Pneumoconiosis. Silicosis. Silicatosis.

Vibration disease
Asist. O.S. Kvasnitska
Internal medicine department 2
Recent decades have seen a marked
increase in concern about the
adverse health effects of hazardous
exposures in the workplace and
elsewhere in the environment

Endless array of hazardous
substances in industrial and
agriculture sectors

The lung with its extensive
surface area, high blood flow and
thin alveolar epithelium is an
important site of contact with these
substances in the environment
Introduction
Occupational lung diseases are a
broad group of diagnoses caused by the
inhalation of dusts, chemicals, or
proteins

Pneumoconiosis is the term used for
the diseases associated with inhaling
mineral dusts

The severity of the disease is
related to the material inhaled and the
intensity and duration of the exposure

Individuals who do not work in the
industry can develop occupational
disease through indirect exposure

These diseases have been
documented as far back as ancient
Greece and Rome; the incidence of the
disease increased dramatically with the
development of modern industry.
Importance of occupational lung
diseases
Knowledge of cause may affect patient
management and prognosis and may prevent
further disease progression in the affected
person
Establishment of cause may have significant
legal, financial and social implications for
the patient
The recognition of occupational and
environmental risk factors can also have
important public health and policy
Occupational and environmental lung
diseases can also serve as important
disease models

Inorganic dust (consists of particles
of minerals and metals)
Organic dust (contains particles of
plant and animal origin, and also
microorganisms that are on them, and
their waste products)
Mixed dust

Industrial dust
Inorganic dust
Asbestos fibers under
the electron microscope
Talc - hydrated aluminum silicate
oal dust of mining enterprises
Organic dust
Dust generated during processing of raw cotton Moldy hay
Classification
1996 year, The Russian Academy of Medical Sciences
Research institute of Health Medicine
1. Pneumoconiosis, which develops by influence moderately and highly
fibrogenic dust (with containing free silica more than 10 %)
silicosis, antracosilicosis, silicosiderhosis, silicisilicatosis
2. Pneumoconiosis, which develops by influence mild fibrogenic dust
(with containing free silica less than 10 % or not containing it)
silicatosis (asbestosis, talcosis, caolinosis, olivinosis, nephelinosis,
pneumoconiosis from exposure to cement dust) carboconiosis
(anthracosis, graphitosis, black-lung carbon disease etc.), polishers
and emerys pneumoconiosis, metalloconiosis or pneumoconiosis
from exposure radiopaque dusts (siderosis, including of aerosol
electric welding or gas cutting iron products, baritoz, stanioz,
manganokonioz etc).
3. Pneumoconiosis, which develops by influence toxic-allergic aerosols
(dust, which containing metals-allergens, plastic and other polymeric
material compounds, organic dust etc) berylliosis, aluminosis,
farmer's lung and other hypersensitivity pneumonitis
International Labour organization, Geneva.
List of occupational Diseases (2002)
1. Diseases caused by agents
1.1 Chemical agents ( 32 items)
1.2 Physical agents ( 8 items )
1.3 Biological agents ( infectious and
parasitic diseases contracted in an occupation
where there is a par contracted in an occupation
where there is a particular risk of contamination )
2. Diseases by target organ systems
2.1 Occupational respiratory diseases
2.2 Occupational skin diseases
2.3 Occupational musculoskeletal disorders

International Labour organization, Geneva.
List of occupational Diseases (2002)
3. Occupational cancer ( 15 items )
(Asbestos, Benzidine and compounds,
Bischloromethylether, chromium and
compounds, coal tar, beta-naphthylamine,
Vinylchloride, Benzene, Toxic nitro and amino
derivatives of benzene, Ionizing radiations, Tar,
pitch bitumen, mineral oil, and related
compounds, coke oven emission, coke oven
emission, wood dust ).
4. Other diseases
4.1 Miners nystagmus

2.1 Occupational respiratory diseases
2.1.1 Pneumoconioses caused by sclerogenic mineral dusts
2.1.2 Bronchopulmonary disease caused by hard-metal
dust
2.1.3 Bronchopulmonary disease caused by cotton, flax,
hemp or sisal dust
2.1.4 Occupational asthma
2.1.5 Extrinsic allergic alveolitis
2.1.5 Siderosis
2.1.6 Chronic obstructive pulmonary diseases
2.1.7 Diseases caused by aluminium
2.1.9 Upper airways disorders
2.1.10 Any other respiratory disease not mentioned in the
proceeding items caused by an agent where the casual
relationship is established

Basic principles of occupational lung diseases
Certain principles apply broadly to the full range
of occupational respiratory disorders
While a few environmental and occupational
lung diseases may present with
pathognomonic features, most are difficult to
distinguish from disorders of
nonenvironmental origin
A given substance in the workplace or
environment can cause more than one clinical
or pathologic entity
The etiology of many lung diseases may be
multifactorial and occupational factors may
interact with other factors
The dose of exposure is an important
determinant of the proportion of people
affected or the severity of disease
Individual differences in susceptibility to
exposures do exist
The effects of a given occupational or
environmental lung exposure occur after the
exposure with a predictable latency interval
Pathogenesis
The effects of an inhaled agent depend
on many factors
its physical and chemical properties
the susceptibility of the exposed
person
the site of deposition within the
bronchial tree
Physical properties
physical state (solid
particulates, mist, vapor and gases)
solubility
size, shape and density
concentration
penetrability
radioactivity
Chemical properties
alkalinity and acidity
fibrogenicity
antigenicity
Susceptibility of exposed person
Integrity of local defense
mechanisms
Immunological status ( atopy,
HLA type)
Airway geometry
Site of deposition
When airborne particles come in
contact with the wall of the conducting
airway or a respiratory unit they do not
become airborne again
Governs the lung response
substantially
Mechanisms of dust deposition:
Sedimentation
Inertial impaction
Diffusion
Interception
Electrostatic precipitation
10- 5 -
Upper Respiratory tract
5 - 3
Mid respiratory tract
3 - 1
Alveoli
Pathogenesis
Size of Dust
Clinical approach to the
patient
There are two important phases in the workup of
any patient with a potential occupational or
environmental lung disease.
1. General approach: To define and characterize
the nature and extent of the respiratory illness,
regardless of the suspected origin
A detailed history
Physical examination
Appropriate diagnostic tools
2. To determine the extent to which the disease or
symptom complex is caused or exacerbated by
an exposure at work or in the environment


Occupational and environmental history single
most helpful tool in the diagnostic workup
1. Employment details
Job title
Type of industry and specific work
Name of employer
Years employed
2. Exposure information
General description of job process and
overall hygiene
Materials used by worker and others
Specific workplace exposures
Ventilation / exhaust system
Use of respiratory protection
Industrial hygiene informations provided by
the employer to the employee
3. Environmental nonoccupational factors
Smoking
Diet
Hobbies
4. Details about past employments in
chronological order
5. Other details
Does the patient think symptoms / problem
is related to anything at work?
Are other workers affected?
Work absenteeism
Prior pulmonary problems and medications
used
Physical examinations
Generally unrevealing about specific
cause
It is most helpful in ruling out
nonoccupational causes of respiratory
symptoms or diseases (cardiac
problems or connective tissue
disorders)
Chest radiography - is the most important
diagnostic test for occupational lung diseases
Limitations:
The chest radiographic findings can
be nonspecific.
Conventional chest radiography is
insensitive, missing as many as 10 to
15 percent of cases with pathologically
documented disease.
Interpersonal variations
ILO International Classification of
radiographs of pneumoconiosis,1971, 2002
1. Film quality : Grades I to IV
2. Small opacities:
round opacities: p (<1.5mm)
q (1.5 3mm)
r (3 - 10mm)
Irregular opacities: s (<1.5mm)
t (1.5 3mm)
u (3 10mm)
ILO International Classification of
radiographs of pneumoconiosis,1971,
2002
Profusion:
Category 0: small rounded opacities absent or less
profuse than in category 1
Category 1: small rounded opacities definitely
present but few in number
Category 2: small rounded opacities numerous.
The normal lung markings are still visible
Category 3: small rounded opacities very
numerous. The lung markings are partially or
totally obscured
ILO International Classification of
radiographs of pneumoconiosis,1971,
2002
Large opacities
Category A: one or more large opacities
not exceeding a combined diameter of
5 cm
Category B: large opacities with
combined diameter greater than 5 cm
but does not exceed the equivalent of
the right upper zone
Category C: bigger than B
ILO International Classification of
radiographs of pneumoconiosis,1971, 2002
Pleural Abnormalities:
Location
width
extent
degree of calcification
Other abnormal features
Computed tomography
Conventional and HRCT scanning are highly sensitive
for diagnosis of pleural diseases and useful for
improved visualization of parenchymal abnormalities.

HRCT findings are usually non specific, but
occasionally certain features and distribution pattern
may suggest a specific cause and may help narrow the
differential diagnosis
Silicosis
Silica is silicon dioxide, the oxide of silicon, chemical
formula SiO
2

SiO
2
is the most abundant mineral on earth; comprises
large part of granite, sandstone and slate.
Silicosis is lung disease caused by inhalation of fine silica
dust; the dust causes inflammation and then scarring of the
lungs. Scarring shows up on chest x-ray.
Silicosis is one type of pneumoconiosis, the medical term
for lung scarring from inhaled dust. Pneumoconiosis can
also occur from inhaled asbestos (asbestosis), coal (coal
workers pneumonconiosis), beryllium (berylliosis), and
other respirable dusts.
There is no effective treatment for any pneumoconiosis,
including silicosis
Silica Dust Exposure Risk Factors
Any work that exposes
silica dust:
mining
stone cutting
quarrying
road and building
construction
work with abrasives
glass manufacturing
sand blasting
also, some hobbies can
involve exposure to silica
(sculptor, glass blower)

Silicosis - Sandblasting
Silicosis Foundry work

Silicosis - Stone cutting
Silicosis Glass Factory
Workers

Sumathi, 19, admitted to
Government Hospital,
Pondicherry, India, suffers
from severe silicosis. She
worked in the sand plant
(where silica is sieved) of
a glass-container
manufacturing plant.

Silicosis - Tunnel construction
Worst single incidence of silicosis in U.S.
Came to national attention 1930-1931 with construction of Hawks
Nest Tunnel in Gauley Bridge, West Virginia. Called the worst
industrial accident in U.S. history. At least 764 tunnel workers died
from silicosis. Hawks Nest disaster led to Congressional hearings
in 1936, and new laws protecting workers in many states

Silicosis history
Full description by
Bernardino Ramazzini
(1633-1714) in early 18
th

century. ...when the
bodies of such workers
are dissected, they have
been found to be stuffed
with small stones.
Diseases of Workers
(De Morbis Artificum
Diatriba, 1713).

Pathology
Fibrotic nodules
develop by a particular
process in which
fibrous tissue is laid
down in concentric
rings around a central
core of silica particles
as an onion
Healthy lung Silicosis
Manifestions
Symptoms
shortness of breath
while exercising
fever
occasional bluish skin at
ear lobes or lips
fatigue
loss of appetite

Three types of silicosis
Simple chronic silicosis From long-term exposure
(10-20 years) to low amounts of silica dust. Nodules of
chronic inflammation and scarring, provoked by the silica
dust, form in the lungs and chest lymph nodes. Patients
often asymptomatic, seen for other reasons.
Accelerated silicosis (= PMF, progressive massive
fibrosis) Occurs after exposure to larger amounts of silica
over a shorter period of time (5-10 years). Inflammation,
scarring, and symptoms progress faster in accelerated
silicosis than in simple silicosis. Patients have symptoms,
especially shortness of breath.
Acute silicosis From short-term exposure to very large
amounts of silica dust. The lungs become very inflamed,
causing severe shortness of breath and low blood oxygen
level.

Simple Silicosis


normal chest x-ray simple silicosis
Accelerated Silicosis
(= Progressive Massive Fibrosis)

normal chest x-ray
PMF
Accelerated Silicosis (PMF)

chest x-ray
CT scan
Eggshell calcification
almost exclusively silicosis
Silicosis associated risks
Having silicosis increases risk of contracting
tuberculosis & lung cancer.
Degree of increased risk is highly variable;
depends on several OTHER factors, including
immune system & exposure history (for TB),
and amount of lung scarring, age & smoking
history (for cancer).
Silicosis also strongly associated with
scleroderma and rheumatoid arthritis.
Other associations less well established:
lupus, systemic vasculitis, end-stage kidney
disease.


Diagnosis of silicosis
Abnormal chest X-ray or chest CT scan
History of significant exposure to silica dust
Medical evaluation to rule out other causes of
abnormal x-ray
Pulmonary function tests
Lung biopsy rarely used
Silicosis can be mis-diagnosed
as something else
Silicosis can mimic:
Sarcoidosis (benign inflammation of unknown cause)
Idiopathic pulmonary fibrosis (lung scarring of
unknown cause)
Lung cancer
Several other lung conditions (chronic infection,
collagen-vascular disease, etc.)

Can usually make right diagnosis with
detailed history (occupational & medical)
or, rarely, a lung biopsy.
Treatment

Early revealing and change of occupation to
industry without dust.
Oxygen therapy to improve lung ventilation.
Corticosteroids are used in the period of
fast progression, in Rheumatoid Silicosis.
Treatment of Heart failure
Treatment of Complication (Pleuritis,
Pneumonia, Tuberculosis)
Symptomatic Therapy.

Silicatosis (Asbestosis)
Parenchymal lung fibrosis with or without pleural involvement due
to inhalation of asbestos fibres.
5- 20 years to develop
Inflammation from fibres causes scarring (fibrosis) and stiffening
of the lung. This causes less oxygen exchange. Damage leads to
bronchitis, bronhiectasis.
Damage leads to pleural changes (pleuritis, spikes, enlargement
of lymph nodes at the lung hila (containing asbestos).
It is more dangerous than silicosis as it predisposes to
bronchogenic carcinoma and mesothelioma of the pleura and
peritoneum
Symptoms shortness of breath, a dry, persistant cough , chest
tightness, deformed, club-shaped fingers

Asbestos fibers
Chest X- Ray :

Interstitial
pneumoscelerosis

Diagnostic Particularities:

a) In sputum - asbestos
bodies
b) In skin - asbestos Warts
(containing asbestos)
Diagnosis of Asbestosis
Typical dumbbell shaped ferruginous bodies seen in a bronchial washing
specimen
asbestos warts
Complications
Bronchogenic carcinoma
Mesothelioma
65-year-old asymptomatic man who had been employed in construction and demolition for over
forty years Radiologic Findings PA (A) and lateral (B) chest radiographs demonstrate the
presence of bilateral, relatively symmetric, multi-focal, discontinuous areas of pleural thickening and
calcification primarily distributed along the anterolateral and posterolateral chest wall and domes of
each hemidiaphragm. The apices and costophrenic angles are spared. Lesions seen en face on the
frontal exam (A) exhibit scalloped morphology, whereas those seen in profile on the lateral exam
(B) appear more linear confirming the lesions change morphology from one orthogonal plane to the
next and are therefore pleural-based.
Diagnosis: Asbestos-Related Pleural Plaques
A B
Coal Worker's Pneumoconiosis
(CWP)
CWP is a lung disease that results from
breathing in dust from coal, graphite, or
man-made carbon over a long period of
time
Necessary to differentiate from silico-
tuberculosis, disseminated tuberculosis,
metastatic lung cancer, and other diffuse
infiltrative pulmonary diseases
The disease is divided into 2 categories:
simple CWP and complicated CWP or
progressive massive fibrosis (PMF)
Particularities
Slow growth, benign character of
current, active phagocytosis, saved
lung protective mechanism.
Causes chronic bronchitis, lung
emphysema
Radiological investigation interstitial
or interstitial nodular fibrosis of the
lung.
Symptoms and Diagnosis
Simple CWP:
It is said to exist in the presence of
radiological opacities < 1cm in diameter.
It is benign disease if no complications.
Cough, expectoration and dyspnea are
frequently present.
Slight decrease in FVC and FEV1/FVC
Simple CWP

Minute opacities are
diffusely scatterred
throughout both lung fields,
providing a crude measure
of excessive exposure.
Early pneumoconiosis is
essentially a focal disorder
and may produce little
physiologycal disorders
Complicated CWP (PMF):
Is diagnosed when large opacity of 1cm or more in
diameter is observed in the chest X-ray.
Pathologically it is characterized by large masses of
black colored fibrous tissue.
The large lesions may cavitate as a result of
ischemic necrosis or infection (T.B)
The severe stages of PMF cause cough and often
disabling shortness of breath.
Pulmonary function test reveals decreased FVC,
FEV1/FVC and increased residual volume
These pictures show complicated coal workers
pneumoconiosis. There are diffuse, small, light areas (more
than 1 cm) in all areas on both sides of the lungs. There are
large light areas which run together with poorly defined
borders in the upper areas on both sides of the lungs.

If coal worker's pneumoconiosis
occurs with rheumatoid arthritis it is
called Caplan syndrome.
Caplan's syndrome (or Caplan's
disease) is a combination of rheumatoid
arthritis and pneumoconiosis that
manifests as intrapulmonary nodules,
which appear homogenous and well-
defined on chest X-ray
Caplan's syndrome presents with
Cough, shortness of breath
features of rheumatoid arthritis (painful joints and
morning stiffness)
Examination should reveal tender, swollen MCP
joints and rheumatoid nodules
Auscultation of the chest may reveal diffuse rales that
do not disappear on coughing or taking a deep breath.
Other types of occupational lung
disease
Byssinosis
Byssinosis is a narrowing of the
airways caused by inhaling cotton,
flax, or hemp particles.
The substance or substances in the
material that cause the disease are
not known, but it is believed that the
protein component rather than the
cellulose or mineral constituents is
responsible
Other types of occupational lung
disease
Hypersensitivity Pneumonitis
Hypersensitivity Pneumonitis (also referred to
as extrinsic allergic alveolitis) is an
immunologic-induced, non-IgE mediated
inflammatory pulmonary disease. It affects
primarily the interstitium, alveoli, and terminal
airways, and is caused by prolonged,
repeated inhalation of organic dusts or
certain chemicals (Farmers lung, Bagassosis
etc.)
Other types of occupational lung
disease
Occupational Asthma
Reversible airflow obstruction caused
by workplace exposures
With latency period (sensitization)
Without latency period (irritant)
Causes: a broad group of vegetable,
animal products, chemicals, metals-
referred to as asthmagens
New Occupational Lung
Diseases
Popcorn workers lung
Obstructive airways disease, some with
bronchitis obliterans
Caused by a ketone (diacetyl) in the
artificial butter flavoring used in microwave
popcorn processing



Kreiss et al., NEJM 2002; 347: 330-8
Prevention of occupational
lung diseases
Respirators
Prevention of occupational
lung diseases
Ventilation and exhaust systems

Occupational disease,
caused by influence
physical factors.
Vibration disease
Vibration disease - an
occupational disease caused by
exposure to vibration. This
pathology was first described by
Lrig in 1911 as a syndrome of
stonecutters dead fingers, and in
1955 it was named vibration
disease

OCCUPATIONAL VIBRATION -
A SHORT HISTORY

1839 - Pneumatic tools were first used in French mines
1862 - Primary Raynaud's Phenomenon (Raynaud's
Disease) identified.
1911 - Professor Loriga first described vascular spasm
in the hands of Italian miners using pneumatic tools.
1918 - Alice Hamilton studied miners using drills in
limestone quarries describing spastic anaemia of the
hands.
1930-40s - Cases of white finger were identified
studies in fettlers, riveters, boot and shoe industry
workers and users of electrical powered rotating tools
1950s - Research links signs and symptoms in nerves,
bones, joints and muscles with vibrating tools.
1968-69 - After 12-14 years of continuous chain saw
use widespread complaints of VWF (Vibration white
finger) in operators.
1975 - Scale for assessing the extent of vascular injury
associated with vibration white finger published by
Taylor-Pelmear
1985 - VWF becomes a prescribed disease for
Industrial Injuries Disablement Benefit purposes
1987 - Stockholm scale for assessment of VWF
published. Standard for measurement of vibration
published in BS 6842.
WHAT IS VIBRATION?
Frequency
Amplitude
Acceleration
TYPES OF
VIBRATION

low-frequency (8 15 Hz)
medium-frequency (16 64 Hz)
high-frequency (more than 64 Hz)
Dangerous for the development of
disease is the vibration with the
frequency 16 250 Hz.

73
VIBRATION
EXPOSURE
Segmental (Local) Vibration
Segment of body such as hand-transmitted
vibration (known as hand-arm vibration or HAV)

Whole Body Vibration
Vibration transmitted through the seat or
feet (known as whole-body vibration or
WBV)


ACTING DIRECTIONS OF
THE MECHANICAL
VIBRATIONS
TRANSMITTED TO THE
WHOLE BODY THROUGH
THE SUPPORTING AREA
Industry

Type of
Vibration

Common Source of
Vibration

Agriculture

Whole body

Tractors

Construction

Whole body
Local

Heavy equipment vehicles
Pneumatic tools,
Jackhammers

Forestry

Whole body
Local
Tractors
Chain saws

Furniture
manufacture

Local Pneumatic chisels

Machine tools

Local Vibrating hand tools

Textile

Local Sewing machines, Looms

Transportation

Whole body

Vehicles

Mining

Whole body
Local
Vehicle operation
Rock drills




PATHOGENESIS:
LOCAL EFFECTS
These effects occur under the influence of
afferent impulses in the spinal cord neurons,
sympathetic ganglia, and the reticular
formation of the brain, including the levels of
autonomic-vascular centers.
The state of regional circulation disturbs,
there are specific manifestations of
vasospasm. The greater the altered vibration
sensitivity, so vasospasm is significant.
Direct mechanical damage and irritation of
smooth muscle cells of blood vessels is
expressed, which contributes to their spasm
or atony. Further dystrophic changes
develops.
Pathological process is in general has
character of angiotrophoneurosis that at
some stage has a tendency to generalize.
However, trophic disorders relate primarily to
the neuromuscular and musculoskeletal
system, especially the shoulder girdle
muscles, bones and joints.
In parallel with the progressive decline
in the perception of vibration in vibration
disease pain, tactile and thermal
sensitivity disturbed.
Vibrational excitation irradiating to
neighboring areas, especially in the
vasomotor center, changing the
functional state of the peripheral vessel.
Later irritation radiating to vasomotor,
pain and temperature centers if the
disease development of vibration centers
in stagnant excitation (parabiosis).
PATHOGENESIS: CENTRAL EFFECTS
PATHOGENESIS
Defeat of
Cardiovascular system
Nervous system
Locomotor system
Metabolism
Decreasing of
Vibrational sensitivity
Algesthesia (pain sensitivity)
Tactile sensitivity
Thermoesthesia (temperature sensitivity)


TYPES OF
VIBRATION
DISEASE
Vibration disease from local
vibration impact
Vibration disease from general
vibration impact
Vibration disease from combine
vibration (local and general) impact

CLASSIFICATION
I. Initial stage (mild manifestation)
II. Moderately expressed (dystrophic
disorders)
III. Expressed (irreversible organic
changes)
IV.Generalized (very rare)

MAIN SYNDROMES IN
VIBRATION DISEASE
1. Angiodistonic syndrome
2. Angiospastic syndrome
3. Syndrome of vegetative polyneuritis
4. Syndrome of vegetative myofascitis
5. Syndrome of somatic neuritis (cubital,
median), plexitis, radiculitis
6. Diencephalic syndrome with
neurocirculatory disturbance
7. Vestibular syndrome

ANGIODISTONIC
SYNDROME
Main symptoms The nature of vibration and
the stage of disease at which
a given syndrome
Vegetative-vascular disease in
the limbs, impaired capillary
blood circulation (atonic or
spastic-atonic state)
At high-frequency vibration
and overall in the early stages,
with the midrange - in
elementary and moderate
stages, the low-frequency
vibrations - in all stages
ANGIOSPASTIC
SYNDROME
Main symptoms The nature of vibration and
the stage of disease at which
a given syndrome
White finger attack, spasms of
the capillaries, skin
temperature violation,
marked reduction of vibration
sensitivity preferentially
localized to the hands and
feet
At high-frequency vibration in
severe stages, and the stage
of generalization, with a total
of vibration - in the initial
stages and marked
SYNDROME OF
VEGETATIVE
POLYNEURITIS
Main symptoms The nature of vibration and
the stage of disease at which
a given syndrome
Pain phenomena, violation of
skin sensitivity, reduced skin
temperature, vegetative
symptoms
At low-frequency vibrations -
in the initial stages, with a
total of vibration - in the initial
stages
SYNDROME OF
VEGETATIVE
MYOFASCITIS
Main symptoms The nature of vibration and
the stage of disease at which
a given syndrome
Painful phenomena, vascular
disorders, changes in
sensitivity by peripheral or
segmental type
At low-frequency vibration
(especially in the presence of
static stress and significant
return impact) and less
frequently in middle
frequency vibration in various
stages
SYNDROME OF SOMATIC
NEURITIS
Main symptoms The nature of vibration and
the stage of disease at which
a given syndrome
Electoral amyotrophy,
impaired of sensitivity and
reflex areas
Low-frequency vibration,
combined with significant
blowback, with emphasis
trauma tool in severe stages
DIENCEPHALIC SYNDROME
WITH
NEUROCIRCULATORY
DISTURBANCE
Main symptoms The nature of vibration and
the stage of disease at which
a given syndrome
Generalized vascular disorders
and crises (cerebral,
coronary), metabolic
endocrine disorders
At high-frequency vibration
(local and general) in the
terminal stage
VIBRATION
DISEASE FROM
THE ACTION OF
LOCAL VIBRATION
(HAND ARM
VIBRATION,
VIBRATION
WHITE FINGER)
91
HAND ARM
VIBRATION
WHAT IS HAV?
HAV is vibration transmitted from work
processes into workers hands and
arms. It can be caused by operating
hand-held power tools such as road
breakers, hand-guided equipment such
as lawn mowers, or by holding materials
being processed by machines such as
pedestal grinders.

WHEN IS IT HAZARDOUS?
Regular and frequent exposure to high
levels of vibration can lead to
permanent injury. This is most likely
when contact with a vibrating tool or
process is a regular part of a persons
job.

92
HAND ARM
VIBRATION
WHAT SORT OF TOOLS AND EQUIPMENT CAN
CAUSE VIBRATION INJURY?
Chainsaws
Concrete breakers/road drills
Hammer drills
Hand-held grinders
Hand-held sanders
Nut runners
Pedestal grinders
Power hammers and chisels
Powered lawnmowers
Riveting hammers and bolsters
Strimmers/brush cutters
Swaging machines.

Con
sultn
et
Limit
ed
9
3

HAND ARM VIBRATION
Moderate vibration
High vibration
impact wrenches
chain saws
percussive tools
jack hammers
scalers
riveting or chipping hammers
grinders
sanders
jig saws
HAND ARM VIBRATION
- CAUSES & EFFECTS
Neurological component
Vascular component
Muscular and soft tissue
component
HAND ARM VIBRATION
- CAUSES & EFFECTS
WHAT INJURIES CAN HAV
CAUSE?
Regular exposure to HAV can cause
a range of permanent injuries to
hands and arms including damage
to the:
Blood circulatory system (e.g.
vibration white finger)
Sensory nerves
Muscles
Bones
Joints

CLASSIFICATION
initial manifestations:
1) Peripheral angiodystonic syndrome of the
upper extremities, including fingers with rare
angiospasm;
2) neuro-sensory upper limb polyneuropathy
CLASSIFICATION
II mild manifestations:
1) Peripheral angiodystonic syndrome of
the upper extremities with frequent
fingers angiospasm;
2) neuro-sensory polyneuropathy
syndrome of upper extremities with:
a) frequent fingers angiospasm;
b) persistent vegetative and trophic
disorders on the hands;
c) with degenerative disorders device
support and movement of the upper limbs
and their zone (miofibrosis, periartrosis,
arthritis);
d) cervical-brachial plexopathy;
e) with cerebral angiodystonic syndrome.

CLASSIFICATION
III - pronounced symptoms:
1) sensory motor polyneuropathy syndrome of
the upper extremities;
2) Encephalopolineuropathy syndrome;
3) syndrome polineuropathy with generalized
angiospasm.
Consultnet Limited 99
STOCKHOLM
WORKSHOP SCALES
VASCULAR
COMPONENT
Stage Grade Description
0 No attacks
1v Mild Occasional attacks affecting
only the tips of one or more
fingers
2v Moderate Occasional attacks affecting
distal and middle (rarely also
proximal)
phalanges of one or more
fingers
3v Severe Frequent attacks affecting all
phalanges of most fingers
4v Very severe As in stage 3, with trophic
changes in the fingertips
STOCKHOLM
WORKSHOP SCALES
SENSORINEURAL
COMPONENT
Stage Grade Description
0 Vibration-exposed but no
symptoms
1sn Mild Intermittent numbness with
or without tingling
2sn Moderate Intermittent or persistent
numbness, reduced sensory
perception
3sn Severe Intermittent or persistent
numbness, reduced tactile
discrimination
and/or manipulative dexterity
Numerical scoring of vascular symptoms of
HAVS (after Griffin, 1982)
VIBRATION INDUCED GANGRENE
ATROPHY OF MUSCLES
DURING VIBRATION
DISEASES
DIAGNOSIS OF HAVS
History of symptoms
History of vibration exposure
Various clinical tests to exclude other disorders
Objective measurement of vascular, neurological and
musculoskeletal function:
Vascular tests:
Finger systolic blood pressures
Rewarming time after cold provocation
Neurological tests:
Clinical tactile threshold tests
Thermal thresholds
Vibrotactile thresholds
Nerve conductive velocity
Musculoskeletal function:
Finger dexterity
Hand grip force

VASCULAR TESTS
Finger systolic blood pressures
Rewarming time after cold provocation
NEUROLOGICAL
TESTS
Clinical tactile threshold tests
Thermal thresholds
Vibrotactile thresholds
Nerve conductive velocity

MUSCULOSKELETAL
FUNCTION
Finger dexterity
Hand grip force
DIAGNOSIS OF
VIBRATION DISEASE
FROM EXPOSURE TO
LOCAL VIBRATION
The typical additional signs of vascular disorders
1. Symptom of "white spot". You ask a patient
to clench firmly the first of hand and through 5
sec quickly unclench it. In a norm the white spots
which appeared have to vanish in 5 sec. If spots
do not disappear quickly the test is positive
2. Piles symptom. A pulse is found on both radial
arteries, and then by rapid motion lift up the hands
of patient. Thus a pulse can vanish on a few
seconds. Such test is positive.
3. Test on reactive hyperemia. You impose a cuff
on a shoulder and pump a pressure 180 - 200 mm
of Hg. Then ask to lift hands up, in 2 min. to put
hands down, take cuff off and write down time of
hands reddening. In a norm the reddening begins
in 1,5 - 2 sec. and passes in 15 sec. Lengthening
of this time testifies to the spasm of vessels, and
shortening - about their atony
DIAGNOSIS OF
VIBRATION DISEASE
FROM EXPOSURE TO
LOCAL VIBRATION
The typical additional signs of vascular disorders
4. Boholyepovs test. A patient stretches both hands
with the unbended fingers ahead. At that you pay
attention on colouring of skin, state of veins and
capillary net of nail bed of fingers. Then a patient
lifts a right hand up, and put down a left on 30
sec. After it, returns hands in previous position.
We look after the change of vein and capillary
circulation of blood. Normally, the changes of
blood filling are normalized in 30 sec. At
insufficiency of circulation of blood, pallor or
cyanosis, which arose up disappear slower, than
the more expressed is a disorder of peripheral
circulation of blood.
DIAGNOSIS OF
VIBRATION DISEASE
FROM EXPOSURE TO
LOCAL VIBRATION
The typical additional signs of vascular disorders
5. Cold test. The hands of explored are dipped into
a cold water (+10) on 5 min. At albication of
fingers the test is considered positive. Pay
attention on prevalence and intensity of the
process, mark the time of renewal of skin
temperature after cooling. Normally it does not
exceed 20 min. At patients with vibration disease
there is an acute deceleration of renewal of skin
temperature.
8Channel Temperature Monitor
CAPILLAROS
COPE
DIAGNOSTIC OF SENSORY
DURING VIBRATION
DISEASE
DIAGNOSTIC OF SENSORY
DURING VIBRATION
DISEASE
TREATMENT
Therapeutic interventions
Pharmaceutical agents for the
treatment of HAVS
1. Calcium antagonists
2. Alpha-adreno receptor antagonists
3. Antifibrinolytics
4. Prostaglandin analogues
Surgical interventions for HAVS
WHOLE BODY
VIBRATION
initial manifestation:
1) angiodystonic syndrome (cerebral or
peripheral);
2) neuro-vestibular syndrome;
3) sensory syndrome (neuro-sensory)
polyneuropathy of the lower extremities.
WHOLE BODY
VIBRATION
II - moderate symptoms:
1) cerebro-peripheral angiodystonic syndrome;
2) sensory syndrome (neuro-sensory)
polyneuropathy in combination:
a) polyradiculoneuropathy syndrome;
b) secondary lumbosacral radicular syndrome
(due to degenerative disc disease of the lumbar
spine);
c) with functional disorders of the nervous
system (neurasthenia syndrome).
WHOLE BODY
VIBRATION
III - pronounced symptoms:
1) sensorimotor polyneuropathy syndrome;
2) dyscirculatory encephalopathy syndrome in
combination with peripheral neuropathy
syndrome (encephalopolineuropathy)
VIBRATION DISEASE
FROM
THE INFLUENCE OF
GENERAL VIBRATION
Syndromes of vibration disease conditioned
by general vibration:
- cerebral-peripheral,
- angiodistonic,
- vegetative-vestibular,
- vegetative-sensory polyneuropathy.
SENSORY DECREMENT
BY THE PERIPHERAL
TYPE
Roentgenograms can reveal ossific
formations and centers of osteosclerosis. In
a spinal column, the changes in
intervertebral disks and joints prevail,
mainly of degenerative-dystrophic
character.
PROPHYLAXIS
The contra-indications to the
employment on the work related with
influence of vibration are
chronic diseases of the peripheral nervous
system
obliterating endarteritis
Raynaud's disease
angina pectoris, arterial hypertension of -
III stages,
endocrine disease (diabetus mellitus)
ulcer disease
neuritis, polyneuritis
stable hearing loss of any aetiology,
otosclerosis
chronic gynecological diseases
PREVENTI
ON
Development of HAV is dose related,
meaning that effective control
procedures should be:

reducing the intensity of the vibration
reducing the duration of the exposure
to vibration
early recognition of signs and
symptoms
identifying vibration sensitive
individuals
CONTROLS
Buy lower vibration
tools

A link to the European Hand Arm Vibration
Database is in the Links and
References at the end of
this presentation
Tape
existing
handles with
vibration
dampening
tape
Regularly
maintain
and
balance
hand
tools
Use full
fingered anti-
vibration
gloves
Suspend tools
from tool
balancers to
reduce hand
grip force
REMOTE CONTROL
VIBRATORY PLATE
OPERATOR VIBRATION
EXPOSURE - ZERO
VIBRATION REDUCED
BREAKER
Keep the moil point sharp
Break a little at a time
Dont get jammed
Dont force anti-vibration
handles
Stop breaker before pulling
out
MECHANISATION
REMOVES THE RISK
MACHINE-MOUNTED PICK
REPLACES HAND-OPERATED
BREAKERS
Thanks for attention!