Rates of Vitamin D Production from Solar Ultraviolet B Irradiance in San Francisco During One Year

William B. Grant, Ph.D.
SUNARC
2107 Van Ness Ave., Suite 403B
San Francisco, CA 94109-2529
USA
www.sunarc.org
grant@sunarc.org

Vitamin D is very important for the health of man and animals alike. Human skin has adapted over periods of millennia to the typical ultraviolet (UV) irradiance levels, light enough to permit vitamin D production, dark enough to reduce the production of free radicals and destruction of folate [Jablonski and Chaplin, 2000, 2002]. Unfortunately, many people are now living at latitudes far removed from their ancestors, so they either burn easily in the bright sunlight or don’t produce enough vitamin D for optimal health.

Vitamin D deficiency was first associated with rickets [Rajakumar, 2003] and then osteoporosis [Holick, 2004a,b]. More recently, attention has turned to soft-tissue diseases. The one that particularly interests me is cancer. The ultraviolet-B (UVB)/vitamin D/cancer hypothesis was first proposed in 1980 based on reviewing the atlas of colon cancer mortality rates in the U.S., where it was obvious that rates in the sunny southwest were about half those in the northeast [Garland and Garland, 1980]. The hypothesis is rapidly gaining support but has not reached the level of acceptance by governmental agencies or major disease organizations. A number of recent papers have provided additional support for the hypothesis [Grant, 2002, 2006; Robsahm et al., 2004; Giovannucci et al., 2006; Grant and Garland, 2006]. Vitamin D is also very important for reducing the risk of developing a number of other conditions and diseases or their progression including bone conditions and diseases, muscle pain, neuromuscular control, autoimmune diseases such as arthritis and multiple sclerosis, and heart disease [Holick, 2004a,b; Grant and Holick, 2005].

Solar UVB (290-315 nm) is the primary source of vitamin D for most people. Dietary sources provide about 250-300 I.U./day in the U.S., but it was recently determined that it takes about 1000 I.U. per day to reduce the risk of colon cancer by 50% [Gorham et al., 2005]. One can produce 10,000-20,000 I.U. of vitamin D from solar UVB in a day. On the other hand, solar UV, especially the longer wave UVA (315-400 nm), is an important risk factor for melanoma and basal cell carcinoma, the most common type of skin cancer in the U.S. Thus, it is worthwhile to determine how long one needs to be in the sun at what time of the day and with how much of the body exposed in order to optimize vitamin D production while minimizing UVA irradiance.

Fortunately, there is a meter developed for just that purpose, the Vitamin D3 meter from Solartech, Inc. The action spectrum for vitamin D production peaks a bit short of 300 nm. This meter measures the UVB irradiance virtually in accordance with the vitamin D action spectrum and gives a value of the number of international units of vitamin D that could be produced by a fair-skinned Caucasian (Fitzgerald skin type II) with 10% of his body exposed. There is also a second meter that measures solar UVB without weighting for vitamin D production. I have one of each and have used them to measure the vitamin D production potential and UVB from my rooftop in San Francisco (37.8° N, 122.4° W) during the past year. I describe the measurements in this article.

Since vitamin D production rates (VDPR) are highest near solar noon, assuming that aerosol and cloud optical depths are similar during the daylight hours, I tried to make measurements at that time. Solar noon is half way between sunrise and sunset. At standard time, it is about 12:15 p.m. at my location. The clear-sky values are plotted in Fig. 1. For this location, VDPR varies from about 15 I.U./minute in winter to about 67 I.U./min in summer. These values compare very favorably with those calculated for Melbourne, Australia [Samanek et al., 2006], even though the Earth-Sun distance is 3.4% less during the Austral summer, thereby increasing the solar UVB there by 6.8%, and the column ozone amount is a bit lower. However, it should be noted that the vitamin D action spectrum, i.e., the wavelength dependence of the vitamin D production, is not known with a high degree of certainty. The primary measurement was made in 1982 [MacLaughlin et al., 1982], and since it is a difficult measurement, has not been replicated. Thus, the values given here should be regarded as approximate. Note that readings were not made on many days. That was because it is frequently foggy or cloudy in San Francisco, and that I occasionally travel out of town.

Figure 1. Vitamin D production rates near solar noon, San Francisco. The dots represent clear sky values on typical days; the circles represent the same on days when the stratospheric ozone layer was thinner due to transport from the tropics [Grant et al., 2000].

Apart from clouds and aerosols, the primary variable is the solar zenith angle (SZA). The SZA can be calculated using a web-based tool. SZA varies by season and time of day. There are two primary factors that change with SZA: the path length through ozone and the path length through the molecular atmosphere. The effect of ozone can be modeled to first order as the logarithm of the path length. The path length is proportional to 1/cos (SZA). Plotting this value times the VDPR should result in a horizontal straight line. As seen in Fig. 2, there is a 30% reduction in winter compared to summer.

Figure 2. The product of the vitamin D production rate times the exponential function of the air mass vs. day of the year. If ozone were the only factor affecting UVB hitting the surface in San Francisco, the best fit to the data would be a horizontal line. The deviation from a straight line is mostly due to attenuation by molecular scattering, with a 7% increase in winter due to differences in Earth-Sun distance with season.

The primary unmodeled contribution to the change in VDPR with season is the attenuation of the atmosphere due to molecular scattering. Attenuation by molecular scatter increases as the inverse fourth power of the wavelength. In order to estimate the effect of molecular scatter with SZA, data taken from 7:20 a.m. to 1:00 p.m. on 26 March 2006 were used. It was assumed that column ozone levels were constant during this period and that the effect of ozone absorption could be modeled as just discussed. It was found that as the SZA decreased from 60 to 35 degrees, the product of VDPR x exponent(1/cos(SZA)) increased by 31% (Fig. 3). These results are supported by measurements of UV at the surface in Lauder, New Zealand (0.37 km elevation) and Mauna Loa Observatory, Hawaii (3.4 km elevation) for the wavelengths just long of the UVB and ozone absorption band [McKenzie et al., 2001]. Plotting the data during the year vs. SZA and fitting the data to a third order polynomial yielded a 35% change with an uncertainty of 10%. Thus, the variation observed is nearly within experimental uncertainty of what was expected, recalling that there is also the 6.8% increase in winter due to differences in Earth-Sun distance with season.

Figure 3. The product of VDPR x exponent(1/cos(SZA)) vs. SZA, showing the effect of extinction by molecular scattering.

An additional contribution to the difference might be higher column ozone in winter. Stratospheric ozone is produced in or near the tropics and transported towards the polar region in winter as the polar atmosphere cools and condenses. However, that does not appear to be the case for San Francisco through a quick inspection of the data at the Total Ozone Mapping Spectrometer (TOMS) web site.

Going further, as can be seen in Fig. 1, there are several periods when the vitamin D production rates are about 10 I.U./min higher than the regression curve. These are times when the stratospheric ozone layer is thinner due to transport of tropical air masses overhead. During the mid-May 2006 (near day 133) event, the surface air was unseasonably warm. This is a well-known phenomenon. I happened to be measuring tropospheric ozone with a differential absorption lidar (DIAL) system on a NASA flight from Moffett Field, California to Bangor, Maine on 13 October 1997 when we passed through the warm conveyor belt transport from the Rocky Mountains all the way to Maine [Grant et al., 2000]. With this DIAL system, we were able to measure the vertical profiles of ozone and aerosols from the surface to the lower stratosphere along the flight path. Tropospheric ozone was as low as 18 ppbv at 10 km and the tropopause was pushed up to 16 km in some locations, well above the 13 km encountered in California.

To check that there was, indeed, tropical air transported over San Francisco, I checked the UVB measurements made at the U.S. Department of Agriculture UVB Monitoring and Research Program station in Davis, California (121.8˚ W, 38.5˚ N). I used the lamp-calibrated channel plots for 300, 305.5, and 311.4 nm. The USDA data clearly showed increased UVB values during the three periods indicated on Fig. 1.

There are two other UVB and vitamin D web sites I’d like to recommend as well. One is where I obtained the July 1992 DNA-weighted UVB doses for the U.S. It was developed for an article in Scientific American on UV and skin cancer [Leffell and Brash, 1996]. I’ve used this map in linking UVB and vitamin D to risk reduction for a number of cancers [Grant, 2002; 2006; Grant and Garland, 2006]. The other is a daily forecast of vitamin D production rates around the Earth, (choose the horizontal map). Both URLs clearly show that UVB and vitamin D production rates are higher from the Rocky Mountains to the west in the U.S.

This occurs for two reasons: (1) the surface elevation is generally higher in the west; and (2) the stratospheric ozone layer is thinner due to the prevailing westerly winds pushing up the tropopause as the air masses cross the Rocky Mountains. However, it should be noted that it is easy to produce vitamin D from solar UVB in summer, but difficult in winter, so it may be that there is a fortuitous agreement between the July 1992 UVB data and annual UVB levels.

So, what does this information about vitamin D production rates mean for the average person? First, recall that 1000 I.U./day of vitamin D is associated with a 50% reduction in risk of colorectal cancer [Gorham et al., 2005]. For other cancers, values of about 1500 I.U./day are probably required for 50% reductions [Giovannucci et al., 2006]. Another paper suggests that people need 3000-5000 I.U./day in general [Heaney et al., 2003]. Thus, one can use information about the SZA and surface elevation (6% increase in UVB for each km in elevation [Cutchis, 1980]) to determine VDPRs and time required for the desired vitamin D production for a given fraction of body surface area exposed.

However, vitamin D production saturates after an equivalent of about 15,000 I.U. during a day [Holick et al., 1981; Holick, 1994], so that UVB irradiance beyond that amount on the exposed skin is not useful. In addition, it should be noted that it is the long-wave UV (UVA) (315-400 nm) that is associated with risk of melanoma [Moan et al., 1999] and basal cell carcinoma, the most common form of skin cancer, so that one would do better to obtain UVB near solar noon, when the ratio of UVB to UVA is highest and exposure times can be minimized.

Given the problems of being in a location and season with available solar UVB, having the time to be out of doors, worrying about the risk of skin cancer and melanoma, etc., many people may want to obtain vitamin D from supplements rather than solar UVB irradiance. Vitamin D from solar UVB irradiance, fortified food, and supplements has the same physiological effect as long as it is in the form D3 (cholecalciferol) rather than D2 (ergocalciferol) [Armas et al., 2004]. There is not enough vitamin D in fortified food to have a strong beneficial effect; the average American obtains about 300 I.U. of vitamin D per day from food. Also, vitamin D should not be combined with high amounts of vitamin A, which competes with vitamin D.

Also, it is noted that sunscreen sold in the U.S. blocks UVB radiation very well but UVA poorly. A tan provides as much protection against UVA irradiance as does sunscreen in the U.S. (protection factor of 2-4). Thus, a Caucasian who does not rapidly burn might consider going into the sun without sunscreen for the first 10-15 minutes, and not rely on sunscreen for long-term protection against UVA. Since melanoma arises from free radicals produced deep in the skin from UVA, one should try to maintain a good antioxidant status through diet, as well as maintain high vitamin D levels [Millen et al., 2004].

Hopefully this work not only provides useful information on vitamin D production and its role in reducing the risk of cancer and other diseases but also shows how a dedicated scientist, working without research funding, can have an impact on the course of scientific research and understanding.

References

(Abstracts of most papers and full text of some can be obtained from http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?)

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