Transcript Medicina del Lavoro Prof. Francesco S. Violante

Occupational Medicine
Prof. Francesco S. Violante
Noise, Ionizing and Non-ionizing Radiations,
Lung Diseases caused by Dust and Chemical
Agents, Occupational Dermatites, Solvent and
Pesticide Intoxications
Noise


Sound = a series of pressure variances
(oscillations) propagating through an elastic
medium (a solid, a liquid or a gas) and
perceived by the human ear as sound
sensation
Noise = an undesired and annoying sound
that, due to its physical characteristics, is
potentially able to cause a temporary or
permanent physical or psychic damage to
the human organism (Giaccai, 1995 mod.)
Physical Characteristics
Λ = Wavelength: horizontal distance
between two subsequent crests or troughs
 A = Amplitude of the wave: maximum
wave range
 T = Period: time required for one
oscillation

Physical Characteristics

Frequency = Number of oscillations per
second. It is measured in Hz (the human ear
can detect frequencies between 16 and 16000 HZ)

Acoustic intensity = sound energy
radiated by the source (acoustic power, W)
per unit area perpendicular to the direction
of propagation (W/m2)

Timbre = refers to sound quality and is
determined by the wave shape
Unit of measurement

Noise intensity is usually measured in
Decibels (dB). The Decibel is the logarithm
of the ratio between a reference sound
intensity and the intensity which is being
measured
minimum pressure variance value
detectable by the human ear for a pure tone
of 1000 HZ

Range: from 0 dB, which corresponds to the
hearing threshold level, to 120 dB, which
corresponds to the pain threshold level
Perception

Sound is transmitted through air (external
ear middle ear) and bone conduction (middle
ear  inner ear)

The auditory apparatus (inner ear, organ of
Corti) transforms sound (mechanical energy
carried by sound waves) into action potentials
that reach the cortical acoustic areas
through the acoustic nerve, determining
the sound sensation
Perception

External ear: gathers sound waves
and transmits them to the middle ear

Middle ear: transmits and amplifies the
sound energy from the eardrum to the
oval window through the ossicular chain
and the contraction of the stapedius and
tensor tympani muscles

Inner ear: transduction of mechanical
energy (acoustic waves) into an electric
signal (action potentials of the acoustic
nerve)
Anatomy of the Ear
Organ of Corti
Perception

The discrimination of sound frequency
takes place at the level of the organ of
Corti thanks to a tonotopic localization
of receptors (high frequencies near the
staples, low frequencies at the cochlea)

The discrimination of sound intensity
depends on the number of impulses
reaching the cortex
Perception

Sounds with intensity levels >70-75
dB induce a reflex contraction of the
stapedius and tensor tympani muscles,
which attenuates by 20 dB the acoustic
energy reaching the inner ear (lowpitched tones)

This mechanism is not effective in case of:
 chronic exposures
(due to adaptation and muscular fatigue)

Impulsive noises (reaching the inner ear
before the reflex occurrs)
Intensity of noise: examples
Clock ticking
20 dB
Whispering
30 dB
Conversation
60-70 dB
Motor vehicles on a highway
100 dB
Rock concert, circular saw
110 dB
Taking off airplane
120 dB
Occupational Exposure

Industrial sectors with noise rates
frequently ≥ 85 dBA:
 Engineering sector
 Building sector
 Wood sector
 Textile sector
 Paper mills
 Food industry
Distribution of 9.368.000 Production Workers
who had Noise Exposure Levels of 80 dB or
greater (USA)
Percentage trend of noise-induced hypoacusias and
deafness with respect to the total number of
occupational diseases (diseases “tabled” in D.P.R 336; year of
manifestation: 1985-1999)
90
80
70
60
50
40
30
20
10
0
1985
1986
1987
1988
1989
INDUSTRIA
Chimica
Elettricità
M etallurgia
Tessile e Abbigliamento
Varie
Source: INAIL data processed by ISPESL
1990
1991
1992
1993
1994
1995
1996
1997
1998
Lavorazioni agricole a carattere industriale
Costruzioni
Legno e Affini
M ineraria
Trasporti
1999
Percentage trend of hearing loss cases
compensated by INAIL, by occupation
(“tabled” occupational diseases only)
Altre occupazioni
Minatore
TOTALE
(85-99)
Fabbro ferraio
Tessitore
1995-1999
Montatore
Saldatore
1990-1994
Carpentiere (e aiuto)
Operatore
1985-1989
Falegname
Muratore
Meccanico
0
Source: INAIL
5
10
15
20
25
30
35
40
45
50
Prevalence of Hearing Loss > 45 Dbhl for the
General Population in Great Britain
(Davis, 1988)
Percentage trend of hearing loss cases
compensated by INAIL, by age (”tabled”
occupational diseases only)
65 ed oltre
60 - 64
55 - 59
50 - 54
1995-1999
45 - 49
40 - 44
1990-1994
35 - 39
1985-1989
30 - 34
25 - 29
20 - 24
15 - 19
Fino a 14
0
Source: INAIL
5
10
15
20
25
30
Noise effects

Auditory effects




Temporary Threshold Shift (TTS)
Hypoacusia due to chronic acoustic trauma
Hypoacusia due to acute acoustic trauma
(injury)
Extraauditory effects
Auditory effects

Temporary Threshold Shift (TTS) =
elevation of the auditory threshold as
compared to rest

TTS2 or physiological auditory fatigue
is measured 2 minutes after the end of exposure
and has a duration of 16 hours

TTS16 or pathologic auditory fatigue
is masured 2 minutes after end of exposure and has
a duration of more than 16 hours
Auditory effects

Physiological auditory fatigue (TTS2)

It varies among subjects but remains constant in the same
subject

It increases proportionally with sound pressure, for
stimuli over 70 dB

It begins with stimulating frequency and then extends to
other frequencies according to increase in intensity

Recovery is proportional to the logarithm of time (most of
the recovery takes place within the first hours)

It does not usually exceed 30 dB
Auditory effects
Hypoacusia due to chronic acoustic
trauma

If noise exposure persists (daily occupational
exposure≥ 85 dBA or attention value) the
temporary damage to auditory cells (TTS)
progressively tends to become permanent
Permanent Threshold Shift (PTS) or
hypoacusia due to chronic acoustic
trauma or noise-induced hypoacusia
Example of audiometric tracing of
noise-induced hypoacusia
Auditory effects

The damage affects the organ of Corti (external
ciliated cells)

It is a bilateral neurosensorial (or perceptive)
hypoacusia, almost always symmetrical,
progressively irreversible and evolutive, as a
result of persistent exposure to noise

It mainly concerns high frequencies ranging from
3000 to 6000 Hz with an initial peak at 4000
Hz
Hypoacusia due to chronic acoustic
trauma
Onset is progressive (and nearly always insidious),
and develops in four phases:
p
Initial phase: at the end of the work-shift,
the worker complains of tinnitus (buzzing,
ringing) ,“full ear” feeling, headache,
giddiness, daze, asthenia, etc.
p
Audiometric phase: symptomatology is
absent (a slight intermittent tinnitus at most)
and the damage is revealed only by an
audiometric test (deficit at 4000 Hz)
Hypoacusia due to chronic acoustic trauma
p
Onset phase: appearance of auditory deficits
(hypoacusia) for high-pitched tones (4000 and
6000 Hz), combined with difficulty
conversating, especially in noisy
environments, and need to turn up the volume
of radio or TV
p
Illness phase: appearance of auditory deficits
(hypoacusia) for speech frequencies (500 and
2000 Hz), which can affect social life;
permanent and/or nocturnal tinnitus (with
insomnia) and appearance of the “recruitment”
phenomenon (distorted and annoying
perception of noises of relatively high
intensity) are also possible
Hypoacusia due to chronic acoustic
trauma
Diagnosis






Pathological and working anamnesis
Risk assessment for exposure to noise
Tonal audiometry (with determination of air and
bone conduction) performed in silent cabin in
conditions of acoustic rest, preceded by otoscopic
examination
Vocal audiometry
Tympanometry and reflectometry
Evoked auditory potentials
Hypoacusia due to chronic acoustic trauma
Synergic effects with noise

Vibrations

High temperatures

Organic solvents (derived from benzene)

Carbon sulphide

Carbon Oxide


Cyanides
Methylmercury

Pesticides
Epidemiological studies
Risk factors associated with hearing loss:
- Old age
- Previous ear surgery
- Decline of cognitive function
- Diabetes mellitus
- Hypercholesterolemia
- Use of analgesics
- Smoking
(E. Toppilla et al., Individual Risk Factors in the Development of Noise-Induced
HearingLoss. Noise Health. 2000; 2(8): 59-70)
Extra-auditory effects

They seem to be attributable to the
connections between the acoustic
pathways and CNS areas different from
the auditory cortex

E.g. the reticular zone, which is connected
via descending pathways to the
mechanisms that control voluntary
motility, spinal reflexes, with the
hypothalamus (and the neurovegetative
system)
Extraauditory effects







They seem to be attributable to the
connections between acoustic
pathways and CNS areas, different from
the auditory cortex, related to the
neurovegetative system
Sleep disorders
Reduced attention and concentration
Anxiety and irritation
Reduction in working efficiency
Increase in cardiac frequency and arterial pressure
Increase in gastric secretion
Ionizing and Non-ionizing Radiations
Ionizing Radiations

Ionizing radiations are electromagnetic
particles and waves whose energy is
sufficient to directly or indirectly ionize
the atoms they pass through, so as to
modify matter properties

It is believed that any exposure to
ionizing radiations provokes “biological
effects”, which are generally harmful;
type, appearance and severity of such
effects can differ widely
Ionizing Radiations

Electromagnetic Radiations



X rays
Gamma rays
Corpuscular Radiations




Alpha particle
Beta particle
Neutrons
Nrotons
Ionizing Radiations
Alpha rays

Particles carrying a double positive charge,
composed of two helium nuclei (2 neutrons and 2
protons)


Source: radioactive atomic nuclei with a high
atomic number
Penetrating power: extremely weak, skin basal
layer (100-fold weaker than beta rays) Radius in tissues:
few µ

Ionizing power: very high (1000-fold higher than

Dangerousness: dangerous only if emitted inside
the human body
that of beta particles)
Ionizing Radiations
Beta rays



Particles made of electrons (beta-) and positrons
(beta+) emitted by a decaying nucleus. Some
high-speed beta particles interact with matter,
emitting x rays (natural x rays)
Source: radioactive atomic nuclei, accelerators
Penetrating Power: weak, 1 cm below skin
surface (100-fold stronger than alpha rays, but 100-fold
weaker than gamma rays) Radius in tissues:: few mm
Ionizing Radiations


Ionizing power: minimal
Dangerousness: always harmful with internal
sources; harmful for structures at less than 1 cm
from the skin
Ionizing Radiations
Neutrons



The neutron is, together with the proton, one of
the two components of atomic nuclei; neutrons
have no electric charge and lose energy through
interaction with the atomic nuclei of the materials
they pass through
Source: nuclear reactors and accelerators,
nuclear explosions
Dangerousness: high. The source is always
external and emissions cease only when the
source is switched off
Ionizing Radiations
Gamma rays




Source: radioactive atomic nuclei, nuclear
explosions
Penetrating power: strong (100-fold stronger
than that of beta rays). A few centimeters of lead
reduce the intensity of these rays by a factor of 2
Ionizing power: they produce secondary
electrons that ionize air
Dangerousness: always dangerous, even when
emitted by external sources
Ionizing Radiations
X rays





Electromagnetic radiations similar to gamma
rays, but with a lower frequency
Source: artificial production (x-rays tube),
collision between electrons and matter
Penetrating power: high
Ionizing power: high
Dangerousness: high, but lower than that of
gamma rays
Ionizing Radiations
Ionizing Radiations
Natural background
 Radioactivity is a natural phenomenon, we
are constantly exposed to natural radiations
 External sources
cosmic radiations, radioactive substances contained in the
soil and in building materials

Internal sources
radioactive substances which are inhaled or ingested and
the radioactive constituents of our body, especially
potassium 40
Ionizing Radiations
Absorbed dose (D)



Indicates the quantity of energy imparted by
radiation and absorbed by tissues and results
from the interaction of radiation with matter
D = dE / dm = ratio of energy imparted to a
given volume to the mass contained in that
volume; the higher the absorbed dose, the more
severe the effect of a radiation
The unit of measurement (SI) is the Gray (Gy)
Ionizing Radiations
In order to compare the effects of different types of
IR, a numeric coefficient or QF is used (it depends
on the LET# and is linearly proportional to the RBE*
of each type of IR)
# number of ionizations produced per unit path length in the biological
medium
* ratio of the dose of a “standard” radiation (produced by a 250-kv x-ray
source), expressed as D250, to the dose of the analysed radiation (Dr) that is
necessary to obtain the same biological effect (= D250/Dr)
Ionizing Radiations
Dose equivalent (H)



The product of absorbed dose in tissue (D) and the
quality factor (QF) is defined as dose equivalent
(H=QFD).
The unit of measurement (SI) is the Sievert (Sv)
Since the QF for x and  rays is 1, Sv and Gy for x
and  rays are equivalent
We often refer to dose or absorbed dose equivalent per unit
time, that is intensity or absorbed dose rate (Gy· s-1), or
dose equivalent rate (Sv· s-1)
BIOLOGICAL EFFECTS OF
IONIZING RADIATIONS
IONIZING
RADIATIONS
LIVING
MATTER


ELEMENTARY PHYSICAL PHENOMENA

IONIZATIONS

FREE RADICALS

DIRECT AND INDIRECT ACTIONS

BIOLOGICAL EFFECTS
BIOLOGICAL EFFECTS OF
IONIZING RADIATIONS

It is believed that, to inactivate cells, IR
damage some essential macromolecules
(biological target) as DNA, proteins,
sugars and complex lipids

The effect of IR on the biological target
can occur either by direct or indirect
action
BIOLOGICAL EFFECTS OF
IONIZING RADIATIONS
> ionizing ability> damage
Direct action


Target molecules are directly damaged by rupture
of molecular links
The target is a structure, which is:
 Sensitive to IR
 Essential in the biological system
Direct action

Cellular macromolecules get damaged by free
radicals, resulting from water radiolysis
BIOLOGICAL EFFECTS OF
IONIZING RADIATIONS
Ionizing radiations damages





DETERMINISTIC DAMAGES:
Somatic effects: appearing in the
irradiated individual
STOCHASTIC DAMAGES:
Somatic effects
Genetic effects: occurring in the offspring
of the irradiated individual
DETERMINISTIC DAMAGE
(graded or non-stochastic damage)






●
●
●
●
This damage is exclusively somatic
There is a threshold level
The severity of damage depends on the dose
The latent period is usually short (late onset in
some cases)
Dose-effect relationship is represented by a
sigmoid curve
Damage can be:
direct (early):mainly affecting parenchymal cells
indirect (late): affecting vascular and connective
tissue structure
generalized
localized
DETERMINISTIC DAMAGE
(graded or non-stochastic damage)
Dose-effect relationship
DETERMINISTIC DAMAGE
(graded or non-stochastic damage)
Law of Bergonié and Tribondeau
Cells sensitivity to IR radiation is:
 directly proportional to their mitotic
activity
 inversely proportional to their degree of
differentiation
 On the basis of this principle, a tissue
radiosensitivity scale can be defined

Tissue
Relative Radiosensitivity
Linfatic tissue, hemopoietic marrow, germinal
epithelium of the skin and of the small
intestine
Very High
Skin, other epithelial tissues (cornea,
crystalline lens, mucosa of the digestive tract)
High
Growing bone and cartilage
Moderate
Salivary glands' epithelium and liver
epithelium; renal and pulmonary epithelium
Medium
Muscle, nervous tissue (CNS and peripheral
tissue), mature bone and cartilage
Low
GENERALIZED DETERMINISTIC
DAMAGE
Whole-Body Radiation Syndrome
 Acute radiation to the whole body or to a
large portion of the body (global
radiation) gives rise to the so-called
Acute Radiation Syndrome:
 It is characterized by three worsening
clinical stages (hematologic,
gastrointestinal and neurologic stage)
developing according to their respective
dose thresholds
GENERALIZED DETERMINISTIC
DAMAGE
Radiation disease (prodromic phase)
Dose = 1-2,5 Gy


Severity of radiation is inversely
proportional to the latency of symptoms
nausea, vomiting, diarrhea, anorexia, headache,
dizziness, asthenia, olfactory and taste anomalies,
cardiac arrhythmias, hypotension, irritability,
insomnia
GENERALIZED DETERMINISTIC
DAMAGE
Hematologic Syndrome
Dose = 2.5 – 4.5 Gy



It results from the damage affecting the
staminal compartment of hematic cells
Early fall of lymphocytes and granulocytes (24 –
48 ore), followed by a latency period of two
weeks, associated with relative well-being
Late fall of erythrocytes and platelets
GENERALIZED DETERMINISTIC
DAMAGE
Trend of blood cells as a function of time, following wholebody radiation at moderate dose rate (< 10 Gy)
100
Lymphocytes
Granulocytes
60
Platelets
Erythrocytes
20
Cell %.
vs controls
5
10
15
20
25 Days after
radiation
GENERALIZED DETERMINISTIC
DAMAGE
Hematologic Sindrome



Fever associated with shivering, asthenia,
malaise, headache, hair loss
Appearance of petechias, gum hemorrhages,
worsening anemia, marked asthenia and
disphnea, infections
Death by cardiovascular collapse
GENERALIZED DETERMINISTIC
DAMAGE
Gastroenteric Syndrome
Dose = 5 - 20 Gy
It results from the damage affecting the
intestinal mucosa, due to failed maturation of
stem cells
Early appearance of nausea and vomiting, with
significant worsening after 3-5 days from radiation
 Violent diarrhea with watery and bloody stools
 Electrolytic imbalance with malnutrition
 Septicaemia
 Death within 1 or 2 weeks in conditions of
hyperpyrexia, septic status, dehydration

GENERALIZED DETERMINISTIC
DAMAGE
Neurologic Syndrome
Dose = 10 - 50 Gy




It results from the increase in permeability
of encephalic vessels
cerebral oedema, endocranic hypertension with
nervous tissue damage (always lethal).
sudden onset and fast development
rapid exitus due to marked prostration, apathy,
drowsiness, coma with or without convulsions
THE LITVINENKO CASE
THE LITVINENKO CASE
Polonium is a rare radioactive metalloid
found in uranium minerals
 Polonium-210: isotope of polonium,
alpha-emitter with a half-life of 138,39
days (1 milligram of this metalloid emits as
many alpha particles as 5 grams of radium)

THE LITVINENKO CASE
Polonium is a toxic element, it is highly
radiactive and dangerous to
manipulate
 It emits alpha particles, which travel only
a few centimetres in the air and can be
easily shielded, although in case of
penetration into the organism (by
inhalation or ingestion), they have a high
ionizing power and can cause damage to
the tissues

THE LITVINENKO CASE
The symptomatology of polonium
poisoning presents with the usual
symptomatology of whole-body radiation:
From vomiting, nausea and diarrhea (all the more
violent, the higher the radiation) to bone marrow
destruction and the consequent increase in infections
and hematic losses

In order for damages to be detectable, the
absorbed dose has to be about 1 Sv (a thoracic
radiography is about 20 millionths of an SV and the natural
radiation background is about 2 thousandths of an SV per
year)
THE LITVINENKO CASE




It is not clear how much polonium was
used to kill the former spy
The duration of his agony, about 3 weeks,
gives us some clues …
Subjects exposed to less than 5 Sv live
longer than 3 weeks and can even survive
The former secret agent is likely to have
received a dose comprised between 5 and
15 Sv
THE LITVINENKO CASE



i.e. the same quantity of radiations
absorbed by those who were about 800 m
from the Hiroshima explosion
If ingested, this radiation dose would
correspond to a ten-millionth of a gram of
Polonium
Estimates on the lethal dose vary widely
THE LITVINENKO CASE
DETERMINISTIC LOCALIZED
DAMAGE
Skin



In the past, it was used as a “biological
dosimeter”.
Doses ≥ 2 Gy in single fraction initially provoke
erythema (following dilation of skin
capillaries) lasting 48-72 hours; at a late stage,
dermic and hypodermic lesions (secondary
lesions to the microcircle) appear, associated
with fibrosis and possible thrombosis and
formation of microvascular telangiectases.
In more severe cases, chronic radiodermitis
may develop (sclerosis and ulcer).
DETERMINISTIC LOCALIZED
DAMAGE
Male Gonads



Germinal cells are more radiosensitive than
hormone-secreting cells, and radiosensitivity
also varies according to degree of maturation
(B spermatogonia  spermatozoa)
Doses of 4-6 Gy (4.000-6.000 mSv) cause
temporary infertility after 1–2 months
(generally lasting for at least 2 years)
For doses > 6 Gy (6.000 mSv), infertility may
be permanent
DETERMINISTIC LOCALIZED
DAMAGE
Female Gonads


The dose needed to cause temporary
infertility in women is higher than that
needed to cause temporary infertility in men
Doses of 20-30 Gy – 20.000-30.000 mSv
cause permanent infertility
DETERMINISTIC LOCALIZED
DAMAGE
Eye



The damage caused by radiation occurs in the
crystalline lens at the level of the epithelial cells
covering the lens
Opacities develop at the posterior pole. Over
time, the confluence of these lesions leads to a
total opacification of the lens, which is defined
as cataract
A threshold dose was defined for the
development of opacity and cataracts
DETERMINISTIC LOCALIZED
DAMAGE
Estimate of the threshold dose for deterministic effects to the crystalline lens
in an adult subject (ICRP 41 and ICRP 60)
Target organ and
effect
CRYSTALLINE
LENS: observable
opacities
VISUAL DEFICIT
(cataract)
Total dose
equivalent received
in a single
exposure (Sv)
Total dose
equivalent received
during repeated or
prolonged
exposures (Sv)
Annual dose
received during
repeated
exposures or
exposures
prolonged over
many years (Sv a1)
0.5-2.0
5
> 0.1
5.0
>8
> 0.15
STOCHASTIC DAMAGES
(probability-based damages)

Lack of threshold dose (precautionary
hypothesis assumed for the preventive purposes of
radiation protection)


The dose-effect relationship is linear without
threshold
Severity is independent of dose
STOCHASTIC DAMAGES
(probability-based damages)



They have long latent periods and are
randomly distributed in the exposed
population
The probability of appearance increases as
dose increases
They were demonstrated for high doses by
radiobiological experimentation and
epidemiological evidence
STOCHASTIC DAMAGES
(probability-based damages)
Dose-effect relationship
STOCHASTIC DAMAGES
(probability-based damages)
Genetic

Modifications of chromosome structure :





Variations in chromosome number:





deletion
duplication
inversion
translocation
nullisomy
monosomy
trisomy
tetrasomy
Point mutations
Somatic stochastic damage
 Represented


by:
Leukemias
Solid tumours
Somatic stochastic damage

The Law of Bergonié and Tribondeaux
seems to apply also to this case:

Tissues with a high mitotic index seem more
susceptible to neoplasia than tissues with a low
mitotic index.
Non-ionizing Radiations
Radiazioni Non Ionizzanti
Non-ionizing Radiations
Definition
Electromagnetic waves that:

Propagate through space, vibrating at a certain
frequency (Hz) with a certain wavelength (metric
units  nm  m).

Have an energy lower than 12 eV (minimum
energy needed to turn a stable atom into an ion).
Radiazioni
Non
Ionizzanti
Non-ionizing Radiations
ENERGY
The energy carried by a NIR increases as its
frequency increases:

High-energy NIRs have:



a high wave frequency
a short wavelength
Low-energy NIRs have:


A low wave frequency
A long wavelength
Types of NIR
NIRs in ascending wavelength order:

Optic damage:







Ultraviolet radiations(UV)
Visible radiations (VSBL)(400-760 nm)
Infrared radiations (IR)
Microwaves
Radiofrequencies
Electric and magnetic fields with extremely low
frequencies (ELF)
Static electromagnetic fields
Types of NIR
Laser (Light Amplification by
Stimulated Emission of Radiation)
Definition

A beam of optical radiation (Ultraviolet,
visible or infrared radiation):

Monochromatic

Coherent

Collimated
Laser (Light Amplification by
Stimulated Emission of Radiation)
Harmful effects of Lasers

The eye is the main target organ for Laser
damage, but skin can also be affected (burns),
although to a smaller extent

Its penetrating power into the ocular structures
varies widely depending on laser radiation
wavelength
Laser (Light Amplification by
Stimulated Emission of Radiation)
Harmful effects of Lasers

UV-B, UV-C , IR-B and IR-C laser radiations
stop at the conjunctiva and cornea

UV-A laser radiations can reach the crystalline
lens

VSBL and IR-A laser radiations can reach the
retina.
Ultraviolet Radiations (UV)

Invisible to the human eye

They are produced by special mercuryvapour lamps. These lamps are made of
quartz and special glasses and allow
filtering of electromagnetic waves with
wavelengths of 115-400 nm

UV radiation can penetrate:



ordinary glass
various types of plastic
any opaque material
Ultraviolet Radiations (UV)
UV radiations are divided according to
decreasing wavelength:

UV-A  longer wavelength (400-315 nm)
and lower energy rate

UV-B  intermediate wavelength (315 -280
nm)

UV-C  shorter wavelength (280-115 nm)
and higher energy
Ultraviolet Radiations (UV)
Occupational Exposure

Phototherapy

Photodiagnostics

Sterilization of surfaces and environments

Photohardening of resins

Arc welding, etc.
Ultraviolet Radiations (UV)
Harmful effects of UV radiation




The eye and skin are the main target organs of UV
radiation
The damaging effect is higher for UV-C radiation,
whereas UV-A radiation has a higher penetrating
power
UV-A radiation is unable to penetrate further than
the skin and crystalline lens (the retina is never
reached)
The penetrating depth is greater in subjects with fair
complexion, particularly albinos, who have no melanocytes
 no melanin, <cutaneous pigment able to absorb a part of the
UV-A radiation affecting the skin, thus preventing it from
penetrating deeper into the tissues
Ultraviolet Radiations (UV)
Harmful effects of UV radiation
Skin


Tanning (UV-A radiations stimulate the transfer of
melanin granules to the epidermis)
Erythemas (mainly induced by UV-B and UV-C)
the above-mentioned effects vary not only according to UV
type, but also according to length of exposure


Skin ageing, due to loss of skin elasticity caused
by UV radiation
Actinic Keratosis offers a fertile ground for the
onset of skin tumours (basocellular and
spinocellular carcinoma, melanoma)
Ultraviolet Radiations (UV)
Harmful effects of UV radiation
Eye

Photoconjunctivae

Photokeratitis

Opacity of the crystalline lens leading up to
actinic cataract
the above-mentioned effects vary not only according to UV type
(in this case, UV-B radiation is more effective), but also
according to length of exposure These ocular manifestations
appear 2 to 24 hours after eye UV irradiation
Infrared Radiations (IR)
UV radiations are divided according to increasing
wavelength:
IR-A 
shorter wavelength (760-1400 nm) and higher

IR-B 
intermediate wavelength (1400-3000 nm)

IR-C 
longer wavelength (3000-10000 nm) and lower

energy
energy
Infrared Radiations (IR)
Occupational Exposure

Glass processing (melting)

Smelting industry (blast furnaces)

Engineering sector (electric arc welding)

Others
Infrared Radiations (IR)
Harmful effects of IR radiation
The eye and skin are the main target
organs of UV radiation
 The damaging effect is higher for IR-A
radiation, whereas IR-C radiation has a
higher penetrating power
 However, also IR-C radiation is unable to
penetrate further than the skin and
crystalline lens (the retina is never
reached)

Infrared Radiations (IR)
Thermal Effects

Eye:
•
•
•
•

Blepharitis
Blepharoconjunctivitis
Keratitis
Posterior capsular cataract
Skin: superficial or deep burns, whose
severity depends on:
•
•
•
Incident thermal energy
Degree of pigmentation
Efficiency of local thermoregulation phenomena
Radiofrequencies and
Microwaves

Microwaves (MW)
 electromagnetic waves with wavelengths
ranging from 1 mm and 1 m and frequencies
between 100 Khz and 300 MHz

Radiofrequencies(RF)
 electromagnetic waves with wavelengths > 1
and frequencies between 300 MHz and 300 GHz
Radiofrequencies and
Microwaves
Extra-occupational Exposure


Domestic microwave ovens
Telecommunications:
a.
b.
c.
Diffusion systems (amplitude modulation aerials, TV
aerials)
Directive links (radio link)
Mobile telephony aerials
Radiofrequencies and
Microwaves
Occupational Exposure

Workers employed in the maintenance of
power plants and instruments producing
high electric fields

Plastic welding and moulding

Rapid wood gluing

Smelting and tempering of metals

Sanitary operators using Marconitherapy
(RF) and Radartherapy (MW) devices.
Radiofrequencies and
Microwaves
Thermal Effects

Temperature rise in the irradiated tissues
due to faster molecular movement and
consequent heat production

Hypersusceptibility of some organs:



Eye  possible development of cataract
Testes  atrophy and fibrosis with possibility of
temporary sterility
Ovaries  alteration of the reproductive cycle,
increase in abortions
Radiofrequencies and
Microwaves
Non-thermal Effects

Cardiovascular system: vasodilatation,
hypo or hyperkinetic arrhythmias

Nervous system: irritability, depression,
tremor, dizziness, sleep disorders

Endocrine system: hyperthyroidism,
hypercorticosurrenalism, etc.
Radiofrequencies and
Microwaves
Oncogenic Effects
TYPE OF TUMOUR
SIGNIFICANT
CORRELATION
STUDIES
GLIOMA
YES
Auvinen 2002
No
Christensen 2005
Johansen 2002
Inskip 2001
YES
_
No
Christensen 2005
Johansen 2002
Inskip 2001
YES
Hardell 2003
No
Christensen 2004
Muscat 2002
Inskip 2001
Hardell 1999
MENINGIOMA
ACOUSTIC
NEURINOMA
Extremely Low Frequency (ELF)
Electric and Magnetic Fields

Sinusoidal electromagnetic
fields with frequencies ranging
from 30 and 300 Hz.

Any electrically powered device
is a source of ELF electric and
magnetic fields:


In the domestic setting,
electric fields are always
present regardless of
whether appliances are
being used or not.
On the other hand, a
magnetic field is present
only when appliances are
turned on and current flows
through them.
Extremely Low Frequency (ELF)
Electric and Magnetic Fields
Occupational Exposure
 Use of automatic welders, arc furnaces

Induction heating systems and other
widespread devices

Tempering and degasification of metals

Glass-metal welding

Sealing of plastic containers

Processing of precious metals
Extremely Low Frequency (ELF)
Electric and Magnetic Fields
Short-term Effects

Interaction with transport of Na+, k-, Ca++
ions through the membranes

Biological effects on the:
 Nervous system
 Endocrine system
 Cardiocirculatory system

These effects occurr in acute form when
threshold values are exceeded
Extremely Low Frequency (ELF)
Electric and Magnetic Fields
Short-term Effects

In 2001, IARC (International Agency for
Research on Cancer) classified ELF
magnetic fields in group 2B
Possible carcinogens, which should be carefully considered for
their possible carcinogenic effects in man
Extremely Low Frequency (ELF)
Electric and Magnetic Fields
Short-term Effects

In 2001, IARC (International Agency for
Research on Cancer) classified ELF electric
fields in group 3
Not classifiable as to their carcinogenicity to humans:
substances whose carcinogenicity has not been assessed
Extremely Low Frequency (ELF)
Electric and Magnetic Fields
Long-term Effects
TYPE OF
TUMOUR
CEREBRAL
TUMOURS
SIGNIFICANT
CORRELATION
Yes
No
STUDIES
• Hakansson 2002
• Villeneuve 2002
• Van Wijngaarden
2001
• Klaebol 2004
• Sorahan 2001
Extremely Low Frequency (ELF)
Electric and Magnetic Fields
Long-term Effects
TYPE OF
TUMOUR
SIGNIFICANT
CORRELATION
Yes
CHILD
LEUKEMIA
No
STUDIES
• Ahlbom 2000 #
• London 1991
• Wertheimer e
Leeper 1979
• Ahlbom 2000 *
• Verkasalo 1993
• Savitz 1988
STATIC ELECTRIC AND
MAGNETIC FIELDS
Occupational Exposure

Electrochemical plants (e.g. Production
of aluminium)

Continuous current transport (trains,
trams, underground trains)

High energy accelerators:
•
•
•
MNR
Particles accelerators
Nuclear reactors
STATIC ELECTRIC AND
MAGNETIC FIELDS
Harmful Effects

Sensory group

Stress group

Genetic code group

Indirect effects
STATIC ELECTRIC AND
MAGNETIC FIELDS
Sensory group

They can be associated with sensory
magnetoreception, also in the case of
fields of the order of the geomagnetic
field, and regulate:



The navigation of migratory birds
The directional sense in insects
The kinetic movement of shellfish
STATIC ELECTRIC AND
MAGNETIC FIELDS
Stress group






Hematologic effects: leukopenia
CNS: magnetophosphene
phenomenon, caused by stimulation of
the retina by induced currents, and change
in cerebral bioelectrical activity in high
intensity fields
Delay in wound healing and tissue
regeneration
Decrease in body temperature
Delay in growth
Interruption of the estrous cycle
STATIC ELECTRIC AND
MAGNETIC FIELDS
Genetic code group

They have been hypothesized as
perturbative mechanisms in proton
tunneling during DNA replication, with
possible errors in the genetic code

Experimental evidence is insufficient
STATIC ELECTRIC AND
MAGNETIC FIELDS
Indirect Effects

Interaction with and possible malfunction
of various devices:




Pacemakers
Electrocardiographs
Insulin pumps, etc
Interaction with external or internal
ferromagnetic materials:


prostheses, clips, etc
tools, gas cylinders, etc