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Medical & Health Physics Med Phys 772 · PDF file•“Arcs” in free air...

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Ultraviolet Radiation
Transcript

Ultraviolet Radiation

What is it?

• Photons

• Energies between X-rays and visible light

• Natural and man-made exposure

Why Do We Care?

• Skin cancer

• Other effects in the skin

• Immunosuppression

• Eye damage

Why Do We Care?

• Regulatory

– Not much

– Radiation Emitting Devices Act (REDA or RED Act) for tanning beds

Physical Principles

Biological Divisions

UV-C UV-B UV-A Ionizing Visible

Energy (eV)

Wavelength (nm)

12.4 4.4 3.9 3.1

100 280 320 400

1240E

UV-C

• Ionization energy for water 12.4 eV

• UV-C 100 ≤ ≤ 280 nm

• “Germicidal”

• Exposure only from manufactured sources

UV-B

• 280 ≤ ≤ 320 nm

– Was 315 nm based on erythema action spectrum; current wavelength based on DNA damage

• Erythema-inducing region

• “Direct action” damage

• Hazardous solar ultraviolet

UV-A

• 320 ≤ ≤ 400 nm

• “Blacklight”

• “Indirect action” damage

• Induces fluorescence in many substances

Physical Divisions

Vacuum Far UV Near UV Ionizing Visible

Wavelength (nm)

100 190 300 400

Sources

Man-Made Sources

Man-Made Sources

• Incandescent

• Gas discharges

• Electrical discharges

• Fluorescent lamps

• Lasers

Incandescent

• “Blackbody” sources

• Very inefficient (0.1 – 0.2%)

• Rarely used for UV production

– Previously used for small spaces, e.g. dashboard phosphors

Gas Discharge

~

Gas Discharge

• Electrodes: W, Mo, Ta typical

• Glass walls

– Fused silica (quartz) 190nm

– “Suprasil” quartz 165nm

– Ti alloy doping to filter UV-C

– Filtering to block visible light

• Gases: Hg typical (10 – 25% UV)

– Inert; metal halides in high pressure lamps to increase output

Low Pressure Lamps

• 1 Pa, 500 K

• Discrete lines

High Pressure Lamps

• 1 MPa, 6000 – 8000K

Electrical Discharges

• “Arcs” in free air

• Spectrum depends on electrode composition

– W – arc welding; C – electrodes consumed

• Occupational hazard for arc welders

Fluorescent Lamps

• Low pressure Hg lamp (253.7nm main emission) with phosphor coating to convert UV into visible or UVA

• Blacklight phosphor (350 – 400nm) to induce fluorescence

• Sunlamp emission 280 – 400nm

UV Lasers

• Gas: He-Cd (325nm), N (337nm), excimer (various)

• Solid state: Nd:YAG frequency quadrupled (1064 → 266nm) using non-linear optical components

Solar UV

Solar UV

• Emitted from surface of sun

• Blackbody-like radiation 5600K

Solar UV at Sea Level

Wavelength

band

UV-C UV-B UV-A VIS NIR

Irradiance

(W/m2)

0 1 50 500 450

Terrestrial UV typically limited to > 290 nm due

to attenuation by ozone.

Variations in Intensity

Pathlength

• Latitude

• Season

• Altitude

Attenuators

• Ozone concentration

• Aerosols

• Smoke/Dust

• Rain

Attenuation of UV

Attenuation

• Absorption (ozone, oxygen, aerosolized water)

• Scattering (smoke, dust, other aerosols)

– Rayleigh

– Mie (“large” mm particles)

Aside: Rayleigh Scattering

• Elastic scattering of EM waves by particles much smaller than the wavelength

Aside: Mie Scattering

• Particle size comparable to or larger than wavelength

• Solution to Maxwell’s equations

Geometry

a

dO

d

Ozone: mO

Atmosphere

mR, mM

Direct Solar UV Irradiance

• a: solar zenith angle

• d: atmosphere thickness

• dO: ozone thickness (~0.32cm at STP)

• mR,M,O: Rayleigh, Mie scatter coefficients, ozone absorption coefficient

ammma seccos OOMR dd

o eEE

Aside: Irradiance

• What is it??

• Defined as the “radiant power incident on an infinitesimal surface element containing the point of interest, divided by the area of that surface element”.

– “Power density”, “Flux density” …

• Not to be confused with fluence rate, which is used for free space rather than a surface.

Geometry

a

dO

d

Ozone: mO

Atmosphere

mR, mM

Estimating Solar Altitude for Time of Day

80equinox for vernal

1day 1 Jan year ofday

plane eliptical tilt wrt sEarth'4.23

3652sinsinsin

plane equatorial & line

Earth-to-sun between angle ndeclinatiosolar

noonsolar after hr per 15 anglehour solar

latitude geographic

sinsincoscoscossin

o

max

max

1

o

dd

d

dd

h

ve

ve

How Do We Use These Equations?

• Many calculations involve numerical integration or heavy approximation

– Changes in UV attenuation in the atmosphere

– Estimating dose (e.g. changing the time of day you walk)

– Changes in cancer incidence due to either of the above

Attenuation Changes

• Ozone column/thickness of atmosphere, attenuation coefficient, time of day/year changes

– Calculations often relative to something else

– Ozone attenuation usually dominates scattering

ammma seccos OOMR dd

o eEE

Estimating UV Dose

• Integral of E() over wavelength (), time of day (t), days of the year (day)

• Use relationship h=90-a to bring time variables into play

– May be easier to substitute dt for d (see Solar Altitude calculation)

a am

dddaydteSE ood

o cossec

Solar UV “Dose”

• Standard Erythema Dose (SED) = 100 J/m2

erythemally weighted

• Minimum Erythema Dose (MED) is the weighted UV dose required to initiate erythema in an individual (clinical measure), about 200 J/m2 erythemally weighted

Intensity: Solar Altitude

Solar altitude h = 90 - a

Solar altitude h = 90 - a

Intensity: Ozone

Intensity: Altitude

• dE/E ~ +4% (net) for each 300 m above sea level

– Direct UV irradiance increases

– Scattered UV decreases

Intensity: Latitude

Intensity: Cloud Cover

Intensity: Seasonal Variations

Intensity: Surface Reflections

Practical Points

• Water is a weak reflector (<5%) and a poor absorber (>40% transmission through 50cm) of UV-B

– Sunburn under water

Practical Points

• Solar irradiance at sea level ~50% scattered and ~50% direct

– Exposure under localized clouds or in the shade

Practical Points

• Window glass absorbs UV-B strongly

– Longer to sunburn behind glass

Practical Points

• Sunlamps with UV-B filters not necessarily “safe”

• UV-A still causes

– Aging (“dermatoheliosis”)

– Immunosupression

– Erythema (much less than UV-B)

Interactions with Tissues

What Tissues?

• Skin

• Eyes

• Oral cavity (dentistry)

What Interactions?

• Absorption, primarily

– Scattering negligible (short pathlength)

• Important biomolecules

– Nucleic acids (pyrimidines: cytosine, thymine)

– Amino acids in proteins (tyrosine, tryptophan)

• Chromophores (melanin, hemoglobin, carotenes)

Nucleic Acids

0

1000

2000

3000

4000

5000

6000

7000

8000

9000

220 245 270 295 320

Cytosine

Thymine

Exti

nct

ion

Co

effi

cie

nt

(cm

-1 M

-1)

Wavelength (nm)

Amino Acids

Amino Acids

0

2000

4000

6000

8000

10000

12000

14000

220 270 320

Phenylalanine

Tryptophan

Tyrosine

Exti

nct

ion

Co

effi

cie

nt

(cm

-1 M

-1)

Wavelength (nm)

Chromophores

0

100000

200000

300000

400000

500000

600000

700000

800000

200 300 400 500 600 700 800

Melanin

HbO2

Hb

beta-Carotene

x 100

Exti

nct

ion

Co

effi

cie

nt

(cm

-1 M

-1)

Wavelength (nm)

Attenuation in the Skin

~200 µm

~1-4 mm

Attenuation in the Skin

Practically all UV absorbed in the epidermis

Attenuation in the Eye

Attenuation in the Eye

UV Photochemistry

• UV absorption by molecules generates photoproducts

• Principal target for UV is DNA

• Photoproducts constitute:

– Pyrimidine dimers (UV-B direct action)

– Single strand breaks (UV-A indirect action from OH●)

UV Photochemistry

1. Absorption 2. Fluorescence 3. Phosphorescence 4. Vibrational relaxation 5. Internal Conversion 6. Intersystem Crossing 7. Quenching

Energ

y

Ground electronic state (singlet)

First excited singlet state

First excited triplet state

1 3

2

5

4

6

7 4

4

4

7

UV Photochemistry

• Excited singlet or triplet state may:

– React with another molecule

– Transfer its energy / electron spin to another molecule

– Break apart (common source of OH●)

UV Photosensitivity

• UV interacts with exogenous molecules (photosensitizers) to produce a biologically strong reactant

• “Photodermatosis”: rashes, et cetera that appear after exposure to sun

UV Photosensitivity

• Light sensitivity diseases

– Polymorphic light eruption (looks like boils)

– Actinic reticuloid (chronic inflammation upon sun exposure)

– Solar urticaria (hives)

– Porphyria (over production and accumulation of porphyrins)

UV Photosensitizers

• Things you might not expect...

– Phenobarbitone (hypnotics)

– Chlorpromazine (tranquilizer)

– Thiazide (diuretics)

– Tetracyclines & sulphurs (antibiotics)

– Cosmetics containing eosin or psoralens

UV Photosensitizers

• Intentional (clinical) use

– Methoxypsoralens (e.g. 8-MOP) causes cross-linking to prevent DNA replication

– Hematoporphyrin derivative (HPD) for photodynamic therapy (skin sensitivity a few weeks after treatment)

UV Photosensitization

OXXO

OSOT

*

2

1

*

2

1

2

3*

Quenching Singlet Oxygen

• Quenchers de-excite the singlet oxygen prior to it reacting with anything useful

– Collisional quenching (energy transfer)

– Static quenching (binding)

• Common quenchers

– Vitamin E

– Carotenes

– Ascorbic acid (vitamin C)

Biological Effects

Cellular Level Effects

• Melanogenesis

– DNA damage

– Activation of tyrosinase

– Liberation of cell membrane lipids

• Immunosuppression

– Decrease in Langerhans cells (T-cell antigens)

– Change urocanic acid trans to cis

– Alter epidermal cytokine production

Cellular Level Effects

• Carcinogenesis

– Activation of oncogenes

– Inactivation of tumour suppressor genes

• Cell growth arrest

• Apoptosis

– Both mainly during UV sterilization

Organ Level Effects

• Stochastic

– Probability increases with dose

• Deterministic

– Severity increases with dose beyond some threshold

• Effects are somatic

– No inheritable genetic damage

Responses To UV

Skin

Attenuation in the Skin

~200 µm

~1-4 mm

Attenuation in the Skin

Practically all UV absorbed in the epidermis

Deterministic Effects

• Erythema & subsequent melanogenesis

– Inflammatory response – epidermal & dermal vasodilation

– Mechanisms – direct action on vessels, indirect action in response to diffusion of prostaglandins in the epidermis to the dermis, response to DNA damage

– Edema, pain, blistering at high UV doses

– Thickening of the stratum corneum (3-5x)

Blood Flow in the Skin

Erythema Time Course

Early onset

erythema

High UV dose

Late onset

erythema visible

MED exposures

Maximum

erythema

Erythema

fades

Immediate pigment

darkening (IPD)

Delayed melanogenesis

becomes noticeable

0 4 1-2 12-24 hours 1-2 days

Minimal Erythemal Dose

• MED

• Minimum biologically effective dose (really radiant exposure) required to induce erythema in an individual (~ 200 J/m2 in melano-compromised individuals)

• Highly dependent on individual factors, standard erythema dose ( 1 SED = 100 J/m2) introduced for standardization

Skin Types

Fitzpatrick et al. 1975

Skin Types

1 SED = 100 J/m²

Biologically Effective Irradiance

• E(): Spectral Irradiance (W/m²/nm)

• S(): Biological Effectiveness curve

– e.g. erythema action spectrum

dSEEeff

Erythema Action Spectrum

Erythema Action Spectrum

CIE (1998) ▬

Anders (1995) ▲

CIE (1935) ■

CIE: International Commission on Illumination

Wavelength Dependence of MED

Erythema Action Spectrum, In Action

• Small changes in UV-B (different ozone conditions) can result in large changes to biologically effective dose (FxB)

Aside: Dobson Units

• 1 DU = 10 µm of ozone at STP

• Reference level is 220 DU, corresponding to development of the Antarctica ozone hole

Aside: SPF

• Sun Protection Factor

• Really a dose reduction factor

– e.g. SPF 15 reduces dose to skin by 15x

– Dactual = Do/SPF

Melanin Production

• “Melanogenesis”

• Produced in melanocytes in basal layer

– Boundary between epidermis & dermis

• Melanin redistributes to keratinocytes in epidermis

• Skin pigmentation (“tanning”) and thickening (“conditioning”) may increase MED for UV-B exposure at least 4x

Deterministic Effects

• Immunosuppression

– Loss of epidermal antigen presenting Langerhans cells

– Alteration of urocanic acid (trans to cis) activates “suppressor T-cells”

Deterministic Effects

• Aging of the skin – “Late effect”

– Structural changes in the dermis

– Dryness, loss of elasticity, mottled complexion, deep wrinkling

– Difficult to determine action spectrum due to long term nature of the changes

• Actinic Keratosis (AK) – hard, precancerous skin lesions

Deterministic Effects

• Vitamin D production

– Conversion of 7-dehydrocholesterol in epidermis to D3 previtamin

– Conversion in liver to useful 25-hydroxyvitamin D

– D3 broken down by UV

– Only 15 minutes exposure to hands, arms, face, during spring to fall on a clear day

Stochastic Effects

• Cancer

– Basal cell, squamous cell: highly treatable

– Malignant melanoma: challenging

• Modeling skin cancer incidence

– Rate of Incidence, UV Dose, amPlification factor

pDI

BCC/SCC

• Both highly treatable (99% CR BCC, 97% CR SCC)

• Mainly UV-B

• p~2.5 SCC, ~1.5 BCC

• Higher incidence with lower pigmentation

• Incidence ~50% in Americans age>65

• Unknown latency

• SCC often accompanied by AK

Non-Melanoma Action Spectrum

Relative Risk for BCC/SCC

Melanoma

• Highly metastatic

• Action spectrum is unknown, although UV-B irradiation seems to be the main risk

• Often found on covered regions (e.g. trunk) – “Acute exposure hypothesis”

• 10-15 year latency

• Rising incidence (doubles every ~15 yrs)

The Eye

Attenuation in the Eye

Attenuation in the Eye

Exposure Levels Required To Produce Ocular Effects

Mainly in the cornea and conjunctiva.

Deterministic Effects

• Conjunctivitis (conjunctiva)

• Photokeratitis (cornea)

– Welder’s flash, arc eye, snow blindness

– Primarily caused by excessive UV-B

– Inflammation of the cornea, resolves spontaneously in about 36 hours

– Thresholds 270nm (~50), 310nm (~550), 315nm (~22,500 J/m²)

Deterministic Effects

• Cataract formation

– Evidence from animal models and human epidemiology, 295 – 320 nm range

– Relatively high exposures required (> 5 MED for transient cataracts)

• Retinal damage

– Not observed (< 1% UV-A penetration)

Stochastic Effects

• Tumours

– Some epidemiological evidence of ocular melanoma

– Choroid & ciliary body melanomas positively correlated with time outdoors (Australian study: Vajdic 2002)

– Hypothesis that UV exposure from the horizon rather than overhead

Medical Applications

Phototherapy

• UV-B for skin conditions such as:

– Psoriasis (scaling due to rapid cell division)

– Vitiligo (depigmentation, possibly due to autoimmune effects)

– Atopic dermatitis / eczema (chronic rash, may be heriditary)

• Light source tends to be fluorescent lightbulbs with various filter materials added to select spectral content

Phototherapy

• Psoriasis

– Suppresses cell division, changes the inflammatory environment of the site

Phototherapy

• Vitiligo

– Suppresses immune system in irradiated region

Phototherapy

• Eczema

– Helps to suppress inflammatory response

Phototherapy

• Old school – broad band ultraviolet A+B

Images from Solarc Systems

Phototherapy

• New school – narrow band UV-B (311 nm)

– Minimizes erythema while catching the edge of the psoriasis/vitiligo “action spectrum”

Images from Solarc Systems

PUVA Therapy

• Psoralen + UV-A

– Psoriasis (scaling of the skin) & vitiligo (autoimmune/inflammatory depigmentation)

– Cutaneous T-cell lymphoma (photophoresis technique)

– 8-MOP (methoxy psoralen, topic or oral) + UV-A (360nm)

Psoralens

• 3 ring compounds that bind to DNA non-covalently

• Irradiation @ 365nm causes covalent binding to thiamine, and subsequent irreversible cross-linking

• Fatal to healthy cells

General psoralen structure

8-methoxy psoralen

Extra-Corporal Photopheresis

Damaged white blood cells

recognized by immune system,

which makes healthy lymphocytes

to fight against those abnormal cells.

Treatment is used for cutaneous

T-cell lymphoma.

Neonatal Jaundice

• “Hyperbilirubinemia”

• 10 – 20% of newborns

• Excessive bilirubin photodecomposed by UV-A and blue light (400 – 480nm)

Dentistry

• Polymerization of resins

• Fluorescence of tooth enamel

– Decreased fluorescence in the vicinity of cavities

– Not used routinely

Pathology/Biology/Other

• Sterilization of air and flow hoods in various biological laboratories

• New UV-C based technologies used for terminal cleaning of hospital rooms

– High intensity pulsed xenon arc lamps

– 1 pulse is enough to exceed the occupational effective limit of 30 J/m² (coming up)

Detection & Dosimetry

Terms & Units

Symbol Name Relationship Units

Q Radiant energy J

φ Radiant flux ∂Q/∂t W

I Radiant

intensity ∂φ/∂Ω W/sr

L Radiance ∂φ/∂Ω/∂s W/m²/sr

E Irradiance ∂φ/∂s W/m²

H Radiant

exposure ∂Q/∂s J/m²

Biologically Effective Irradiance

• Recall:

dSEEeff

Detection Theory

• Rather than biologically effective irradiance we measure:

• In practice, a correction factor is applied so signal can be directly correlated to a dosimetric quantity (e.g. SED/MED)

dGESignal

dGE

dSECF

known

known

UV Dosimeters

• Thermal

• Photon counting

• Chemical

• “Biological”

Thermopile Detectors

• Incorporated into “Pyranometers”

• Principle: Voltage α ∆T

• Sensitivity: 10 µV / [W/m²]

• Accuracy: ±1% typical

• Spectrum: 250 – 2000 nm

• Uses: Secondary calibration standards, field instruments

Thermopile Detectors

V

Envelope

Thin

window

Pt electrode Heat sink

Receiver

(Au, Pt)

Semiconductor

Photon Counting

• Photomultiplier tube

• Photodiode

Photomultiplier Tubes

• Principle: photoelectrons from photocathode multiplied by accelerating through a series of dynodes

• Advantages: very high sensitivity

• Problems: fragile, stable voltage required

• Uses: measuring low irradiances

Photomultiplier Tubes

Photodiodes

• Principle: photoconductivity (reverse bias) or photovoltaic (no applied voltage – photoelectric current only)

• Advantages: inexpensive, stable, robust

• Disadvantages: poor UV sensitivity

• Uses: routine portable usage

Photodiodes

Chemical Sensors

• “Actinometry”

• Principle: absorbed photon induces a detectable chemical change

• Advantages: passive device (no p/s required)

• Disadvantages: calibration, reproducibility

• Uses: dosimetry in microbiological specimens

Biological Sensors

• Real systems

– Example: determine a treatment time based on erythema onset on a small patch of skin

• Simulated

– Attempt to match the “detector’s” response G() to some appropriate action spectrum S()

– Problems: person-to-person S() variability, small mismatches may amplify dose differences, angular response of detector same as what is being modeled?

Protective Measures

General Health & Safety

• Administrative Controls

• Engineering Controls

• Personal Controls

Administrative Controls

• Limit access (necessary personnel only)

• Information on hazards (education, policies and procedures)

• Signs and warning lights

• Substitution

• Distance and time limits (based on MPE)

Engineering Controls

• Containment (barriers, instrument housing)

• Machine guards

• Interlocking (device turns off or doesn’t operate under certain conditions)

• Screens, UV filters

• Elimination of reflective surfaces

Personal Controls

• Personal Protective Equipment (PPE)

• Skin

– Clothing is best

– UV-A+B sunblocks, but industrial setting UV-C may also be a concern (SPF 30 minimum preferred)

• Eyes

– Glasses: opaque for <400nm, side shields, good visible transmission

– Welding shades: helmet or mask with filters

Ozone Production

• UV-C produces ozone in air <260nm

• Smell sensitivity ~ 0.1 ppm

• Occupational limits in Ontario

– 0.1 ppm daily average, 0.3 ppm 15 minute exposure

• Lethal concentration ~ 50 ppm for 0.5 hours

Exposure Standards

Historical

• CIE (1935) – Standard erythema curve

• AMA (1942) – 1 EU = 100 mW/cm2 * S(297)/S()

• NRPB, NIOSH (1977, 1972) – Modern standards

– 2004 International Commission on Non-Ionizing Radiation Protection (ICNIRP)

Radiation Protection from Modern Standards

• Based on an envelope action spectrum incorporating erythema and photokeratitis

• Not valid for photosensitive individuals (type 1 skin)

• Sets effective exposure limits

• NO CANADIAN STANDARDS (or US, really)

– American Conference of Governmental Industrial Hygienists (ACGIH)

• 30 J/m² “Threshold Limit Value”

Ontario Ministry Of Labour

• “…an employer shall take every precaution reasonable…” (s.25(2)(h) of the Occupational Health & Safety Act)

• MoL uses ACGIH exposure guidelines to establish if a workplace is using due diligence in protecting its workers

• Guidelines do not apply to workers using UV lasers or hypersensitizing substances

Envelope Action Spectrum

ICNIRP 2004

Envelope Action Spectrum

Effective Irradiance and Exposure

dttEH

dSH

dttEH

dStEtE

T

T

effeff

eff

0

0

,

,

Polychromatic & UV-B Exposure

• UV-B exposure limit chosen conservatively

– 30 J/m² of Effective Radiant Exposure

– Total over any 8 hour period

• Tabulated as Radiant Exposure limits for monochromatic radiation

• Compare with MED

ICNIRP 2004

MPE Based on Effective Irradiance

30 J/m2 maximum exposure (UV-B&C) ICNIRP 2004 (ACGIH uses same table) NIOSH uses 254nm as reference, so permits 0.2 µW/cm² for 8 hours or 100 µW/cm² for 1 minute (2x above, why?)

Maximum Permissible Exposure (8h Period)

UV-A Exposure

• Maximum permissible exposure (MPE) based on irradiance (long times) or radiant exposure (short times)

• 10 W/m² for t > 10³ s

• 10 kJ/m² for t < 10³ s

– Why?

• No annual exposure limit

Associated Regulators / Regulations

• Radiation Emitting Devices Act & Regulations (Tanning Equipment)

– Canadian regulations administered by Health Canada

• ICNIRP & WHO reports

• EC Health & Consumer Protection Directorate-General

• Ministry of Labour (Ontario)

REDA

• “Radiation” means energy in the form of electromagnetic waves or acoustical waves

• “Radiation emitting device” means

– (a) any device that is capable of producing and emitting radiation, and

– (b) any component of or accessory to a device described in paragraph (a)

REDA

• Prohibits the sale, lease, or importation of any radiation emitting device in Canada that:

• (a) does not comply with the standards, if any, prescribed under paragraph 13(1)(b) and applicable thereto; or

• (b) creates a risk to any person of genetic or personal injury, impairment of health or death from radiation by reason of the fact that it – (i) does not perform according to the performance

characteristics claimed for it, – (ii) does not accomplish its claimed purpose, or – (iii) emits radiation that is not necessary in order for it to

accomplish its claimed purpose.

REDA

13.1(b) The Governor in Council may make regulations prescribing standards regulating the design, construction and functioning of any prescribed class of radiation emitting devices for the purpose of protecting persons against genetic or personal injury, impairment of health or death from radiation.

REDA

• Governor in Council = Prime Minister + Cabinet – Executive authority is vested in the Crown

• Acts versus Regulations – Laws passed by a legislative body versus directions

adopted by the executive branch that have the binding effect of law. Generalized laws are often passed that empower a particular department of the executive branch (through the appropriate cabinet minister) to make regulations to implement the intent of the general law.

REDA

• Prohibits deceptive claims

• Sets regulations for labeling, packaging, safety and functional features, and advertising

Tanning Equipment Regulations In Canada

• “Tanning equipment” means a device that – Can be equipped with one or more ultraviolet lamps

– Induces skin tanning or other cosmetic effects and is advertised as inducing such effects.

• No occupational UV standards, but… – “Prevent over exposure” – any dose that exceeds the

amount required to produce daily vitamin D requirement

– “Tanning is not safe”, but the evidence is not strong enough to ban tanning equipment (regulations FAQ)

Tanning Equipment Regulations In Canada

• Exposure time calculations – 100 J/m2 for the first session, and up to 625 J/m2

per session beyond the first (usually increase gradually)

– Similar to FDA dosing schedule, but uses CIE(1998) action spectrum from previous lectures (unlike FDA)

ES

mJDose

Time2


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