Geography
103
Weather
Lecture No. 2.2 : Ultraviolet Radiation (UVR, Quiz 1)
1. 3-bands of UVR (by Saidman, 1932)
(1). UVC:
A. Wavelengths < 280 nm (0.28µ). µ = micrometer, 1µ = 10-6 m
B. Completely absorbed by the stratospheric ozone.
(2). UVB
A. Wavelengths: 280 nm to 320 nm.
B. Partially absorbed by the stratospheric ozone.
C. Responsible for sunburn, eye disorder, suppression of immune system, and skin cancers.
(3). UVA
A. Wavelengths: > 320 nm.
B. Little absorption by ozone.
C. Exacerbates the damaging effects of UVB.
(A). 1000-fold less effective than UVB in producing erythema (skin redness or sunburn).
(B). About 100-fold more UVA than UVB energy reaching the earth’s surface.
(C). Contributes about 10-20% to the sunburn in summer.
D. Responsible for skin aging.
E. Generates photochemical smog and degrades materials such as plastics, paints, and
fabrics, etc.
2. Health Impacts
(1). Short-term effect: Sunburn.
(2). Long-term effects:
A. Photoaging (prior to age 30).
(A). Damage the elastic fibers responsible for skin’s strength and resilience.
(B). Liver spots: Leathery texture, wrinkles, and irregular pigmentation.
B. Eye disorders
(A). Damage to lens of eye
a. Retina cells are more sensitive to UVR than are skin cells.
b. Lens of eye strongly absorbs UVB thereby shielding the retina cells.
(B). Cataracts
a. Cloudy (opaque) regions scatter and absorb light.
b. 20% of cataracts are related to UV exposure.
C. DNA damage
(A). UVR penetrates through the outer shield (melanin-containing stratum corneum) to
underlying living cells where this energetic rays can inflict considerable damage to
DNA molecules.
(B). Genetic materials containing instruction that direct the body’s activities.
(C). Damage to DNA molecules may lead to skin cancer:
a. Fair-skinned individuals:
Melanocytes produce less melanin, high risk of skin cancer.
b. Dark complexions: Not immune to skin cancer.
(D). Repair capability of UV-damaged DNA (DNA-repair enzyme)
a. DNA repair system locates and repairs DNA lesions by making a cut on each
end of the damaged segment of DNA and excision the lesions.
b. Without a mechanism for continual repairs, the number of damaged sites in a
cell’s gene builds up over time, a tumor develops.
(E). Xeroderma pigmentosum
a. A rare genetic disease lack of a DNA repair mechanism.
b. So sensitive to UVB that skin cancer develops prior to age 10.
D. Skin cancer
(A). Gradual accumulation of damaged DNA sites:
A declining ability to repair damaged DNA molecules due to aging.
(B). Most common form of cancer in the
a. About one in seven Americans will contract this disease during their lifetime.
b. 90% of these cases will be due to overexposure to the sun’s UVB rays.
3. Epidermis (The outermost layer of the skin, Figure 3.2)
(1). Stratum corneum
A. The outermost portion of the epidermis.
B. Tightly packed dead cells about 20 cells thick.
C. Protects the underlying living cells by absorbing UVR:
Absorbs a portion of UVR.
D. Gradually erodes as dead cells are shed from the skin.
(2). Squamous cells
A. Basal cells that migrate toward the surface of the skin.
Die on the way to the skin surface.
B. Become part of stratum corneum
C. The sequence from cell division to shedding: 3-4 weeks.
(3). Basal cells
A. At the base of the epidermis.
B. Regularly divide and produce new cells.
C. Some of these cells migrate toward surface of the skin (sequamoa cells).
(4). Melanocytes
A. Scatter among basal cells.
B. Produce melanin.
(5). Basement membrane.
4. Body’s natural UV defenses
(1). Stratum corneum absorbs a portion of UVR.
(2). UVR that penetrates downward accelerates division of basal cells to form thicker layer of
dead cells that protect the underlying living cells.
(3). Melanin produced by melanocytes
A. Penetrating UV rays stimulate melanocytes to produce melanin (a brownish-black
pigments that absorbs UVR and darkens the skin).
B. Synthesis of this natural sunscreen (melanin) takes place in microscopic vesicles
(membrane-bound sacs within the cytoplasm of cells).
C. Skin tan
(A). Squamous cells carrying melanin-containing vesicles moves toward the surface of the
skin.
(B). The skin gradually becomes darker as an increasing portion of the stratum corneum
consists of melanin-containing cells.
(C). Skin fades as melanin production decline due to less penetrating UV rays to the base
of epidermis (melanocytes).
D. Addition of melanin to stratum corneum does not provide total protection from UVR.
(A). Several days elapse between the skin’s initial exposure to UVR and the development
of a tan.
(B). Severe damage (sunburn) caused by initial exposure to UV rays.
Initial exposure to UVR should be limited in duration to permit synthesis of greater
amounts of protective melanin.
(C) Melanin is not a perfect absorber of UVR.
(4). DNA repair system
5. Forms of skin cancer
UVB damages the DNA of the respective epidermal cells resulting in uncontrolled growth and
subsequent formation of tumors.
(1). Basal cell carcinoma
A. Grows slowly and rarely spreads to other parts of the body.
B. On the face and ears.
C. 75% of all skin cancers.
D. Easily treatable if detected early.
E. Most common warning sign: A new growth or a sore that does not heal.
(2). Squamous cell carcinoma
A. Grows more rapidly than the basal cell carcinoma.
B. More likely to invade the underlying skin structures and other parts of the body.
C. Forms on the face, ears, neck, lips, and hands.
D. About 20% of all skin cancers.
E. Warning sign: same as basal cell carcinoma.
(3). Malignant melanoma
A. Originates in the melanocytes.
B. On the body’s trunk or legs.
C. Grows quickly and spreads rapidly throughout the body.
D. Dark brown or black spots on the skin: accelerated production of melanin.
E. Mnemonic to describe four major visual characteristics of malignant melanoma lesions:
ABCD (Asymmetry, Border irregularity, Color variation, and Diameter greater than 6 mm,
the diameter of a pencil eraser).
F. Once tumors begin to spread, the cure rate plummets.
G. Responsible for about 95% (38,000 annually) of all skin cancer fatalities.
H. Accounts for about 5% of all cases of skin cancers.
I. The incidence of malignant melanoma is growing faster (4% per year) than that of any
other form of cancer and has more than double since 1980.
6. Time required for skin cancer development
(1). On the average 20 years.
(2). Average age of discovery of skin cancer: age 50.
(3). Declining age:
An estimated one quarter of the approximately 32,000 new cases of malignant melanoma
reported in 1992 were in people age 39 or younger (
7. The Ultraviolet Index (UVI, Figure 3.4; Table 3.2)
(1). Definition:
A next-day forecast of the likely exposure to ultraviolet radiation weighted by the erythemal
action spectrum for the
(2). History
A.
B.
Environmental Prediction) of NWS.
(3). Variables
A. The previous day’s satellite measurements of the total column ozone.
B. Forecasts of the next day’s cloud cover from MOS (model output statistics).
C. Surface albedo (5%).
D. Optical depth (0.2; 0 for total clean atmosphere).
E. Altitude.
F. Solar zenith angle (time of year, latitude).
(4). Computation of UVI (erythemally weighted UV radiation)
A. The spectrum irridiances at individual wavelengths between 290 nm and 400 nm are
calculated using a radiative transfer model, regression equations, and MOS (cloud cover).
B. The spectrum irridiances are weighted (multiplied) by the CIE action spectrum to produce
an erythemal dose rate in watts per square meter (W/m2).
C. Experimental period (June 1994 through April 1995): You do not need to memorize numbers.
(A). UVI = Forecast or measured erythemal dose rate (W/m2) x 36
(B). 1 W/m2 erythemal dose rate = 36 UVIs.
1 W/m2 x 3600 s = 1 Js-1m-2 x 3600 s = 3600 Jm-2 = 36 hJm-2 = 36 units of UVI.
1 UVI = 1 hJm-2 erythema UVB dosage.
(C). The erythemal dose rate of 0.2 W/m2 :
UVI = 0.2 x 36 = 7.2.
D. The international standard (since 1995)
(A). UVI = Forecast or measured erythemal dose rate x 40.
(B). The erythemal dose rate of 0.2 W/m2.
UVI = 0.2 x 40 = 8.
(C). One unit of UVI equals 0.025 W/m2 erythemal dose rate (UVB irridiances x CIE
action spectrum).
(5). Action (effective) spectrum
A. Relative effectiveness of individual wavelengths of radiation in causing the same degree
of a biological response such as erythema, skin tumors, or DNA damage.
B. Reciprocal of the dose required to cause a threshold biological response.
C. The effective radiant dose is normalized to 1 at the most effective wavelength
(297 nm for erythma).
D. The effective radiant exposure of the other wavelengths, which are less than 1, are
computed from statistically-derived normalized equations.
(6). CIE (International Commission on Illumination or Commission Internationaled’Eclairage)
action spectrum (280 nm to 400 nm)
A. The spectral erythema effectiveness is the reciprocal of the minimum erythema dose
(MED).
B. The spectral erythema effectiveness is normalized to 1 at 297 nm (most effective in
causing erythema).
C. MED: The smallest amount of UV dose necessary to induce a barely perceptible
redness of previously unexposed skin within 24 hours of exposure.
8. UVI categories (by EPA)
(1). Five exposure categories
Low: 0, 1, 2
Moderate: 3, 4, 5
High: 6, 7.
Very High: 8, 9, 10
Extreme: 11 through 15.
(2). The public is advised
to minimize outdoor activities between hours of
UVI lies in the category of High or Very High.
Please click on the following URLs for more information:
http://iwin.nws.noaa.gov/iwin/us/ultraviolet.html
http://www.epa.gov/sunwise/uviscale.html
9. Minutes to Burn
(1). Definition:
A. 60 minutes divided by the number of minimum erythema dose (MEDs) in one hour
(60/0.9UVI) for the most sensitive people (skin color is pale, milky white, or alabaster).
B. Approximation: 60 minutes divided by UVI.
C. The time required to sunburn for the least sensitive people is about 5 times as long as that
required for the most sensitive people.
(2). MED : 10 mJ/cm2 for the most sensitive people (never tans/always burns) to 50 mJ/cm2 for
the least sensitive people (always tans /never burns).
mJ = millijoules = 10-3 joules.
(3). 4 skin phototypes (Table 3.3, by EPA):
A. Never tans/always burns.
B. Sometimes tans/usually burns.
C. Usually tans/sometimes burns.
D. Always tans/rarely burns.
10. Spatial variation
of UVI in the
11. Spatial variation
of minutes-to-burns in the
12. Protection measures
(1). Under umbrella on beach
A person may be exposed to much more UVR than the UVI may indicate.
A. Sand reflection of UVB: 50%.
B. Water reflection: 100%.
C. UVB penetration to a water depth of 1 m or so.
(2). High mountains
A. The intensity of UVR at 3,000 meters is about 40% greater than at sea level.
B. Snow reflection: 90% of UVR.
(3). Brief initial exposure to the sun until a protective tan develops.
A. One or more severe sunburns greatly increases a person’s chances of contracting skin
cancer later in life.
B. Only one severe sunburn doubles a child’s chances of developing basal cell or squamous
cell carcinoma as an adult.
(4). Holloway’s study
A. Shadow rule:
If a person’s shadow is shorter than he or she is tall, then they should avoid
the sun or apply sunscreen to exposed skin (Figure 3.7a).
B. The intensity of UVB increases slowly until the solar altitude reaches about 45 degrees.
C. At or higher than 45 degrees solar altitude: Total UVB exposure is about 5 times greater than
the total exposure during the remaining daylight hours.
(5). Protective clothing (wide-brim hats, long-sleeved shirts, long pants and tightly woven fabrics)
reduces the risk of skin cancer on such exposed skin surfaces as forearm, face, and neck, the most
common sites of tumor formation (Figure 3.8).
(6). Eye protection
UV-rated sunglasses along with a wide-brim hat provides an adequate eye protection.
(7). Sunscreens
A. Apply to all exposed skin approximately 20 minutes before beginning outdoor activities.
B. Sunscreens have ingredients that selectively absorb UV wavelengths, augmenting the skin’s
natural UV-defenses.
C. Broad-spectrum sunscreen that provides protection from both UVB and UVA.
D. Sun Protection Factor (SPF)
(A). A measure of how much longer a person can safely stay in the sun when wearing a particular
sunscreen versus wearing no sunscreen.
(B). SPF -15 (minimum protection)
a. No sunscreen: Skin begins to turn pink after 10 minutes in the sun.
b. With sunscreen: 150 minutes (2.5 hours)
10 minutes x 15 = 150 minutes
c. Block 94% of UVR reaching the skin surface.
(C). SPF - 30
a. Block 97% pf UVR reaching the skin surface.
b. No 100% effective sunscreen
(D). SPF – 40 or higher
Too much chemical providing no additional protection.
13. Peak UVR does not coincide with peak temperatures either on a daily or seasonal basis.