- Email: [email protected]
UV RADIATION FROM FLUORESCENT LIGHTS
579
immunofluorescent staining of cervical
antibody
to
detect
chlamydial
Praed Street Clinic, St Mary’s Hospital, London W2 INY
Department of Pathology, St Mary’s Hospital Medical School
smears
with
a
monoclonal
infection.
TABLE I-SPECTRAL POWER IRRADIANCE
(J.iWm -2nm - I) FROM
VARIOUS FLUORESCENT TUBES GIVING AN ILLUMINANCE OF
500 lux
G. FORSTER
R. JHA
Praed Street
Clinic, St Mary’s Hospital
D. CHEETHAM P. MUNDAY
Department of Pathology, St Mary’s Hospital Medical School Clinical Research Centre, Harrow
D. COLEMAN D. TAYLOR-ROBINSON
TABLE II-GROUND LEVEL SOLAR IRRADIANCE
3-3
(E.Wm Znm I FOR
nm OZONE LAYER
UV RADIATION FROM FLUORESCENT LIGHTS
all have raised the possibility of an association lighting and melanoma. At first sight, such a suggestion seems unlikely since ultraviolet (UV) emissions much SIR,-Beral
et
between fluorescent
more intense than those from fluorescent tubes are present in normal sunlight. However, the comparison2was based on integrated intensity measurements over UVA wavelengths (320-400 nm). Solar irradiance at ground level approaches zero at wavelengths around 290 nm because shorter wavelength UV is absorbed by atmospheric ozone.3In contrast, the biological activity of UV, shown for example by DNA damage in vitro, increases rapidly at shorter wavelengths; the induction of non-melanoma skin tumours in animals and short term effects such as erythema in man are produced more readily by UVB (280-320 nm) than by longer wavelengths.4 We have compared the UV emissions expected from exposure to fluorescent light in a typical office environment with those of sunlight at specific wavelengths in the 280-300 nm region. The spectral power distributions of nineteen tubes were supplied by a leading manufacturer. Nine, all commonly used in office lighting, had small but significant intensities of UVB in the region around 290 nm. For each of these, the desk top power irradiance level per unit wavelength range was calculated for a typical office illuminance of 500 lux (table!). Comparison with ground level solar irradiances requires assumptions about the height of the sun, latitude, and depth of stratospheric ozone layer. Ozone depth is especially important in the UVB region. Layer thickness varies with latitude from 2’ 0-2 - 5 mm at the equator to 4 - 0-4 - 5 mm at the poles and is the main factor in the variation of UVB radiation with latitude. Beral’s study was done near Sydney, Australia, so we have assumed an ozone layer of about 3.3 3 mm in deriving the ground level solar irradiance from the results cited by Henderson.3 As a check, these numbers have been used to calculate average daily dose of UVB with 5 nm resolution throughout the year, and they give results which are compatible with the measurements of Klein and Goldberg5for similar northern latitudes. A comparison of tablesand n shows that the irradiance of some fluorescent tubes is comparable to that of sunlight for much of the year in Sydney for wavelengths near 295 nm, and many exceed it substantially for wavelengths near 290 nm. The figures are for uncovered tubes. Styrene diffusers absorb almost all UVB in the 280-315 nm range while acrylic diffusers absorb about 25%. Diffusers giving only partial coverage, such as those of a lattice design, will absorb less. However, we have no reliable information on the distribution of different types of office fitting. We have also calculated the total dose of UV to various wavelengths expected from 8 h a day, 5 days per week exposure to fluorescent light and from daily total outdoor exposure to the sun at latitude 30°. The results are similar to those above: at the wavelength of 290 nm the dose received from fluorescent lights may considerably exceed that from sunlight. These results suggest that the association found by Beral et al may be biologically plausible, if exposure to short wavelength UVB
1 Beral V, Evans S, Shore H, Milton G. Malignant melanoma and exposure to fluorescent lighting at work. Lancet 1982; ii: 290-92. 2 Rigel D, Friedman R, Levenstein M, Greenwald D. Malignant melanoma and exposure to fluorescent lighting at work. Lancet 1983; i: 704. 3 Henderson ST. Daylight and its spectrum. London: Hilger, 1977. 4 National Research Council. Causes and effects of stratospheric ozone reduction: an update. Washington, DC: National Academy Press, 1982. 5 Klein W, Goldberg B. Proc 7th Int Solar Energy Conf (New Delhi, 1978): 400.
around 390 nm has a specific role in the aetiology of melanoma. Alternatively, the ratio of short wavelength UV to longer wavelength UV, which is much higher for fluorescent light than for sunlight, may be important; it may be relevant that pyrimidine dimers produced in DNA by UVB can be split, and the DNA thereby repaired, by longer wavelength UVA or visible light.4 Departments of Physics and Community Health, University of Nottingham, Nottingham NG7 2UH
KENNETH J. MAXWELL J. MARK ELWOOD
VANADATE AND CARDIAC GLYCOSIDES
SIR,-The report in your July 16 issue, describing a correlation serum selenium concentrations and the subsequent
between low
development of cancer will increase scientific interest in selenium and related trace minerals. In Finland, some doctors routinely prescribe selenium and other trace minerals for a variety of illnesses, including cancer and rheumatism. We have recently become aware ofapotentially hazardous form of such treatment. Prescriptions for sodium orthovanadate decahydrate (4 mg) in combination with sodium selenate (4 mg), and chromic chloride (4 mg) have been presented at several Finnish pharmacies. These are compounded as capsules to be taken twice daily, thus the ingested amount of vanadium is 1.1 1 mg (21 mol) per day. Vanadate, the pentavalent form of vanadium, is a potent inhibitor of Na’, K+-ATPase2and patients on cardiac glycosides are at risk if they take these vanadate capsules since the toxicity of cardiac 3 glycosides is related tot he degree ofNa , K + -ATPase inhibition. To illustrate this point, we prepared red blood cell membranes (RBCM)4 from two healthy blood donors. RBCM Na+, K+-ATPase activity was determined by a colorimetric assay, in omitting EDTA. Inclusion of vanadate (10 nmol/1) in the incubation potentiated by three-fold the inhibition of Na, K+-ATPase activity caused by the water soluble cardiac glycoside ouabain (Kl 0.80 emol/1; KI for ouabain plus vanadate = 0 - 27 for ouabain mol/1; p<0 001). This low concentration of vanadate alone caused only 10% inhibition of RBCM Na+, K+-ATPase activity. The interaction between vanadate and ouabain was additive in the linear portion of the dose-response curve. The results are exactly what one would predict from the pharmacology of vanadate and the cardiac glycosides. It is impossible to extrapolate these in vitrol results to the in vivo situation since the biological availability of vanadate is complex, depending on the =
WC, Polk BF, Morris JS, Stampfer MJ, Pressel S, Rosner B, Taylor JO, Schneider K, Hames CG. Prediagnostic serum selenium and risk of cancer. Lancet 1983; ii: 130-34. 2. Cantley LC, Josephson L, Warner R, Yanagisawa M, Lechene C, Guidotti G. Vanadate is a potent (Na, K)-ATPase inhibitor in ATP derived from muscle. J Biol Chem 1977; 252: 7421-23. 3. Aronson JK, Carver JG. Diagnosing digoxin toxicity by combined measurement of plasma digoxin concentrations and erythrocytic 86rubidium uptake. Br J Clin Pharmacol 1983; 15: 618P-619P. 4. Reinila M, MacDonald E, Salem N, Linnoila M, Trams EG. Standardised method for the determination of human erythrocyte membrance adenosine triphosphatases. Anal Biochem 1982; 124: 19-26. 1. Willett
immunofluorescent staining of cervical
antibody
to
detect
chlamydial
Praed Street Clinic, St Mary’s Hospital, London W2 INY
Department of Pathology, St Mary’s Hospital Medical School
smears
with
a
monoclonal
infection.
TABLE I-SPECTRAL POWER IRRADIANCE
(J.iWm -2nm - I) FROM
VARIOUS FLUORESCENT TUBES GIVING AN ILLUMINANCE OF
500 lux
G. FORSTER
R. JHA
Praed Street
Clinic, St Mary’s Hospital
D. CHEETHAM P. MUNDAY
Department of Pathology, St Mary’s Hospital Medical School Clinical Research Centre, Harrow
D. COLEMAN D. TAYLOR-ROBINSON
TABLE II-GROUND LEVEL SOLAR IRRADIANCE
3-3
(E.Wm Znm I FOR
nm OZONE LAYER
UV RADIATION FROM FLUORESCENT LIGHTS
all have raised the possibility of an association lighting and melanoma. At first sight, such a suggestion seems unlikely since ultraviolet (UV) emissions much SIR,-Beral
et
between fluorescent
more intense than those from fluorescent tubes are present in normal sunlight. However, the comparison2was based on integrated intensity measurements over UVA wavelengths (320-400 nm). Solar irradiance at ground level approaches zero at wavelengths around 290 nm because shorter wavelength UV is absorbed by atmospheric ozone.3In contrast, the biological activity of UV, shown for example by DNA damage in vitro, increases rapidly at shorter wavelengths; the induction of non-melanoma skin tumours in animals and short term effects such as erythema in man are produced more readily by UVB (280-320 nm) than by longer wavelengths.4 We have compared the UV emissions expected from exposure to fluorescent light in a typical office environment with those of sunlight at specific wavelengths in the 280-300 nm region. The spectral power distributions of nineteen tubes were supplied by a leading manufacturer. Nine, all commonly used in office lighting, had small but significant intensities of UVB in the region around 290 nm. For each of these, the desk top power irradiance level per unit wavelength range was calculated for a typical office illuminance of 500 lux (table!). Comparison with ground level solar irradiances requires assumptions about the height of the sun, latitude, and depth of stratospheric ozone layer. Ozone depth is especially important in the UVB region. Layer thickness varies with latitude from 2’ 0-2 - 5 mm at the equator to 4 - 0-4 - 5 mm at the poles and is the main factor in the variation of UVB radiation with latitude. Beral’s study was done near Sydney, Australia, so we have assumed an ozone layer of about 3.3 3 mm in deriving the ground level solar irradiance from the results cited by Henderson.3 As a check, these numbers have been used to calculate average daily dose of UVB with 5 nm resolution throughout the year, and they give results which are compatible with the measurements of Klein and Goldberg5for similar northern latitudes. A comparison of tablesand n shows that the irradiance of some fluorescent tubes is comparable to that of sunlight for much of the year in Sydney for wavelengths near 295 nm, and many exceed it substantially for wavelengths near 290 nm. The figures are for uncovered tubes. Styrene diffusers absorb almost all UVB in the 280-315 nm range while acrylic diffusers absorb about 25%. Diffusers giving only partial coverage, such as those of a lattice design, will absorb less. However, we have no reliable information on the distribution of different types of office fitting. We have also calculated the total dose of UV to various wavelengths expected from 8 h a day, 5 days per week exposure to fluorescent light and from daily total outdoor exposure to the sun at latitude 30°. The results are similar to those above: at the wavelength of 290 nm the dose received from fluorescent lights may considerably exceed that from sunlight. These results suggest that the association found by Beral et al may be biologically plausible, if exposure to short wavelength UVB
1 Beral V, Evans S, Shore H, Milton G. Malignant melanoma and exposure to fluorescent lighting at work. Lancet 1982; ii: 290-92. 2 Rigel D, Friedman R, Levenstein M, Greenwald D. Malignant melanoma and exposure to fluorescent lighting at work. Lancet 1983; i: 704. 3 Henderson ST. Daylight and its spectrum. London: Hilger, 1977. 4 National Research Council. Causes and effects of stratospheric ozone reduction: an update. Washington, DC: National Academy Press, 1982. 5 Klein W, Goldberg B. Proc 7th Int Solar Energy Conf (New Delhi, 1978): 400.
around 390 nm has a specific role in the aetiology of melanoma. Alternatively, the ratio of short wavelength UV to longer wavelength UV, which is much higher for fluorescent light than for sunlight, may be important; it may be relevant that pyrimidine dimers produced in DNA by UVB can be split, and the DNA thereby repaired, by longer wavelength UVA or visible light.4 Departments of Physics and Community Health, University of Nottingham, Nottingham NG7 2UH
KENNETH J. MAXWELL J. MARK ELWOOD
VANADATE AND CARDIAC GLYCOSIDES
SIR,-The report in your July 16 issue, describing a correlation serum selenium concentrations and the subsequent
between low
development of cancer will increase scientific interest in selenium and related trace minerals. In Finland, some doctors routinely prescribe selenium and other trace minerals for a variety of illnesses, including cancer and rheumatism. We have recently become aware ofapotentially hazardous form of such treatment. Prescriptions for sodium orthovanadate decahydrate (4 mg) in combination with sodium selenate (4 mg), and chromic chloride (4 mg) have been presented at several Finnish pharmacies. These are compounded as capsules to be taken twice daily, thus the ingested amount of vanadium is 1.1 1 mg (21 mol) per day. Vanadate, the pentavalent form of vanadium, is a potent inhibitor of Na’, K+-ATPase2and patients on cardiac glycosides are at risk if they take these vanadate capsules since the toxicity of cardiac 3 glycosides is related tot he degree ofNa , K + -ATPase inhibition. To illustrate this point, we prepared red blood cell membranes (RBCM)4 from two healthy blood donors. RBCM Na+, K+-ATPase activity was determined by a colorimetric assay, in omitting EDTA. Inclusion of vanadate (10 nmol/1) in the incubation potentiated by three-fold the inhibition of Na, K+-ATPase activity caused by the water soluble cardiac glycoside ouabain (Kl 0.80 emol/1; KI for ouabain plus vanadate = 0 - 27 for ouabain mol/1; p<0 001). This low concentration of vanadate alone caused only 10% inhibition of RBCM Na+, K+-ATPase activity. The interaction between vanadate and ouabain was additive in the linear portion of the dose-response curve. The results are exactly what one would predict from the pharmacology of vanadate and the cardiac glycosides. It is impossible to extrapolate these in vitrol results to the in vivo situation since the biological availability of vanadate is complex, depending on the =
WC, Polk BF, Morris JS, Stampfer MJ, Pressel S, Rosner B, Taylor JO, Schneider K, Hames CG. Prediagnostic serum selenium and risk of cancer. Lancet 1983; ii: 130-34. 2. Cantley LC, Josephson L, Warner R, Yanagisawa M, Lechene C, Guidotti G. Vanadate is a potent (Na, K)-ATPase inhibitor in ATP derived from muscle. J Biol Chem 1977; 252: 7421-23. 3. Aronson JK, Carver JG. Diagnosing digoxin toxicity by combined measurement of plasma digoxin concentrations and erythrocytic 86rubidium uptake. Br J Clin Pharmacol 1983; 15: 618P-619P. 4. Reinila M, MacDonald E, Salem N, Linnoila M, Trams EG. Standardised method for the determination of human erythrocyte membrance adenosine triphosphatases. Anal Biochem 1982; 124: 19-26. 1. Willett