25(OH)D was less than 50 nmol/liter in 3
subjects and less than 75 nmol/liter in 15 subjects. (J Clin
Endocrinol Metab 87: 4952– 4956, 2002)
2) to determine whether these changes are associated with
differences in calcium absorption fraction or urinary calcium
excretion, and 3) when combined with results from earlier
work, to quantify the vitamin D input from summer sun
exposure.
Subjects and Methods
The research protocol, including written informed consent, was approved by the Creighton University institutional review board. We
recruited 30 healthy men who had just completed a summer season of
extended outdoor activity (e.g. landscaping, construction work, farming,
or recreation). We excluded candidates with current medications or
diagnoses known to affect calcium absorption or vitamin D metabolism.
For each subject we scheduled 2 visits, to mark the approximate end
of summer sun exposure (visit 1, in late summer, August 3 to September
2) and the end of winter sun deprivation (visit 2, late in the following
winter, February 1 to March 20). By the time of the second visit, 1 subject
had been lost to follow-up, and 3 others reported having spent extended
periods during the winter in warm, sunny locales; we did not retest these
subjects. Between-visit intervals for the 26 subjects who completed both
visits ranged from 158 –227 d.
Visit 1 included interviews to characterize each subject’s summer sun
exposure in terms of locale, length of outdoor work or recreation season,
usual weekly schedule, sunscreen use, and usual outdoor attire. Table
1 outlines our adaptation of the “rule of nines” for representing adult
body surface area (BSA) to estimate usual skin exposure according each
subject’s combination of shirt, pants, and hat.
We also generated an index combining a measure of time outdoors
during daylight and BSA usually exposed during that time, where sun
index ⫽ hours of sun exposure per week ⫻ fraction of BSA exposed to
sunlight. At both visits, a single observer also used a cosmetic color chart
to record the skintone of sun-exposed areas on a nine-point ordinal scale
ranging from lightest to darkest (i.e. 0 – 8), with half-point values for
intermediate readings.
Both visits included collection of fasting serum for 25(OH)D and 2-h
fasting urine for calcium and creatinine; the urine samples were collected
after an overnight fast without water restriction. For each subject, we
calculated seasonal difference in 25(OH)D by subtracting late winter
from late summer values, and used this figure as an estimate of summer
increment. We measured serum 25(OH)D by use of a competitive bind-
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Barger-Lux and Heaney • Summer Sun Exposure and 25-Hydroxyvitamin D
J Clin Endocrinol Metab, November 2002, 87(11):4952– 4956 4953
TABLE 1. BSA exposed to sunlight
Adapted
“rule of nines”a
Category 1
Category 2
No shirt
Long-sleeved shirt
Short-sleeved shirt
Both arms
Both legs
Anterior trunk
Posterior trunk
Head
Perineum
0.18
0.36
0.18
0.18
0.09
0.01
0.18
0.04
0.14
0.09
0.09
0.00
0.00
0.00
0.00
Column totals
1.00
0.36
0.04
0.14
Category 3
Short pants
Long pants
0.24
0.00
0.00
0.00
0.00
0.00
0.00
0.00
0.24
0.00
No hat
Hat
0.07
0.03
0.07
0.03
a
The “rule of nines” estimates sectors of adult BSA as percentages that are multiples of 9. (See standard texts dealing with burn assessment.)
We adapted this rule to estimate fraction of BSA exposed to sunlight by each subject’s usual outdoor attire, where attire consisted of one selection
from each of three categories.
ing assay with a tritium-labeled ligand (Nichols Institute Diagnostics,
San Juan Capistrano, CA), urinary calcium by atomic absorption spectrophotometry (Perkin-Elmer, Norwalk, CT), and urinary creatinine by
an automated analysis system (Express Plus, Ciba Corning, Inc., Medfield, MA).
Calcium absorption was measured as absorption fraction by use of a
5-h single isotope method described previously (8, 9). This method
measures total absorption, both active and passive, and has been shown
to yield the same results as produced by classical balance methods
adjusted for endogenous fecal calcium losses (10). The calcium load was
7.5 mmol, given as calcium-fortified orange juice and labeled with approximately 324 kBq (equivalent to 8.75 ␮Ci) 45Ca, contained in a submicrogram quantity of high specific activity 45CaCl2 (Amersham Pharmacia Biotech, Arlington Heights, IL). The sd of the difference between
replicate measurements in the same individual with this method is 0.042.
With paired measurements for 26 individuals, we had a 90% likelihood
of finding a difference of as little as 0.027.
We used CRUNCH software (version 4.04, CRUNCH Software,
Oakland, CA) to describe the data, test for differences, and examine
relationships.
Results
Table 2 describes the subjects in terms of age and body size
and presents baseline values for the main variables. Table 3
summarizes the data collected at visit 1 characterizing the
subjects’ summer sun exposure; median exposure values for
the group were a 16-wk season of 38 h/wk.
TABLE 2. Characteristics of participants at entrya
Age (yr)
Height (m)
Weight (kg)
Body mass index (kg/m2)
25-hydroxyvitamin D (nmol/liter)
Fasting urine Ca/creatinine (mmol/mmol)
Calcium absorption fraction
a
As Table 4 shows, median serum 25(OH)D decreased from
122 nmol/liter in late summer to 74 nmol/liter in late winter.
The median seasonal difference of 49 nmol/liter (interquartile range, 29 – 67) was highly significant (P ⬍ 0.0001). There
was a strongly positive relationship between late summer
and late winter values for serum 25(OH)D (r ⫽ 0.8197;
P ⬍ 0.0001).
Figure 1 displays individual changes in serum 25(OH)D.
At the late winter visit, 25(OH)D was less than 75 nmol/liter,
a putative lower limit of repletion, in half (13 of 26) of the
subjects. The lowest values at the 2 visits (50 and 24 nmol/
liter, respectively) occurred in the subject whose natural skin
color (as reflected in late winter skintone) was the darkest
that we recorded (i.e. 7 on our skintone scale). For the group
as a whole, median skintone of 3.8 in late summer had faded
to a median of zero by late winter; this seasonal difference in
skin color was also highly significant (P ⬍ 0.0001).
We also examined the relationships between three measures of sun exposure and the summer increment in
25(OH)D. Table 5 shows the relationships of weekly hours of
Data as median (interquartile range).
TABLE 3. Conditions of summer sun exposurea
Length of sun exposure season (wk)
Sun exposure per week (h)
Total summer sun exposure (h)
Fraction of BSA exposed to sunlight
Sun indexc
16 (14 –17)b
38 (22– 42)
544 (332– 660)
0.41 (0.28 – 0.45)
11.5 (6.7–18.1)
n ⫽ 30.
Data as median (interquartile range).
Hours of sun exposure per week ⫻ fraction of BSA exposed to
sunlight.
a
b
c
TABLE 4. Seasonal variation in serum 25(OH)D
Late summer 25(OH)D (nmol/liter)
Late winter 25(OH)D (nmol/liter)
Seasonal difference in 25(OH)D (nmol/liter)
a
Seasonal differences in serum 25(OH)D and skintone
26 (23– 41)
1.80 (1.75–1.84)
83.7 (71.9 –93.7)
25.4 (23.3–28.3)
122 (100 –154)
0.28 (0.19 – 0.36)
0.28 (0.25– 0.31)
122 (95–154)a
74 (60 –94)
49 (29 – 67)
Data as median (interquartile range).
sun exposure, sun-exposed BSA, and sun index to late summer 25(OH)D and summer increment. Figure 2A plots each
subject’s summer increment in 25(OH)D against his sunexposed BSA; the relationship was such that for every percentage of BSA exposed to sunlight by these subjects, the
summer increment of 25(OH)D was greater by about 0.84
nmol/liter. Figure 2B presents the same relationship, using
the sun index as the independent variable; for every sun
index unit, the summer increment was greater by about 0.45
nmol/liter.
Seasonal differences in calcium absorption fraction and
urinary calcium excretion
Our data showed only a trivial, nonsignificant seasonal
decline in calcium absorption fraction (– 0.010; range, – 0.045
to ⫹0.027) and no change in fasting urinary calcium to creatinine ratio (0.00; range, – 0.10 to ⫹0.06 mmol/mmol). However, within individuals, these variables were highly correlated: there were significant relationships between late
summer and late winter values for calcium absorption frac-
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J Clin Endocrinol Metab, November 2002, 87(11):4952– 4956
FIG. 1. Individual changes in 25(OH)D. The median interval between
the late summer and late winter visits was 175 d. The subject with
the lowest late summer value was the only subject with heavily pigmented skin in late winter (i.e. after summer tanning had faded). Both
subjects with late summer values of less than 75 nmol/liter were also
in the lowest tertile for percent skin exposed and sun index (copyright
Robert P. Heaney, 2000; used with permission).
TABLE 5. Bivariate correlations between measures of sun
exposure and serum 25(OH)D
25(OH)D
Hours of sun exposure per week
Fraction of BSA exposed to sunlight
Sun indexd
Late
summer
Summer
increment
NS
⫹0.5839b
⫹0.4936c
⫹0.3891a
⫹0.6587b
⫹0.6684b
Data as Pearson’s r. NS, Not significant.
a
P ⬍ 0.05; b P ⬍ 0.001; c P ⬍ 0.01.
d
Hours of sun exposure per week ⫻ fraction of BSA exposed to
sunlight.
tion (r ⫽ 0.5706; P ⬍ 0.005) and for fasting urinary calcium
(r ⫽ 0.6242; P ⬍ 0.001).
Seventeen of the 30 subjects reported having used sunscreen. Of these, only 1 may have used sunscreen in a way
that was consistent with effective application (i.e. always on
all exposed areas). This subject was in the highest tertile for
sun index, and his summer increment in 25(OH)D was 41
nmol/liter, in the midtertile for the group. The remaining 17
reported sunscreen use only sometimes or rarely.
Discussion
In his 1999 review, Vieth (11) notes that serum 25(OH)D
levels above 200 nmol/liter are not rare among healthy per-
Barger-Lux and Heaney • Summer Sun Exposure and 25-Hydroxyvitamin D
FIG. 2. Measures of summer sun exposure and summer increment in
25(OH)D. The graphs show the relationships of sun-exposed body
surface area (A) and sun index (B) to summer increment in 25(OH)D
in all 26 subjects with complete data. Values for seasonal difference
(late summer less late winter) were used as the measure of summer
increment in 25(OH)D. As shown in Table 5, the relationships were
both statistically significant. The five subjects with the largest summer increments (at the upper right in B) were at the high ends of the
distributions for both variables that comprise the sun index.
sons with ample sun exposure. Of the 30 outdoor workers in
whom we measured 25(OH)D in late summer, 3 had levels
above 200 nmol/liter (i.e. 211, 205, and 203 nmol/liter); their
sun exposure occurred in Nebraska, Kansas, and North Dakota, at 41.2°, 39.0°, and 46.8°N latitude, respectively.
Among 20 male members of a U.S. submarine crew, mean
serum 25(OH)D fell from 78 to 48 nmol/liter over a 68-d
deployment, an average daily decrease of 0.441 nmol/liter
(12). Among our 26 subjects, serum 25(OH)D fell from 122 to
74 nmol/liter over an interval of 175 d (values are medians),
a median daily decrease of 0.274 nmol/liter. In our study sun
deprivation began less abruptly and was less complete.
Hence, one would expect a somewhat lower value for the rate
of fall of serum 25(OH)D. Given this difference, we consider
the 2 rates congruous.
Of several studies that report effects of artificial UV light
on serum 25(OH)D in healthy, nonelderly adults, most have
involved short courses of total body exposure. The most
recent such study of which we are aware (13) involved 10
treatments over a 2-wk period; among 7 healthy subjects,
serum 25(OH)D increased by 71 nmol/liter (from 53 to 124
nmol/liter; values are means). Our subjects had a summer
increment of 49 nmol/liter, and a late summer value of 122
Barger-Lux and Heaney • Summer Sun Exposure and 25-Hydroxyvitamin D
J Clin Endocrinol Metab, November 2002, 87(11):4952– 4956 4955
nmol/liter; those in the highest tertile for skin exposure
(45– 67%) had corresponding values of 85 and 145 nmol/liter
(medians). The net effect of our subjects’ summer-long sun
exposure rather closely approximated the reported effect of
a short course of total body treatment with artificial UV light.
As shown in Table 5, we found that extent of sun exposure
(i.e. fraction of BSA exposed to sunlight) was more closely
related to serum 25(OH)D than was the duration (i.e. hours
of sun exposure per week). This disparity may be a feature
of our approach to measuring these variables. However, the
data suggest a strategy for optimizing dermal production of
vitamin D without prolonged sun exposure, i.e. by maximizing sun-exposed BSA while limiting unprotected time in
direct sunlight to periods as short as 15 min/d (3). Further
research would be required to determine the effectiveness of
such a strategy.
The idea that adequate vitamin D status can be defined as
the absence of osteomalacia has been largely rejected. Various writers have tied inadequacy to seasonal fluctuation of
PTH (14), elevated or suppressible alkaline phosphatase (15),
or inadequate absorption of calcium at ample intakes (16). In
a recent review, Holick (17) considers the role of vitamin D
in cellular growth and maturation as well as the musculoskeletal system. He concludes that whereas secondary hyperparathyroidism can be averted with 25(OH)D levels of at
least 20 ng/ml (50 nmol/liter), 25(OH)D should probably be
at least 30 ng/ml (75 nmol/liter) to maximize cellular health.
Others have reported that higher 25(OH)D is required to
minimize PTH levels (14, 18, 19). As Fig. 1 shows, by the late
winter visit fully half of our subjects had 25(OH)D levels less
than 75 nmol/liter. At the late summer visit, 25(OH)D for this
subgroup was 104 nmol/liter (median; interquartile range,
82–118); the corresponding median for the subset with
25(OH)D levels of at least 75 nmol/liter at the late winter visit
was 154 nmol/liter (range, 135–176).
In earlier work conducted over the winter to minimize
cutaneous production of vitamin D, we examined the doseresponse relationship between oral vitamin D3 and circulating 25(OH)D in healthy adult men (20). In that study equilibrium concentrations of serum 25(OH)D rose in direct
proportion to daily dose of vitamin D3. For every microgram
of vitamin D3 (40 IU) given daily, serum 25(OH)D settled at
an equilibrium level that was higher by about 0.70 nmol/
liter. Using this relationship to estimate the equivalent daily
skin dose of vitamin D3 among the subjects of the present
study, and assuming equilibrium 25(OH)D values by late
summer, it follows that our subjects’ sunlight exposure was
equivalent [in 25(OH)D production] to a daily oral vitamin
D3 dose of 69.5 ␮g (interquartile range, 41.3–95.6) or 2780 IU
(interquartile range, 1652–3824).
This study has several limitations. First, we substituted
recalled estimates of hours outdoors for actual hours of sun
exposure. Although we limited recorded sun exposure to a
daily maximum of 8 daylight h, we did not obtain or incorporate data on sunny vs. overcast or rainy days. Also, we
present our findings on the relationship of sun exposure and
production of vitamin D3 (e.g. Fig. 2) in simple terms that do
not incorporate other factors that influence the efficiency of
the process (e.g. skin pigmentation, age, time of day, and time
per exposure) (3). Finally, differences of as much as 33% have
been reported when laboratories using different methods
have measured 25(OH)D, (21). We therefore recognize that
caution is appropriate when comparing absolute values from
our results with those of others. (However, directional
changes and proportional differences would not be affected
by such methodological differences.)
Conclusions
Our findings confirm and quantify the relatively large
seasonal fluctuations in circulating 25(OH)D in association
with summer sun exposure among outdoor workers. These
changes did not produce significant changes in calcium absorption fraction or urinary calcium excretion among the
healthy men we studied. Moreover, even rather intensive sun
exposure did not regularly protect against a winter deficit
(and, in some participants, not even a summer one), defined
as serum 25(OH)D levels below 75 nmol/liter. Based on the
average rate of decline observed in our subjects, it can be
estimated that in individuals for whom summer sun exposure is the principal source of vitamin D, a late summer
25(OH)D level of approximately 127 nmol/liter is needed to
avoid levels falling to less than 75 nmol/liter by late winter.
Without another substantial source of vitamin D, it is unlikely that occasional sun exposure by persons who spend
most of their daylight hours indoors can support vitamin D
repletion, a conclusion congruent with that reached by
Glerup et al. (22).
Acknowledgments
Received April 24, 2002. Accepted August 13, 2002.
Address all correspondence and requests for reprints to: M. Janet
Barger-Lux, Creighton University Osteoporosis Research Center, 601
North 30th Street, Suite 5766, Omaha, Nebraska 68131. E-mail:
[email protected].
This work was supported by a grant from the Health Future Foundation (Omaha, NE).
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