OCCUPATIONAL DISEASES

1. Occupational diseases definition, classification. List of

occupational diseases.
They are a group of diseases which appear exclusively or
predominantly due to adverse effects of work environment harmful
factors or of the manufacturing process. It is when a disease is
established by a permanent disability or death directly caused by the
working activity of the employee.
Classification:
- Specific occupational diseases (silicosis, vibration disease)
- Conditioned occupational diseases (occupational asthma,
occupational Bronchitis and some infectious diseases like TB)
- Para-occupational disease or work-related. It only triggers or
aggravated the pathogenesis of the disease ( ulcer,
hypertension)
Main principles:
- Clarification of the etiology. Working history. Location of the
work, length of exposure, the substance involved etc.
- Epidemiological tests. It's +ve if there is increase in incidence
of the disease among workers at the same environment.
- Exposure test. It's +ve when the disease is manifested or
aggravated with exposure to the working substance
- Elimination test, +ve when the symptoms decrease totally or
partially upon removal from the environment and then they
reappear upon subsequent exposure. (allergy, and
musculoskeletal disease)
- Length of service at the working environment.
- Sex and age. Women and young people are more affected.
- Parallel existence of other non-occupational diseases renders
the worker more prone to development of occupational
disease.. Maybe decreased immunity???
- Personal trait. Like family history, adverse habits like smoking
etc.
- Clinical course of the disease is specific for occupational
diseases
- Para-clinical investigations: Toxochemical tests, chest
radiography, functional tests, for respiratory, nervous and
cardiac
systems.
Haematological
and
biochemical
investigations, cytomorphology tests
Prevention:
Periodic physical examinations

 Work placement tests

Protective equipment
Treatment of any non-oppupational diseases
Vaccinations
Ventiliation of work environment
Protective work environment etc
Medical measure:
Preplacement examination
Periodic examination
Medical and health care services- immunizations
Notification- any occupational disease
Supervision of working environment
Maintainance and analysis of records
Health education and counseling
Engineering measures:

Design of building
Good housekeeping
General ventilation
Mechanization
Substitution
Dusts
Enclosure
Isolation
Local exhaust ventilation
Protective devices
Statistical monitoring
Research
2. Occupationa diseases and accidents
The term occupational disease is linked to the identification of
a specific cause-effect relationship between a harmful agent
and the affected human organism. It is when a disease is
established by a permanent disability or death directly caused
by the working activity of the employee. An occupational
accident is an unexpected and unplanned occurrence,
including acts of violence. As occupational accidents are to be
considered travel, transport or road traffic accidents in which
workers are injured and which arise out of or in the course of
work, i.e. while engaged in an economic activity, or at work, or
carrying on the business of the employer.

List of occupational diseases:

Diseases due to physical agents
Diseases due to chemical agents
Diseases due to biologic agents- brucellosis, leptospirosis,
anthrax, actinomycosis, psittacosis, tetanus
Occupational cancers- cancer of skin, lung, bladder
Occupational dermatosis- eczema, detmatitis
Diseases of psychological origin- industrial neurosis,
hypertension, peptic ulcer
Radiation hazards
Accidents and trauma
Another list is: Occupational respiratory diseases,
Occupational musculoskeletal disorders, Occupational diseases of
the nervous system, Occupational otolaryngologic diseases,
Occupational poisonings, Occupational dermatoses, Malignant
occupational diseases
3. Occupational diseases of lungs
Repeated and long-term exposure to certain irritants on the job can
lead to an array of lung diseases that may have lasting effects, even
after exposure ceases. Common symptoms: coughing, shortness of
breath, chest pain, chest tightness, abnormal breathing pattern
Diagnosis: chest x-ray, pulmonary function tests - diagnostic tests
that help to measure the lungs' ability to exchange oxygen and
carbon dioxide appropriately, microscopic examination of tissue,
cells, and fluids from the lungs, biochemical and cellular studies of
lung fluids, measurement of respiratory or gas exchange functions,
examination of airway or bronchial activity
Treatment based on: age, overall health, medical history, extent and
type of lung disease, tolerance for specific medications, procedures,
or therapies, expectations for the course of the disease
4. Pneumoconioses and silicosis
Pathologic classification:
1. Collagenous pneumoconiosis= collagen deposits in lungs
(silicosis, asbestosis, kaolinosis, talcosis, coal worker's
pneumoconiosis)

2. Non-Collagenous pneumoconiosis (baritosis, stanosis, pure

siderosis etc)
Etiologic classification:
1. Silicosis
2. Asbestosis
3. Other silicate pneuomoconiosis-silicatosis
4. Pneumoconiosis related to mixed mineral dusts (silicon dioxide,
kaolin dust, mixed talcum dust)
5. Pneumoconiosis caused by metal containing dusts ( aluminosis,
welder's, corundum etc)
Pneumoconiosis is caused by the dust deposition in the lungs which
retains their aggressive fibrogenic effect for many years and result in
crippling fibrosis in the lungs of the workers.
Clinical forms:
Acute silicosis= short exposure to high concentration in the working
atmosphere.
Chronic silicosis= long lasting exposure or low doses during a long
period of exposure (most frequent)
X-ray findings: ground glass opacity, which tend to appear in peripheral
regions.
1. Micronodular silicosis: bilateral opacities in the midzones of lungs
2. Nodular silicosis: bilaterally small round opacities in all lung field
3. Silicosis progressive massive fibrosis PMF bilaterally present in
the whole lung field.#
Functional disturbance:
Restrictive ventilator defects
Low values of arterial blood gases
Respiratory deficiency in advanced disease, related to intensity of
lung fibrosis and complications in the heart
Diagnosis: History of exposure, Specific radiologic findings, High level
quartz concentration in air of working environment, CT findings of nodal
and PMF
Differential diagnosis:
Diffuse pulmonary fibrosis
Disseminated pulmonary infections
Disseminated pulmonary neoplasms
Systemic autoimmune diseases
Treatment: remove the exposure, therapy with corticosteroids.

5.Silicatosis - asbestosis, talcosis, kaolinosis. Clinic and

diagnosis. Complications.
Asbestosis
Clinical picture: Poor and non-typical pulmonary symptoms,
Tiredness, chest pain, dyspnea on exertion. Upon progression,
symptoms become more severe with bronchiectasis, productive
cough, permanent dyspnea and haemoptysis.
Diagnosis: work environment dust exposure, specific x-ray
findings (honeycomb structure), -irregular subpleural opacities,
transbronchial lung biopsy, Bronchioalveolar lavage fluid
investigation BALF: demonstration of asbestos fibres,
fibrobronchoscopy, spirometry, arterial blood gas parameters,
histological, immunological, cytological and mineralogical
investigations
Complications: When the exposure to the asbestos is very high it
can lead to lung cancer and laryngeal cancer.
Talcosis
Usually asymptomatic until advanced disease, slowly
progeressive dyspnea, productive cough, similar to asbestosis,
crackles-in-base-of-lung-during-auscultation
Diagnosis: talc exposure
Kaolinosis
Initially asymptomatic
Diagnosis: Demonstration of kaolin dust exposure
Chest xray: small round opacities, when advanced-progressive
massive fibrosis PMF
6. Coal pneumoconiosis
Long exposure to coal dust and also long term smokers. Coal
dust is not as fibrogenic as is silica dust. Coal dust that enters the
lungs can neither be destroyed nor removed by the body. The
particles are engulfed by resident alveolar or
interstitial macrophages and remain in the lungs, residing in the
connective tissue or pulmonary lymph nodes.
Diagnosis: chest radiography, exposure history
Treatment: bronchodilator, corticosteroids
7. Occupational bronchitis - classification, etiology,
pathogenesis and clinical picture. Etiologic diagnosis and

criteria for occupational evaluation. Treatment prophylactics

and expertise of working capacity of the occupational
bronchitis.

Etiology: bronchial inflammation induced by harmful effects of

different occupational risk factors in the working environment.
The risk factors are: Organic, nonorganic and mixed dusts, Irritative
aerosols- nitrogen oxides, sulphur oxides, acid and alkaline fumes,
sulphured hydrogen, Non-occupational risk factors are tobacco
smoking, antitrypsin deficiency, igA deficiency and preexisting
chronic bronchitis of viral, bacterial or fungal origin.
Pathogenesis:

Mucociliary paralysis
Destruction of ciliary epithelium
Increased mucous secretion
Lymph and plasma cell infiltration
Initial hypertrophy followed by atrophy of the bronchial mucous
membrane
Clinical picture:
Initially: complains of non-obstructive chronic bronchitis
Chronic cough with/out sputum
In advanced stages: COPD-easy fatigue and breathlessness
Latest stages may develop emphysema, respiratory failure and
cor pulmonale

Diagnosis

Occupational history and evidence

Exclusion of non-occupational causes of chronic cough
Presence of complications- emphysema
Functional respiratory impairments
Positive exposure and elimination test

Therapy: Antibiotics and antivirals, Bronchodilatation, corticosteroids

8. Occupational allergic diseases of the lungs. Occupational
asthma and Byssinosis. Etiology and pathogenesis. Criteria for

etiologic diagnosis. Treatment and expertise of working capacity.

Prevention.
Etiology:
Allergic asthma is caused by exogenous allergen in predisposed
ppl
Agricultural
Stock breeding and processing of animal products
Food, wine and tobacco industries
Textile fabrics and tailoring
Tobacco production and processing
Production and use of animal nourishing mixtures
Production, packaging and usage of drugs
Resins and plastics use and production
Hairdressing
Zoological museum curators beetles
Other production and services
Pathogenesis:
Allergic occupational asthma pathogenesis:
Allergic reaction to an allergen with overproduction of IgE
igE combine with mast cells and lead to degranulation
4-8 hours later an allergic reaction develops
Non-allergic occupational asthma pathogenesis:
Liberation of mediators from mast cells following repeated
exposure to industrial agents
Leukotriens are released in the lungs constriction of
airpassages
Symptoms:
There are attacks of expiratory dyspnea with/out cough. Attacks could
be preceded by restlessness, itching in nose, sneezes and chest pain.
There is low value of FEV1 and low FEV1/VC
Diagnosis:
Detection of allergens and irritants in the occupational air

 Detection of risk factors

Medical records
Exclusion of focal pussy infectious lesions in the upper respiratory
tract=chronic sinusitis which can cause chronic non-occupational
asthma.
Skin allergy test to occupational and non-occupational allergens
Bronchoprovocation tests (+ve when decreased FEV1 is >20%)
Bronchodilatory tests
Chest x-ray
Exposure test to occupational allergens
Treatment:
Corticosteroids
Bronchodilators- beta agonists
Antibacterial therapy
Byssinosis is allergic reaction caused by long exposure to inhalation of
dust of cotton or flax. Usually symptoms appear during non-working
days. Breathing difficulties and chest tiredness, wheezing and cough.
Narrowing of airways, infection or respiratory failure
9.Hypersensetive pneumonitis
inflammation of the alveoli within the lung caused
by hypersensitivity to inhaled organic dusts
Pathophysiology
Hypersensitivity pneumonitis involves inhalation of an antigen. This
leads to an exaggerated immune response (hypersensitivity). Type III
hypersensitivity and type IV hypersensitivity occur in hypersensitivity
pneumonitis.
Symptoms
Hypersensitivity pneumonitis (HP) is categorized as acute, subacute,
and chronic based on the duration of the illness.
Acute form of HP: symptoms may develop 46 hours following heavy
exposure to the provoking antigen. Symptoms
include fever, chills, malaise, cough, chest tightness,dyspnea,
and headache. Symptoms resolve within 12 hours to several days upon
cessation of exposure. On chest radiographs, a diffuse micronodular
interstitial pattern (at times with ground-glass density in the lower and
middle lung zones) may be observed.

Subacute HP: productive cough, dyspnea, fatigue, anorexia, weight

loss, and pleurisy. On chest radiographs, micronodular or reticular
opacities are most prominent in mid-to-lower lung zones
Chronic HP: insidious onset of cough, progressive dyspnea, fatigue,
and weight loss. Clubbing is observed in 50% of patients. Tachypnea,
respiratory distress, and inspiratory crackles over lower lung fields often
are present . On chest radiographs, progressive fibrotic changes with
loss of lung volume particularly affect the upper lobes. Nodular or
ground-glass opacities are not present. Features of emphysema are
found on significant chest films and CT scans
10. Occupational diseases with toxo-chemical etiology (chronic
poisonings)
Chemical poisoning is a condition in which the body is exposed to a
potentially harmful chemical (toxins and toxicants) in an amount that
causes symptoms, disease and/or damage to cells, organs and/or body
systems. Chemicals that are produced by living organisms are called
toxins. Toxicants are chemicals are synthetic or are natural substances
that are not produced by a living organism. There are a wide variety of
toxicants, such as pesticides, chlorine, ammonia, pepper spray, and
acetone.
Diagnosis: medical history, including symptoms, and completing a
physical examination, blood tests, EKG may be performed to test for
cardiac arrhythmias or damage the chemical poisoning has done to the
heart. Arterial blood gasses can measure how a chemical poisoning is
affecting the body's oxygen level and acid-base balance. Imaging tests,
such as X-ray, CT, and MRI, may also be done.
11. Occupational intoxications with irritant gases
HYDROGEN FLUORIDE is a chemical used mainly in car cleaning
products and in the production of integrated circuits. The chemical may
be absorbed through the skin.
Sgns and symptoms: Skin blisters, Skin irritation, Skin burns, Eye
irritation, Eye burns, Eye pain, Eye redness, Permanent vision
impairment, Nausea, Vomiting, Diarrhea, edema in the lungs, Bone
pain, Burning sensation, Headache, Dizziness
AMMONIA

The most common mechanism by which ammonia gas causes damage

occurs when anhydrous ammonia (liquid or gas) reacts with tissue
water to form the strongly alkaline solution, ammonium hydroxide. This
reaction is exothermic and capable of causing significant thermal injury.
Ammonium hydroxide can cause severe alkaline chemical burns to skin,
eyes, and especially the respiratory system. Mild exposures primarily
affect the upper respiratory tract, while more severe exposures tend to
affect the entire respiratory system. The gastrointestinal tract also may
be affected if ammonia is ingested.
Signs and symptoms: Pain (oropharyngeal, retrosternal), Dyspnea,
hemoptysis, Dysphagia, Loss of consciousness, Rhinorrhea, scratchy
throat, chest tightness, cough, dyspnea, and eye irritation and usually
subside within 24-48 hours.
Diagnosis: Serum acetaminophen level in intentional exposures,
Complete blood count (CBC), Electrolytes, blood urea nitrogen (BUN),
and creatinine, Serum lactic acid
CHLORINE
Chlorine gas is a pulmonary irritant with intermediate water solubility
that causes acute damage in the upper and lower respiratory tract.
Chlorine is a greenish-yellow, noncombustible gas at room temperature
and atmospheric pressure. The intermediate water solubility of chlorine
accounts for its effect on the upper airway and the lower respiratory
tract. Exposure to chlorine gas may be prolonged because its moderate
water solubility may not cause upper airway symptoms for several
minutes.
Signs and symptoms: Breathing difficulty (from breathing in the
chlorine), Throat swelling (may also cause breathing difficulty), Water
filling the lungs (pulmonary edema). Severe change in acid levels of the
blood (pH balance), which leads to damage in all of the body organs.
Loss of vision, Severe pain in the throat, Severe pain or burning in the
nose, eyes, ears, lips, or tongue. Blood in the stool, severe abdominal
pain, vomiting
Diagnosis
Arterial blood gas abnormalities include hypoxiaand metabolic acidosis.

Chest x-ray (CXR) findings often are normal, but a CXR may be
indicated to rule out pulmonary edema, pneumonitis and acute ARDS.
H2S (HYDROGEN SULFIDE)
Significant H2 S poisoning usually occurs by inhalation. Local irritant
effects, along with arrest of cellular respiration, may follow. H2 S forms
a complex bond to the ferric moiety causing inhibition of mitochondrial
cytochrome oxidase (iron-containing protein), thereby arresting aerobic
metabolism in an effect similar to cyanide toxicity. Very high lipid
solubility allows it to penetrate easily through biologic membranes.
Signs and symptoms: Headaches, Asthenia, Bronchitis, High-level
exposures of hydrogen sulfide result in more neurologic and pulmonary
symptoms, Cough, Dyspnea, Vertigo, Confusion, Nausea and vomiting,
Very high concentrations lead to cardiorespiratory arrest because of
brainstem toxicity.
Myocardial infarction, Sudden loss of consciousness, Seizure,
Cardiopulmonary arrest
Diagnosis
Arterial blood gas (ABG) usually reveals a marked uncompensated
metabolic acidosis. Acidosis is associated with an elevation in serum
lactate level. Oxygen tension (pO2) and calculated oxygen saturation
are within the reference range unless the patient has concomitant
pulmonary edema.
SO2 (SULFUR DIOXIDE)
It is a poisonous gas with a pungent, irritating smell, that is released by
volcanoes and in various industrial processes. Since coal and
petroleum often contain sulfur compounds, their combustion generates
sulfur dioxide unless the sulfur compounds are removed before burning
the fuel. Further oxidation of SO2, usually in the presence of a catalyst
such as NO2, forms H2SO4, and thus acid rain.[2] Sulfur dioxide
emissions are also a precursor to particulates in the atmosphere. Both
of these impacts are cause for concern over the environmental impact
of these fuels.
Signs and symptoms: Eye irritation, Nose irritation, Throat irritation,
Runny nose, Choking, Cough, Frostbite, Skin burns, Chest pain,
Breathing difficulty, Tearing eyes, Cyanosis

12.Occupational intoxications with irritant gases

OCCUPATIONAL INTOXICATIONS WITH NITROGEN OXIDES
Nitrogen dioxide (NO2) is a brownish gas that is produced primarily as a
byproduct of high-temperature combustion. Workers are exposed to
combustion-produced NO2 in various occupations, including arc
welders, firefighters, military and aerospace personnel, and those
working with explosives. Nitric oxide (NO), NO2 and other oxides of
nitrogen are formed from nitrogen and oxygen during high-temperature
combustion. NO is oxidized to NO2, a precursor of ozone (O3).
Clinical: depends on the history of exposure. Welders, firefighters,
military and aerospace personnel, individuals working with explosives,
and farmers generally have higher risk of exposure than those in other
occupations.
The following may develop 2-6 weeks after initial exposure: Bronchiolitis
obliterans, manifested as fever, cough, and dyspnea
Light-headedness, Loss of consciousness, Restlessness, Agitation,
Confusion, Irritation of mucous membranes, including the eyes,
Conjunctival infection ,Weakness, Fatigue, Nausea, Abdominal pain
Causes: Occupational risk factors for NO2 exposure are high among
farmers, particularly those who work near silos, firefighters, arc welders,
military personnel, and aerospace workers (missile fuel). Any
occupation that involves the production, transportation, or use of nitric
acid is at risk.
Pulmonary function tests, if obtained late in the clinical course when
bronchiolitis obliterans has developed, demonstrate presence of
restrictive and obstructive disease.
Imaging studies: Chest radiography findings, range from normal to
noncardiogenic pulmonary edema to that of soft reticulonodular
infiltrates.
13. Occupational intoxications with carbon monoxide
OCCUPATIONAL INTOXICATIONS WITH CARBON MONOXIDE

Carbon monoxide (CO) is a colorless, odorless gas produced by

incomplete combustion of carbonaceous material. Commonly
overlooked or misdiagnosed, CO intoxication often presents a
significant challenge, as treatment protocols, especially for hyperbaric
oxygen therapy, remain controversial because of a paucity of definitive
clinical studies.
CO is formed as a by-product of burning organic compounds. Although
most fatalities result from fires, stoves, portable heaters, and automobile
exhaust cause approximately one third of deaths. These often are
associated with malfunctioning or obstructed exhaust systems and
suicide attempts. Cigarette smoke is a significant source of CO. Natural
gas contains no CO, but improperly vented gas water heaters, kerosene
space heaters, charcoal grills, hibachis, and Sterno stoves all emit CO.
Other sources of CO exposure include propane-fueled forklifts, gaspowered concrete saws, inhaling spray paint, indoor tractor pulls, and
swimming behind a motorboat.
Pathophysiology
CO toxicity causes impaired oxygen delivery and utilization at the
cellular level. CO affects several different sites within the body but has
its most profound impact on the organs (eg, brain, heart) with the
highest oxygen requirement.
Toxicity primarily results from cellular hypoxia caused by impedance of
oxygen delivery. CO reversibly binds hemoglobin, resulting in relative
functional anemia.
CO binds to cardiac myoglobin with an even greater affinity than to
hemoglobin; the resulting myocardial depression and hypotension
exacerbates the tissue hypoxia. Decrease in oxygen delivery is
insufficient, however, to explain the extent of the CO toxicity. Clinical
status often does not correlate well with HbCO level, leading some to
postulate an additional impairment of cellular respiration.
CO binds to cytochromes c and P450 but with a much lower affinity than
that of oxygen; in experimental studies, it was shown that exposure to
CO produces marked decrease in cytochrome oxidase suggesting
direct toxic effects.
Clinical

Symptoms may not correlate well with HbCO levels. For nonfatal
nonintentional non fire-related exposures, the most common symptom
was headache (37%) followed by dizziness (18%) and nausea (17%).
Acute poisoning
Malaise, flulike symptoms, fatigue, Dyspnea on exertion, Chest pain,
palpitations, Confusion, Depression, Hallucination, confabulation,
Agitation, Nausea, vomiting, diarrhea, Abdominal pain, Headache,
drowsiness, Dizziness, weakness, confusion, Visual disturbance,
syncope, seizure
Diagnosis
HbCO analysis requires direct spectrophotometric measurement in
specific blood gas analyzers. Bedside pulse CO-oximetry is now
available but requires a special unit and is not a component of routine
pulse oximetry. Arterial blood gas.
Chest radiography
CT scan : Obtain a CT scan of the head with severe intoxication or
change in mental status that does not resolve rapidly.
Treatment
Prehospital care : Promptly remove from continued exposure and
immediately institute oxygen therapy with a nonrebreather mask
Emergency Department
Cardiac monitor: Sudden death has occurred in patients with severe
arteriosclerotic disease at HbCO levels of only 20%.
Pulse oximetry: HbCO absorbs light almost identically to that of
oxyhemoglobin. Although a linear drop in oxyhemoglobin occurs as
HbCO level rises, pulse oximetry will not reflect it.
Continue 100% oxygen therapy until the patient is asymptomatic and
HbCO levels are below 10%. In patients with cardiovascular or
pulmonary compromise, lower thresholds of 2% have been suggested.
14. Chronic lead intoxications
CHRONIC LEAD INTOXICATION

A heavy metal, lead is ubiquitous in our environment but has no

physiologic role in biological systems. Its effects are pervasive yet often
subtle, with consequences ranging from cognitive impairment in children
to peripheral neuropathy in adults.
Currently, 3 forms of lead nephropathy are recognized. The first is acute
lead poisoning resulting from acute massive exposure to lead, which
causes classic symptoms, including colic, encephalopathy, anemia,
neuropathy, and Fanconi syndrome. The second is chronic lead
nephropathy (see the image below), which is a slowly progressive
interstitial nephritis resulting from excessive cumulative exposure to
lead and is frequently associated with hypertension and gout. The
thirdis lead-induced hypertension.
Furthermore, lead exposure, at much lower levels than those causing
lead nephropathy, acts as a cofactor with more established renal risk
factors to increase the risk of chronic kidney disease and the rate of
progression. Adverse renal effects have been reported at mean blood
lead levels of less than 5 mcg/dL. Cumulative lead dose has also been
associated with worse renal function.
Pathophysiology
Lead perturbs multiple enzyme systems. As in most heavy metals, any
ligand with sulfhydryl groups is vulnerable. Perhaps the best-known
effect is that on the production of heme. Lead interferes with the critical
phases of the dehydration of aminolevulinic acid and the incorporation
of iron into the protoporphyrin molecule; the result is a decrease in
heme production. Because heme is essential for cellular oxidation,
deficiencies have far-reaching effects.
Lead entering the intravascular space binds quickly to red blood cells.
Lead has a half-life of approximately 30 days in the blood, from where it
diffuses into the soft tissues, including the kidneys, brain, liver, and
bone marrow.
Lead then diffuses into bone and is stored there for a period that
corresponds to a half-life of several decades. Increased bone turnover
with pregnancy, menopause, lactation, or immobilization can increase
blood lead levels.

Lead is primarily excreted in urine and bile, but the elimination rate
varies, depending on the tissue that absorbed the lead. The kidney
excretes lead by means of glomerular filtration and tubular secretion.
Clinical
The clinical presentation varies widely, depending upon the age at
exposure, the amount of exposure, and the duration of exposure.
Younger patients tend to be affected more than older children and
adults, because lead is absorbed from the gastrointestinal (GI) tract of
children more effectively than from that of adults.
Children
No pathognomonic symptoms exist. When symptoms do occur, they are
typically nonspecific. Consider lead poisoning whenever a small child
presents with peculiar symptoms that do not match any particular
disease entity. Common nonspecific symptoms include the following:
Temperamental ability, irritability, behavioral changes
Hyperactivity or decreased activity
Loss of developmental milestones, language delay
Abdominal pain, loss of appetite, vomiting, constipation
Headache, ataxia, somnolence
Lethargy, seizures, stupor, coma
In adults, similar symptoms may develop, although cognitive changes
may be discerned more easily, especially since exposures are more
typically acute. In addition, adults with chronic exposure may develop
other symptoms, such as the following:
Weakness of extensor muscles (eg, foot drop, wrist drop)
Delirium, hallucinations
Adults with lead poisoning frequently have sleep disorders. They may
be hypersomnolent or have difficulty falling asleep at the appropriate
time.
15. Occupational intoxication with tetrathyllead
Tetraethyllead (common name tetraethyl lead), abbreviated TEL, is an
organolead compound with the formula (CH3CH2)4Pb. Its mixing with
gasoline (petrol) as an inexpensive additive beginning in the 1920s

allowed octane ratings and thus engine compression to be boosted

significantly, increasing power and fuel economy.
Toxicity
Lead pollution from engine exhaust is dispersed into the air and into the
vicinity of roads and easily inhaled. Contact with concentrated TEL
leads to acute lead poisoning:
Lead is a toxic metal that accumulates and has subtle and insidious
neurotoxic effects especially at low exposure levels, such as low IQ and
antisocial behavior. It has particularly harmful effects on children. These
concerns eventually led to the ban on TEL in automobile gasoline in
many countries. Some neurologists have speculated that the lead
phaseout may have caused average IQ levels to rise by several points
in the US (by reducing cumulative brain damage throughout the
population, especially in the young. Lead exposure affects the
intelligence quotient (IQ) such that a blood lead level of 30 g/dL is
associated with a 6.9-point reduction of IQ, with most reduction (3.9
points) occurring below 10 g/dL.
16. Chronic mercury intoxication
Signs and symptoms
Common symptoms of mercury poisoning include peripheral neuropathy
(presenting as paresthesia or itching, burning or pain), skin discoloration
(pink cheeks, fingertips and toes), swelling, and desquamation
(shedding of skin).
Mercury irreversibly inhibits selenium-dependent enzymes (see below)
and may also inactivate S-adenosyl-methionine, which is necessary for
catecholamine catabolism by catechol-o-methyl transferase. Due to the
body's inability to degrade catecholamines (e.g. Epinephrine) a person
suffering from mercury poisoning may experience profuse sweating,
tachycardia (persistently faster-than-normal heart beat), increased
salivation, and hypertension (high blood pressure).
Mechanism
Mercury is highly reactive with selenium, an essential dietary element
that is required by ~25 genetically distinct enzyme types
(selenoenzymes). Among their numerous functions, selenoenzymes
prevent and reverse oxidative damage in the brain and endocrine

organs. The molecular mechanism of mercury toxicity involves its

unique ability to irreversibly inhibit activities of selenoenzymes such as
thioredoxin reductase). Although it has many additional functions,
thioredoxin reductase restores vitamin C and E as well as a number of
other important antioxidant molecules back into their reduced forms,
enabling them to counteract oxidative damage within body cells. Since
the rate of oxygen consumption is particularly high in brain tissues,
production of reactive oxygen species (ROS) is accentuated in these
vital cells, making them particularly vulnerable to oxidative damage and
especially dependent upon the antioxidant protection provided by
selenoenzymes. High mercury exposures deplete the amount of cellular
selenium available for the biosynthesis of thioredoxin reductase and
other selenoenzymes that prevent and reverse oxidative damage,
which, if the depletion is severe and long lasting, results in brain cell
dysfunctions that can ultimately cause death.
Diagnosis
Diagnosis of elemental or inorganic mercury poisoning involves
determining the history of exposure, physical findings, and an elevated
body burden of mercury. Although whole-blood mercury concentrations
are typically less than 6 g/L, diets rich in fish can result in blood
mercury concentrations higher than 200 g/L; it is not that useful to
measure these levels for suspected cases of elemental or inorganic
poisoning because of mercury's short half-life in the blood. If the
exposure is chronic, urine levels can be obtained; 24-hour collections
are more reliable than spot collections
Treatment
Identifying and removing the source of the mercury is crucial.
Decontamination requires removal of clothes, washing skin with soap
and water, and flushing the eyes with saline solution as needed.
Inorganic ingestion such as mercuric chloride should be approached as
the ingestion of any other serious caustic. Immediate chelation therapy
is the standard of care for a patient showing symptoms of severe
mercury poisoning or the laboratory evidence of a large total mercury
load.
Chelation therapy for acute inorganic mercury poisoning can be done
with DMSA, 2,3-dimercapto-1-propanesulfonic acid (DMPS), Dpenicillamine (DPCN).

17. Chronic manganese intoxication

Chronic exposure to excessive Mn levels can lead to a variety of
psychiatric and motor disturbances, termed manganism. Generally,
exposure to ambient Mn air concentrations in excess of 5 g Mn/m3 can
lead to Mn-induced symptoms.
In initial stages of manganism, neurological symptoms consist of
reduced response speed, irritability, mood changes, and compulsive
behaviors. Upon protracted exposure symptoms are more prominent
and resemble those of idiopathic Parkinson's disease, which it is often
misdiagnosed as, although there are particular differences in both the
symptoms (nature of tremors, for example), response to drugs such as
levodopa, and affected portion of the basal ganglia. Symptoms are also
similar to Lou Gehrig's disease and multiple sclerosis.
Manganism is also documented in reports of illicit methcathinone
manufacturing. This is due to manganese being a byproduct of
methcathinone synthesis if potassium permanganate is used as an
oxidiser. Symptoms include apathy, bradykinesia, gait disorder with
postural instability, and spastic-hypokinetic dysarthria. Another street
drug sometimes contaminated with manganese is the so-called
"Bazooka", prepared by free-base methods from cocaine using
manganese carbonate.
Mechanism
Manganese may affect liver function, but the threshold of acute toxicity
is very high. On the other hand, more than 95% of manganese is
eliminated by biliary excretion. Any existing liver damage may slow this
process, increasing its concentration in blood plasma. The exact
neurotoxic mechanism of manganese is uncertain but there are clues
pointing at the interaction of manganese with iron, zinc, aluminum, and
copper. Based on a number of studies, disturbed iron metabolism could
underlie the neurotoxic action of manganese.
It participates in Fenton reactions and could thus induce oxidative
damage, a hypothesis corroborated by the evidence from studies of
affected welders. A study of the exposed workers showed that they
have significantly fewer children. This may indicate that long-term
accumulation of manganese affects fertility. Pregnant animals
repeatedly receiving high doses of manganese bore malformed
offspring significantly more often compared to controls. Manganism

mimics Schizophrenia. It is found in large quantities in paint and

steelmaking.
Treatment
The current mainstay of manganism treatment is levodopa and
chelation with EDTA. Both have limited and at best transient efficacy.
Replenishing the deficit of dopamine with levodopa has been shown to
initially improve extrapyramidal symptoms, but the response to
treatment goes down after 2 or 3 years, with worsening condition of the
same patients noted even after 10 years since last exposure to
manganese. Enhanced excretion of manganese prompted by chelation
therapy brings its blood levels down but the symptoms remain largely
unchanged, raising questions about efficacy of this form of treatment.
Increased ferroportin protein expression in human embryonic kidney
(HEK293) cells is associated with decreased intracellular Mn
concentration and attenuated cytotoxicity, characterized by the reversal
of Mn-reduced glutamate uptake and diminished lactate dehydrogenase
(LDH) leakage.
18. Cadmium intoxications
Sources of exposure
Cadmium is regularly found in ores together with zinc, copper and lead.
Therefore volcanic activity is one natural reason for a temporary
increase in environmental cadmium concentrations. Cadmium is widely
used in industrial processes, e.g.: as an anticorrosive agent, as a
stabilizer in PVC products, as a colour pigment, a neutron-absorber in
nuclear power plants, and in the fabrication of nickel-cadmium batteries.
Phosphate fertilizers also show a big cadmium load. Although some
cadmium-containing products can be recycled, a large share of the
general cadmium pollution is caused by dumping and incinerating
cadmium-polluted waste
Signs and Symptoms
Acute exposure to cadmium fumes may cause flu like symptoms
including chills, fever, and muscle ache sometimes referred to as "the
cadmium blues." Symptoms may resolve after a week if there is no
respiratory damage. More severe exposures can cause tracheobronchitis, pneumonitis, and pulmonary edema. Symptoms of
inflammation may start hours after the exposure and include cough,

dryness and irritation of the nose and throat, headache, dizziness,

weakness, fever, chills, and chest pain.
Inhaling cadmium-laden dust quickly leads to respiratory tract and
kidney problems which can be fatal (often from renal failure). Ingestion
of any significant amount of cadmium causes immediate poisoning and
damage to the liver and the kidneys. Compounds containing cadmium
are also carcinogenic
The bones become soft (osteomalacia), lose bone mineral density
(osteoporosis) and become weaker. This causes the pain in the joints
and the back, and also increases the risk of fractures. In extreme cases
of cadmium poisoning, mere body weight causes a fracture.
The kidneys lose their function to remove acids from the blood in
proximal renal tubular dysfunction. The kidney damage inflicted by
cadmium poisoning is irreversible. The proximal renal tubular
dysfunction creates low phosphate levels in the blood
(hypophosphatemia), causing muscle weakness and sometimes coma.
The dysfunction also causes gout, a form of arthritis due to the
accumulation of uric acid crystals in the joints because of high acidity of
the blood (hyperuricemia). Another side effect is increased levels of
chloride in the blood (hyperchloremia). The kidneys can also shrink up
to 30%.
Other patients lose their sense of smell (anosmia).
Diagnosis
Increased concentrations of urinary beta-2 microglobulin can be an
early indicator of renal dysfunction in persons chronically exposed to
low but excessive levels of environmental cadmium. The urinary beta-2
microglobulin test is an indirect method of measuring cadmium
exposure. Blood or urine cadmium concentrations provide a better index
of excessive exposure in industrial situations or following acute
poisoning, whereas organ tissue (lung, liver, kidney) cadmium
concentrations may be useful in fatalities resulting from either acute or
chronic poisoning.
19. Arsene intoxications
Signs and symptoms

Symptoms of arsenic poisoning begin with headaches, confusion,

severe diarrhea, and drowsiness. As the poisoning develops,
convulsions and changes in fingernail pigmentation
called leukonychia may occur. When the poisoning becomes acute,
symptoms may include diarrhea, vomiting, blood in the urine, cramping
muscles, hair loss, stomach pain, and more convulsions. The organs of
the body that are usually affected by arsenic poisoning are the lungs,
skin, kidneys, and liver. The final result of arsenic poisoning is coma to
death.
Arsenic is related to heart disease(hypertension related cardiovascular),
cancer,stroke (cerebrovascular diseases), chronic lower respiratory
diseases, and diabetes
Night blindness
Long term exposure to arsenic is related to vitamin A deficiency which is
related to heart disease and night blindness.
Research has shown that the inorganic arsenites (trivalent forms) in
drinking water have a much higher acute toxicity than organic arsenates
(pentavalent forms). The acute minimal lethal dose of arsenic in adults
is estimated to be 70 to 200 mg or 1 mg/kg/day. Most reported arsenic
poisonings are caused by one of arsenic's compounds, also found in
drinking water, arsenic trioxide which is 500 times more toxic than pure
arsenic.
Occupational exposures
Industries that use inorganic arsenic and its compounds include wood
preservation, glass production, nonferrous metal alloys, and electronic
semiconductor manufacturing. Inorganic arsenic is also found in coke
oven emissions associated with the smelter industry.
Occupational exposure to arsenic may occur with copper or lead
smelting and wood treatment, among workers involved in the production
or application of pesticides containing organic arsenicals. Humans are
exposed to arsenic through air, drinking water, and food (meat, fish, and
poultry); poultry is usually the largest source of food-based arsenic
ingestion due to usage of certain antibiotics in chicken feed. Arsenic
was also found in wine if arsenic pesticides are used in the vineyard.
Arsenic is well absorbed by oral and inhalation routes, widely distributed
and excreted in urine; most of a single, low-level dose is excreted within
a few days after consuming any form of inorganic arsenic. Remains of
arsenic in nails (which show as white spots and lines) and hair can be
detected years after the exposure
Arsenic interferes with cellular longevity by allosteric inhibition of an
essential metabolic enzyme pyruvate dehydrogenase (PDH) complex,
which catalyzes the oxidation of pyruvateto acetyl-CoA by NAD+. With
the enzyme inhibited, the energy system of the cell is disrupted resulting

in a cellular apoptosis episode. Biochemically, arsenic prevents use of

thiamine resulting in a clinical picture resembling thiamine deficiency.
Poisoning with arsenic can raise lactate levels and lead to lactic
acidosis. Low potassium levels in the cells increases the risk of
experiencing a life-threatening heart rhythm problem from arsenic
trioxide. Arsenic in cells clearly stimulates the production of hydrogen
peroxide (H2O2). When the H2O2 reacts with certain metals such
as iron or manganese it produces a highly reactive hydroxyl radical.
Inorganic arsenic trioxide found in ground water particularly
affectsvoltage-gated potassium channels, disrupting cellular electrolytic
function resulting in neurological disturbances, cardiovascular episodes
such as prolonged QT interval,neutropenia, high blood pressure, central
nervous system dysfunction, anemia, and death. Arsenic is a ubiquitous
element present in American drinking water.
Tissue culture studies have shown that arsenic blocks both IKr and Iks
channels and, at the same time, activates IK-ATP channels. Arsenic
also disrupts ATP production through several mechanisms. At the level
of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by
competing with phosphate it uncouples oxidative phosphorylation, thus
inhibiting energy-linked reduction of NAD+, mitochondrial respiration,
and ATP synthesis. Hydrogen peroxide production is also increased,
which might form reactive oxygen species and oxidative stress. These
metabolic interferences lead to death from multi-system organ failure,
probably from necrotic cell death, not apoptosis. A post mortem reveals
brick red colored mucosa, due to severe hemorrhage. Although arsenic
causes toxicity, it can also play a protective role.
Diagnosis
Arsenic may be measured in blood or urine to monitor excessive
environmental or occupational exposure, confirm a diagnosis of
poisoning in hospitalized victims or to assist in the forensic investigation
in a case of fatal over dosage. Some analytical techniques are capable
of distinguishing organic from inorganic forms of the element. Organic
arsenic compounds tend to be eliminated in the urine in unchanged
form, while inorganic forms are largely converted to organic arsenic
compounds in the body prior to urinary excretion. The current biological
exposure index for U.S. workers of 35 g/L total urinary arsenic may
easily be exceeded by a healthy person eating a seafood meal.
There are tests available to diagnose poisoning by measuring arsenic in
blood, urine, hair, and fingernails. The urine test is the most reliable test
for arsenic exposure within the last few days. Urine testing needs to be

done within 2448 hours for an accurate analysis of an acute exposure.

Tests on hair and fingernails can measure exposure to high levels of
arsenic over the past 612 months. These tests can determine if one
has been exposed to above-average levels of arsenic. They cannot
predict, however, whether the arsenic levels in the body will affect
health. Chronic arsenic exposure can remain in the body systems for a
longer period of time than a shorter term or more isolated exposure and
can be detected in a longer time frame after the introduction of the
arsenic, important in trying to determine the source of the exposure.
Hair is a potential bioindicator for arsenic exposure due to its ability to
store trace elements from blood. Incorporated elements maintain their
position during growth of hair. Thus for a temporal estimation of
exposure, an assay of hair composition needs to be carried out with a
single hair which is not possible with older techniques requiring
homogenization and dissolution of several strands of hair. This type of
biomonitoring has been achieved with newer microanalytical techniques
like Synchroton radiation based X ray fluorescence (SXRF)
spectroscopy and Microparticle induced X ray emission (PIXE).The
highly focused and intense beams study small spots on biological
samples allowing analysis to micro level along with the chemical
speciation. In a study, this method has been used to follow arsenic level
before, during and after treatment with Arsenious oxide in patients with
Acute Promyelocytic Leukemia
Treatment
Chelation
Chemical and synthetic methods are now used to treat arsenic
poisoning. Dimercaprol and dimercaptosuccinic acid are chelating
agents which sequester the arsenic away from blood proteins and are
used in treating acute arsenic poisoning. The most important side effect
is hypertension. Dimercaprol is considerably more toxic than succimer.
Mineral supplements
Supplemental potassium decreases the risk of experiencing a lifethreatening heart rhythm problem from arsenic trioxide
Nutritional intervention
Rats daily dosed with arsenic in their water, in levels equivalent to those
found in groundwater in Bangladesh and West Bengal were found to
respond to garlic extracts, with 40 percent less arsenic in their blood
and liver, and passed 45 percent more arsenic in their urine. The
conclusion is that sulfur-containing substances in garlic scavenge
arsenic from tissues and blood. The presentation concludes that people
in areas at risk of arsenic contamination in the water supply should eat
one to three cloves of garlic per day as a preventative.

22) Intoxications with benzene, xylene, styrene, toluene. Pathogenesis,

clinical characteristics, diagnostics, therapy and expertise of working
ability.
Benzene is a clear, oil-based liquid chemical. Sources of potential benzene
exposure range from gasoline and diesel fuel to more unusual substances such
as benzene-containing varnish remover. However, tobacco smoke is one of
the most significant sources of exposure to benzene. When a person touches,
inhales or swallows benzene, he is at risk for benzene poisoning, which
damages cells and can result in many symptoms, some of which are lifethreatening. The short term breathing of high levels of benzene can result in
death, while low levels can cause drowsiness, dizziness, rapid heart rate,
headaches, tremors, confusion and unconsciousness. The major effects of
benzene are manifested via chronic exposure through the blood. Benzene
damages the bone marrow and can cause a decrease in red blood cells,
leading to anemia. It can also cause excessive bleeding and depress the
immune system, increasing the chance of infection. Benzene causes leukemia
and is associated with other blood cancers and pre-cancers of the blood.
Toluene and xylene are powerful compounds that are found in many
household and industrial substances. Toluene and xylene poisoning can occur
when someone swallows these substances, breathes in their vapors, or when
these substances touch the skin. Xylene exhibits neurological effects. High
levels from exposure for acute or chronic periods can cause headaches, lack of
muscle coordination, dizziness, confusion and balance. Exposure to high levels
for short periods can also cause irritation of the skin, eyes, nose, and throat,
difficulty in breathing and other problems with the lungs, delayed reaction
time, memory difficulties, stomach discomfort, and possibly adverse effects
on the liver and kidneys. Styrene is only weakly toxic. It is carcinogen and a
toxin to the gastrointestinal, kidney and respiratory systems. Toluene has
direct negative effects on cardiac automaticity and conduction and can
sensitize the myocardium to circulating catecholamines. Pulmonary effects
include bronchospasm, asphyxia, acute lung injury (ALI) and aspiration
pneumonitis. GI symptoms from inhalation and ingestion may result in
abdominal pain, nausea, vomiting, and hematemesis. Hepatotoxicity
manifests with ascites, jaundice, hepatomegaly and liver failure.

23) Intoxications with nitro- and aminobenzenes. Pathogenesis, clinical

characteristics, diagnostics, therapy and expertise of working ability.

Nitrobenzene is a chemical used mainly in floor polish, shoe dyes, soaps and
the production of other chemicals such as cellulose ether and acetaminophen.
The chemical may be absorbed through the skin. Ingestion and other
exposures to the chemical can cause various symptoms. The type and severity
of symptoms varies depending on the amount of chemical involved and the
nature of the exposure.
Symptoms: prolonged exposure may cause serious damage to the central
nervous system, impair vision, cause liver or kidney damage, anemia and lung
irritation. Inhalation of fumes may induce headache, nausea, fatigue,
dizziness, cyanosis, weakness in the arms and legs, and in rare cases may be
fatal. The oil is readily absorbed through the skin and may increase heart rate,
cause convulsions or rarely death. Ingestion may similarly cause headaches,
dizziness, nausea, vomiting and gastrointestinal irritation.
Tests: blood test (only for resent exposure), urine test.
Treatment: breathing tube, oxygen therapy and symptomatic treatment.
Amino benzene (Aniline) It is used in range of dyes, such as fuchsine,
safranine and induline. It is a starting-product for the manufacture of many
drugs, such as paracetamol. It is used to stain neural RNA blue in the Nissl
stain.
Symptoms: Aniline is toxic by inhalation of the vapour, absorption through the
skin or swallowing. It causes headache, drowsiness, cyanosis, and mental
confusion, and, in severe cases, can cause convulsions. Prolonged exposure to
the vapour or slight skin exposure over a period of time affects the nervous
system and the blood, causing tiredness, loss of appetite, headache, and
dizziness.
Tests: breathe test, blood test (only for resent exposure), urine test.
Treatment: breathing tube, oxygen therapy and symptomatic treatment.

24) Intoxications with carbon disulfide. Pathogenesis, clinical

characteristics, diagnostics, therapy and prophylactics.
Carbon Disulfide: is a chemical used mainly in corrosion inhibitors, cold and
nickel plating, photography applications and as a solvent in gums and resins.
Ingestion and other exposures to the chemical can cause various symptoms.
The type and severity of symptoms varies depending on the amount of

chemical involved and the nature of the exposure. Chronic occupational

poisoning occurs after 10 -15 years it may cause sensory and motor
neuropathy, neuropsychiatric changes and parkinsonism. Atherosclerosis, in
particular coronary heart disease, impaired vision (perception of coloured
rings around lights and retinal changes), renal and hepatic damage and
permanent impairment of reproductive function also occur after long-term
exposures.
Symptoms: sleep disturbance, fatigue, anorexia and weight loss are common
complaints among exposed workers.Local contact may result in irritation,
burning sensation,blistering or deep burns. Conjunctivitis, pain and blurred
vision result from exposure of the eyes to the vapour and severe irritation or
burns occur after direct contact.
In chronic occupational exposure, the diagnosis is made from the presence of
sensory and motor neuropathy, neuropsychiatric changes, parkinsonism, renal
and hepatic damage, sleep disturbance, fatigue, anorexia and weight loss.
Treatment: there is no antidote for carbon disulfide poisoning. Treatment is
typically dependent on an individual's symptoms. Individuals with severe
exposure may need to be hospitalized. Antidepressants may be prescribed for
alterations in mood or symptoms associated with peripheral neuropathy.

25) Occupational intoxications with synthetic plastics and resins.

Classification. Pathogenesis, clinical characteristics, diagnostics,
therapy and expertise of working ability.
Due to their insolubility in water and relative chemical inertness, pure plastics
generally have low toxicity. Some plastic products contain a variety of
additives, some of which can be toxic. For
example, plasticizers like adipates and phthalates are often added to brittle
plastics like polyvinyl chloride to make them pliable enough for use in food
packaging, toys, and many other items. Some compounds leaching from
polystyrene food containers have been proposed to interfere with hormone
functions and are suspected human carcinogens. Whereas the finished plastic
may be non-toxic, the monomers used in the manufacture of the parent
polymers may be toxic. In some cases, small amounts of those chemicals can
remain trapped in the product unless suitable processing is employed. Some
polymers may also decompose into the monomers or other toxic substances
when heated. The primary building block of polycarbonates, bisphenol

A (BPA), is an estrogen-like endocrine disruptor that may leach into food. BPA
leached from the lining of tin cans, dental sealants and polycarbonate bottles
can increase body weight of lab animals' offspring. A recent animal study
suggests that even low-level exposure to BPA results in insulin resistance,
which can lead to inflammation and heart disease.
Resin:
Prehospital care: Plant parts or information regarding surroundings obtained
by prehospital providers may be helpful in identifying the suspected toxin.
Rinse mouth in cases of mucosal irritation to help alleviate symptoms.
Generally, induced vomiting with ipecac syrup is not encouraged, particularly
in cases with potential for altered mental status.
Hospital care: Airway, breathing and circulation must be ensured. Remove any
remaining toxin. Ipecac syrup is not recommended. Gastric lavage is unlikely
to be effective for removal of plant parts. Activated charcoal may be of
benefit, particularly if administered within the first several hours; however, it
may be of little benefit with rapidly absorbed substances such as teas.
These plants cause potentially severe contact dermatitis. Contact dermatitis
develops within 48 hours for most exposures. Highly sensitized individuals
develop eruptions within 8 hours. Eruptions often appear in a linear pattern,
indicating that a portion of bruised plant was rubbed across the skin when
handled or trampled. Symptoms at presentation range from mild erythema to
papules, vesicles and bullae. Although once believed to contain the allergen,
vesicular fluid cannot transmit contact dermatitis. Systemic distribution of
toxin may cause diffuse urticaria or erythema multiforme. Severe cases
require aggressive therapy. In severe cases, oral corticosteroids may be
required and should be tapered over 2-3 weeks. A shorter duration of therapy
is associated with rebound dermatitis. Symptoms in severe cases should be
cleared within 3 weeks; symptoms in milder cases may last only 10 days.
Ingestion of daphne causes vesication and edema of the mouth, lips and
pharynx with secondary hypersalivation and dysphagia. Subsequent
symptoms include extreme thirst, abdominal pain, vomiting and bloody
diarrhea. Daphnetoxin may cause organ damage, usually due to hypovolemia
and electrolyte imbalance; therefore, the kidneys are particularly at risk for
damage secondary to acute tubular necrosis. Fluid and electrolyte balance is
critical to prevent a potentially lethal outcome. Ingestion of only a few daphne
fruits can be fatal to a young child.

26) Intoxications with pesticides. Classification of pesticides.

Pathogenesus, clinical characteristics, therapy and expertise pf working
ability.
A pesticide is any substance or mixture of substances intended for preventing,
destroying, repelling or mitigating any pest. A pesticide may be a chemical
substance, biological agent (such as a virus or bacterium), antimicrobial,
disinfectant or device used against any pest.
Classification: Pesticides can be classified by target organism, chemical
structure and physical state. Pesticides can also be classed as inorganic,
synthetic, or biologicals (biopesticides).
A pesticide poisoning occurs when chemicals intended to control a pest affect
non-target organisms such as humans, wildlife, orbees. There are three types
of pesticide poisoning. The first of the three is a single and short-term very
high-level of exposure which can be experienced by individuals who commit
suicide, as well as pesticide formulators. The second type of poisoning is longterm high-level exposure, which can occur in pesticide formulators and
manufacturers. The third type of poisoning is a long-term low-level exposure,
which individuals are exposed to from sources such as pesticide residues in
food as well as contact with pesticide residues in the air, water, soil, sediment,
food materials, plants and animals.
Symptoms: headache, tears in the eyes, runny nose, increased saliva,
vomiting, diarrhea, sweating, general weakness, muscle twitching, seizures,
shallow breathing, dizziness.
Treatment: Specific treatments for acute pesticide poisoning are often
dependent on the pesticide or class of pesticide responsible for the poisoining.
However, there are basic management techniques that are applicable to most
acute poisonings, including skin decontamination, airway protection,
gastrointestinal decontamination and seizure treatment. The patient is
intubated and oxygen administered, if necessary. In more severe cases,
pulmonary ventilation must sometimes be supported mechanically. Seizures
are typically managed with lorazepam, phenytoin and phenobarbitol, or
diazepam (particularly for organochlorine poisonings).

27) Radial epicondylitis. Tendomyosis of the arms clinical

characteristics, diagnosis, criteria for occupational etiology.

Radial epicondylitis: is a condition where the outer part of the elbow

becomes sore and tender. This condition can also be caused by sports such as
swimming and climbing, the work of manual workers and waiters, as well as
activities of daily living. It is an overuse injury occurring in the lateral side of
the elbow region, but more specifically it occurs at the common extensor
tendon that originates from the lateral epicondyle. The acute pain that a
person might feel occurs as one fully extends the arm. Sportspersons as well
as those who used the same repetitive motion for many years, especially in
their profession, suffered from this. It was also common in individuals who
performed motions they were unaccustomed to. The data also mentioned
that the majority of patients suffered from this in their right arms.
Treatment: rest, apply ice or cold therapy to the elbow (20 min's on up to six
times a day). This will help reduce pain and inflammation if present. Wear a
brace or support to protect the tendon whilst healing and strengthening,
particularly when returning to work. The brace should not be put on the
painful area but rather approximately 10cm down the forearm.
Tendomyosis is a purely functional disturbance of tendons, ligaments and
muscles, without any demonstrable patho anatomical changes. Via sensor
receptors in the painful, spastic musculature, the disorder is kept in being and
amplified by positive feedback. All muscles that are functionally related to the
irritated joint have their own specific pain-radiation zones.
Symptoms: Spontaneous chronic pain of the forearm, challenging pain in:
supination and pronation of the forearm, dorsal extension of the wrist against
resistance, palpatory pain of the forearm muscles, edema, rigid muscles,
depression due to chronic pain.
Treatment: the goal of treatment is to relieve pain and reduce inflammation.
Rest or keeping the affected tendons still is essential for recovery. Applying
heat or cold to the affected area should help reduce the pain and
inflammation. Nonsteroidal anti-inflammatory medications (NSAIDs) can
relieve pain and reduce inflammation. Local injections of corticosteroids may
be useful as well. Some patients need surgery to remove the inflammation
surrounding the tendon.

28) De Quervaines disease. Stenosising tendovaginitis of the fingers

clinical characteristics, diagnosis, criteria for occupational etiology.

De Quervain syndrome: is an inflammation or a tendinosis of the sheath or

tunnel that surrounds two tendons that control movement of the thumb. The
cause is not known. In medical terms, it remains idiopathic. Symptoms: are
pain, tenderness and swelling over the thumb side of the wrist and difficulty
gripping. Finkelstein's test is used to diagnose de Quervain syndrome in
people who have wrist pain. To perform the test, the thumb is placed in the
closed fist and the hand is tilted towards the little finger in order to test for
pain at the wrist below the thumb. Pain can occur in the normal individual,
but if severe, DeQuervain's syndrome is likely. Pain will be located on the
thumb side of the forearm about an in inch below the wrist. Treatment: with
corticosteroids injection and surgery.
Tendovaginitis: is the inflammation of the tendon and its surrounding sheath.
The common signs of tendovaginitis are pain, swelling and tenderness on the
affected joint. Treatment involves a lot of rest and patients who are
recovering from it must avoid putting stress and pressure on the affected
joint. Slow and gentle movements could be done after some time to avoid
stiffness. Ice application as a form of tendonitis treatment helps reduce
swelling and pain. Medications to ease the pain come in the form of
nonsteroidal inflammatory drugs that should not be used for more than seven
to ten days.

29) Humero-scapular periarthritis clinical characteristics, diagnosis,

criteria for occupational etiology.
Humeroscapular periarthritis (HPA): this term includes all regressive and
reactive affections occurring in the region of the shoulder joint proper and has
meanwhile become a synonym for painful shoulder stiffness, a term which
covers many different processes which are not covered in detail here. Patients
suffer from this disability exhibit marked loss of function of the upper
extremity due to pronounced limitation of shoulder function. The etiology is
usually resulting of strain or injury to the joint capsule, the subacromial bursa
and the surrounding fibrous tissue. Persistent pain in the shoulder which often
extends down the arm and up into the neck is the main symptom. Muscle
atrophy occurs and frequently the fingers are swollen and show a marked loss
of function. In early prognosis treatment with active movements and some
passive manipulation may be enough. The goal of treatment of HPA is to
restore the function of the shoulder joint and eliminate the pain. To this end,
various forms of treatment are fundamentally available: 1) conservative

treatment, with medication and physiotherapy; 2) surgical treatment; and 3)

mobilization under anesthetic, with which, comparatively speaking, results
have been best.

30) Occupational injuries of the musculo-skeletal system clinical

characteristics, diagnostics, criteria for occupational etiology.
Work-related musculoskeletal disorders (WMSDs) are a group of painful
disorders of muscles, tendons, and nerves. Carpal tunnel syndrome,
tendonitis, thoracic outlet syndrome, and tension neck syndrome are
examples. Work activities which are frequent and repetitive, or activities with
awkward postures cause these disorders which may be painful during work or
at rest. Almost all work requires the use of the arms and hands. Therefore,
most WMSD affect the hands, wrists, elbows, neck, and shoulders. Work using
the legs can lead to WMSD of the legs, hips, ankles, and feet. Some back
problems also result from repetitive activities.
Etiology: dynamic physical overload, static physical load, handwork with
weights, forced working posture and body position, rate of work, irrational
movements and awkward postures, vibration, sudden temperature changes or
long lasting cooling.
Diseases of the muscles:
Myalgia means "muscle pain" and is a symptom of many diseases and
disorders. The most common causes are the overuse or over-stretching of a
muscle or group of muscles.
Myositis is an inflammation or swelling of the muscles, often caused by injury,
infection, or anautoimmune disorder.
Tendinitis or tendonitis, meaning inflammation of a tendon, is a type of
tendinopathy often confused with the more common tendinosis, which has
similar symptoms but requires different treatment.
Tendinosis is a chronic tendinitis, tendinosus, chronic tendinopathy or chronic
tendon injury, is damage to a tendon at a cellular level. It is thought to be
caused by microtears in the connective tissue in and around the tendon,
leading to an increase in tendon repair cells. This may lead to reduced tensile
strength, thus increasing the chance of tendon rupture.

Tendovaginitis, tenosynovitis, vaginal synovitis and tendinous synovitis is an

inflammation of tendon sheath, the membrane that surrounds and cushions
any of certain tendons passing over a bone or through a joint.
nthesopathy - a disease occurring at the site of attachment of muscle
tendons and ligaments to bones or joint capsules.
Periarthritis - Inflammation of the tissues surrounding a joint.
Arthrosis - fibrosis or degeneration of the articular cartilage affecting one or
various articulations.

31) Occupational radicukopathies clinical characteristics, diagnosis,

criteris for occupational etiology.
Radiculopathy is not a specific condition, but a description of a problem in
which one or more nerves are affected and do not work properly (a
neuropathy). This can result in pain (radicular pain), weakness, numbness, or
difficulty controlling specific muscles. The problem is at or near the root of the
nerve, along the spine. The nerves may be inflamed, compressed, or working
ineffectively due to a lack of blood flow. The nerve could be affected by a
progressive disease that is destroying it in part or in whole. The "straight leg
raise test" can help to diagnosis a lumbar or sacral nerve root radiculopathy.
Common mainstream treatment approaches include physical therapy,
medication, and relaxation. Polyradiculopathy refers to the condition where
more than one spinal nerve root is affected.
Causes: Affected nerves may be inflamed, pinched (compressed), or working
ineffectively due to a lack of blood flow. The nerve could be affected by a
progressive disease that is destroying it in part or in whole. Additionally,
pinched nerves can be caused by excessive pressure caused by surrounding
bones, muscle, cartilage, and tendons. The "straight leg raise test" is often
used to diagnose a lumbar or sacral nerve root radiculopathy. Treatment:
effective treatment aims to resolve the underlying cause and restores the
nerve root to normal function. Common mainstream treatment approaches
include physical therapy, medication and relaxation. A comprehensive
systematic review found moderate quality evidence that spinal manipulation
is effective for the treatment of acute lumbar radiculopathy. Only low level
evidence was found to support spinal manipulation for the treatment of

chronic lumbar and cervical spine-related radiculopathies, and no evidence

was found to exist for treatment of thoracic radiculopathy.

32) Vegetative polyneuropathy of the upper limbs with occupational

genesis clinical characteristics, diagnosis, criteria for occupational
etiology.
Neuropathy affecting just one nerve is called "mononeuropathy" and
neuropathy involving multiple nerves in roughly the same areas on both sides
of the body is called "symmetrical polyneuropathy" or simply
"polyneuropathy." When two or more (typically just a few, but sometimes
many) separate nerves in disparate areas of the body are affected it is called
"mononeuritis multiplex," "multifocal mononeuropathy" or "multiple
mononeuropathy". Neuropathy may cause painful cramps, fasciculations (fine
muscle twitching), muscle loss, bone degeneration, and changes in the skin,
hair, and nails. Additionally, motor neuropathy may cause impaired balance
and coordination or, most commonly, muscle weakness; sensory neuropathy
may cause numbness to touch and vibration, reduced position sense causing
poorer coordination and balance, reduced sensitivity to pain and temperature
change, tingling or burning pain, or skin allodynia (severe pain from normally
nonpainful stimuli, such as light touch).
Polyneuropathy is a pattern of nerve damage which is quite different from
mononeuropathy, often more serious and affecting more areas of the body.
The term "peripheral neuropathy" is sometimes used loosely to refer to
polyneuropathy. In cases of polyneuropathy, many nerve cells in various parts
of the body are affected, without regard to the nerve through which they
pass; not all nerve cells are affected in any particular case. The effect of this is
to cause symptoms in more than one part of the body, often on left and right
sides symmetrically. As for any neuropathy, the chief symptoms include
weakness or clumsiness of movement (motor); unusual or unpleasant
sensations such as tingling or burning; reduction in the ability to feel texture,
temperature, etc.; and impaired balance when standing or walking (sensory).
In many polyneuropathies, these symptoms occur first and most severely in
the feet. Autonomic symptoms may also occur, such as dizziness on standing
up, erectile dysfunction, and difficulty controlling urination. Polyneuropathies
are usually caused by processes that affect the body as a
whole. Diabetes and impaired glucose tolerance are the most common
causes. Other causes relate to the particular type of polyneuropathy, and

there are many different causes of each type, including inflammatory diseases
such as lyme disease, vitamin deficiencies, blood disorders, and toxins
(including alcohol and certain prescribed drugs). The treatment of
polyneuropathies is aimed firstly at eliminating or controlling the cause,
secondly at maintaining muscle strength and physical function and thirdly at
controlling symptoms such as neuropathic pain.

33) Toxic polyneuropathies clinical characteristics, diagnosis, criteria

for occupational etiology.
Polyneuropathy is a serious, unpredictable, occasionally progressive, and life
threatening neurological disorder that occurs when many nerves throughout
the body malfunction simultaneously. It may be acute and appear without
warning, or chronic and develop gradually over a longer period of time. Many
polyneuropathies have both motor and sensory involvement; some also
involve dysfunction of the autonomic nervous system. These disorders are
often symmetric and frequently affect the feet and hands, causing weakness,
loss of sensation, pins-and-needle sensations or burning pain. There are
numerous conditions that can cause polyneuropathy.
- Toxic polyneuropathy is usually contracted from drug abuse or chemical
exposure in the workplace.
Causes: drug abuse and chemical exposure in the workplace are the most
common causes of toxic neuropathy. Exposure to lead, mercury, arsenic and
thailum in the workplace makes you more vulnerable to toxic neuropathy. In
addition to drug abuse, sniffing substances like glue can lead to toxic
neuropathy. Herbal medicine remedies, especially Chinese remedies, can be
another cause of toxic neuropathy because herbal medicines can contain
dangerous chemicals.
Symptoms: of toxic neuropathy are the same as standard forms of
neuropathy. Pain, spasms and weakness in the muscles are the most common
symptoms. Some people with neuropathy experience difficulty walking. Pain
associated with neuropathy usually comes in the form of numbness or
shooting pain. Numbness results from nerves inside the body falling asleep.
Shooting pain occurs when nerve signals violently thrust through the body.

Diagnosis: doctors usually recognize symptoms of neuropathy during a

physical examination. Neurological evaluations, electromyography and blood
tests are among methods doctors use to confirm a diagnosis of neuropathy.
Treatment: depends on the cause of the disease. If the cause is exposure to
chemicals, the first step in treatment is removing the patient from the
environment of exposure. For drug-related neuropathy, giving up drug habits
is the first step.

34) Mononeuropathies connected with compressive syndromes of the

carpal, cubital and ulnar canals clinical characteristics, diagnosis,
criteria for occupational etiology.
External pressure reduces flow in the vessels supplying the nerve with blood.
This causes local ischaemia, which has an immediate effect on the ability of
the nerve axons to transmit action potentials. As the compression becomes
more severe over time, focal demyelination occurs, followed by axonal
damage, and finally scarring. The symptoms and signs depend on which nerve
is affected, where along its length the nerve is affected, and how severely the
nerve is affected. Positive sensory symptoms are usually the earliest to occur,
particularly tingling and neuropathic pain followed or accompanied by
reduced sensation or complete numbness. Muscle weakness is usually noticed
later, and is often associated with muscle atrophy. A compression neuropathy
can usually be diagnosed confidently on the basis of the symptoms and signs
alone. However, nerve conduction studies are helpful in confirming the
diagnosis, quantifying the severity, and ruling out involvement of other nerves
(suggesting a mononeuritis multiplex or polyneuropathy). A scan is not usually
necessary, but may be helpful if a tumor or other local compressive lesion is
suspected. Nerve injury, as a mononeuropathy, may cause similar symptoms
to compression neuropathy. This may occasionally cause diagnostic confusion,
particularly if the patient does not remember the injury and there are no
obvious physical signs to suggest it. When an underlying medical condition is
causing the neuropathy, treatment should first be directed at this condition.
Some compression neuropathies are amenable to surgery: carpal tunnel
syndrome and cubital tunnel syndrome are two common examples.
-Carpal tunnel syndrome (CTS) is a median entrapment neuropathy that
causes paresthesia, pain, numbness and other symptoms in the distribution of
the median nerve due to its compression at the wrist in the carpal tunnel.
Conservative treatments include use of night splints
and corticosteroid injection. The only scientifically established disease
modifying treatment is surgery to cut the transverse carpal ligament.

-Cubital tunnel syndrome occurs when the ulnar nerve is obstructed during its
path along the cubital tunnel, the outer edge of the elbow. This compression
of the nerve often leads to a tingling or 'pins and needles' sensation in the
little and ring fingers. Most cases will be minor and tend to come and go with
time. Common causes are sleeping with the arm folded up, so the hand is at
the person's neck and the elbow is sharply bent.
-Ulnar nerve entrapment is a condition where the ulnar nerve becomes
trapped or pinched due to some physiological abnormalities. The ulnar nerve
passes through many tunnels and outlets which could cause the nerve to be
compressed or "pinched".

35) Vibration disease from local vibrations. Pathogenesis, clinical

characteristics, therapy, expertise of working ability, prophylactics.
Vibration is oscillatory motion. Effects may be variously described as pleasant
or unpleasant, beneficial or harmful. Hand transmitted vibration is the
vibration that enters the body through hands. It can be caused by agriculture,
industry, mining and construction. Exposure to hand-transmitted vibration can
lead to five types of disorders:
A) Type A Circulatory disorders
B) Type B bone and joint disorders
C) Type C Neurological disorders
D) Type D Muscle disorders
E) Type E other general disorders-CNSVibration induced health conditions progress slowly. In the beginning it starts
as a pain. As the vibration exposure continues, the pain may develop into an
injury or disease. Pain is the first health condition that is noticed and should
be addressed in order to stop the injury. Vibration-induced white finger (VWF)
is the most common condition among the operators of hand-held vibrating
tools. Vibration can cause changes in tendons, muscles, bones and joints, and
can affect the nervous system. Collectively, these effects are known as HandArm Vibration Syndrome (HAVS). The symptoms of VWF are aggravated when
the hands are exposed to cold. Workers affected by HAVS commonly report:
attacks of whitening (blanching) of one or more fingers when exposed to cold,
tingling and loss of sensation in the fingers, loss of light touch, pain and cold

sensations between periodic white finger attacks, loss of grip strength, bone
cysts in fingers and wrists. The development of HAVS is gradual and increases
in severity over time. It may take a few months to several years for the
symptoms of HAVS to become clinically noticeable. Hand-arm vibration
exposure affects the blood flow (vascular effect) and causes loss of touch
sensation (neurological effect) in fingers.
Classification scale for cold-induced vascular (blood flow) symptoms in fingers
with hand-arm vibration syndrome: 1. Mild, Occasional attacks affecting only
the tips of one or more fingers. 2. Moderate, Occasional attacks affecting
finger tips and middle of the finger and rarely also the finger parts close to the
palm. 3. Severe Frequent attacks affecting most fingers. 4. Very Severe Same
symptoms as in stage 3 with degenerate skin changes in the finger tips. Since
most vibrating machines and tools produce noise, a vibration-exposed worker
is likely to be exposed to noise at the same time. Simultaneous exposure to
noise and vibration produces greater temporary hearing loss than noise alone.

36) Vibration disease from vibrations with whole body impact.

Pathogenesis, clinical characteristics, therapy, expertise of working
ability, prophylactics.
Vibration is oscillatory motion. Effects may be variously described as pleasant
or unpleasant, beneficial or harmful. Hand transmitted vibration is the
vibration that enters the body through hands. It can be caused by agriculture,
industry, mining and construction. Exposure to hand-transmitted vibration can
lead to five types of disorders:
A) Type A Circulatory disorders
B) Type B bone and joint disorders
C) Type C Neurological disorders
D) Type D Muscle disorders
E) Type E other general disorders-CNSWhole-body vibration can cause fatigue, insomnia, stomach problems,
headache and "shakiness" shortly after or during exposure. The symptoms are
similar to those that many people experience after a long car or boat trip.
After daily exposure over a number of years, whole-body vibration can affect
the entire body and result in a number of health disorders. Sea, air or land

vehicles cause motion sickness when the vibration exposure occurs in the 0.1
to 0.6 Hz frequency range. Studies of bus and truck drivers found that
occupational exposure to whole-body vibration could have contributed to a
number of circulatory, bowel, respiratory, muscular and back disorders. The
combined effects of body posture, postural fatigue, dietary habits and wholebody vibration are the possible causes for these disorders. Studies show that
whole-body vibration can increase heart rate, oxygen uptake and respiratory
rate, and can produce changes in blood and urine. East European researchers
have noted that exposure to whole-body vibration can produce an overall ill
feeling which they call "vibration sickness." Many studies have reported
decreased performance in workers exposed to whole-body vibration. Studies
of the effect of separate and simultaneous exposure to noise and whole-body
vibration have concluded that whole-body vibration alone does not cause
hearing loss. However, simultaneous exposure to noise and vibration
produces greater temporary hearing loss than noise alone.

37) Occupational damages of the hearing clinical characteristics,

diagnostics, therapy, expertise of working ability and prophylactics.
Injuries by infra- and ultrasounds.
Occupational hearing loss is damage to the inner ear from noise or vibrations
due to certain types of jobs. Sounds above 90 decibels may cause vibration
intense enough to damage the inner ear, especially if the sound continues for
a long time. Some jobs carry a high risk for hearing loss, such as: Airline
ground maintenance, construction farming jobs involving loud music or
machinery. The main symptom is partial or complete hearing loss. The hearing
loss may get worse over time. Sometimes hearing loss is accompanied by
noise in the ear. A physical examination will not usually show any specific
changes. Tests that may be performed include: Audiology/audiometry, CT
scan of the head, Head x-ray. The hearing loss may be permanent. The goal of
treatment is to improve any remaining hearing and develop coping skills (such
as lip reading). Using a hearing aid may improve communication. Always the
patient needs to protect the ear from further damage. For example, wear ear
plugs in noisy areas.
Hearing loss can be of two types: Acoustic trauma results in damage of the ear
from a sharply rising wave front such as explosion. The second type noise
induced hearing loss is much more common resulting from long term
exposure to intense sound. Noise control in working places should be
classified in three categories:

-Engineering out of the noise hazard

-Attentuating the noise hazard
-Use of hearing protection programs (using hearing protectors)
Treatment: The hearing loss is usually permanent. The goal of treatment is to
prevent further hearing loss, improve communication with any remaining
hearing and develop coping skills (such as lip reading). Using a hearing aid may
improve communication. For example, wear ear plugs in noisy areas.

38) Occupational diseases of the upper respiratory tract clinical

characteristics, diagnosis, criteria for occupational etiology.
We can define them as chronic or acute rhino sinusitis or reactive airways
dysfunction syndrome (RADS).
Sinusitis or rhinosinusitis is inflammation of the paranasal sinuses. It can be
due to infection, allergy, or autoimmune problems. Most cases are due to a
viral infection and resolve over the course of 10 days.
Acute sinusitis is usually precipitated by an earlier upper respiratory tract
infection, generally of viral origin. If the infection is of bacterial origin, the
most common three causative agents are Streptococcus
pneumoniae, Haemophilus influenzae and Moraxella catarrhalis. Viral sinusitis
typically lasts for 7 to 10 days, whereas bacterial sinusitis is more persistent.
Chemical irritation can also trigger sinusitis, commonly from cigarette smoke
and chlorine fumes. Rarely, it may be caused by a tooth infection.
Chronic sinusitis lasts longer than three months and can be caused by many
different diseases that share chronic inflammation of the sinuses as a common
symptom. Symptoms of chronic sinusitis may include any combination of the
following: nasal congestion, facial pain, headache, night-time coughing, an
increase in previously minor or controlled asthma symptoms, general malaise,
thick green or yellow discharge, feeling of facial 'fullness' or 'tightness' that
may worsen when bending over, dizziness, aching teeth and/or halitosis.
Unless complications occur, fever is not a feature of chronic sinusitis. Often
chronic sinusitis can lead to anosmia, a reduced sense of smell. In a small
number of cases, chronic maxillary sinusitis is associated with a dental
infection. Chronic sinusitis cases are subdivided into cases with polyps and
cases without polyps. When polyps are present, the condition is called chronic

hyperplastic sinusitis. Chronic rhino sinusitis represents a multifactorial

inflammatory disorder, rather than simply a persistent bacterial infection. The
medical management of chronic rhino sinusitis is now focused upon
controlling the inflammation that predisposes patients to obstruction,
reducing the incidence of infections.
The phrase "reactive airways dysfunction syndrome" (RADS) denotes the
development of a persistent asthma-like condition with airway hyperresponsiveness developing in a previously healthy asymptomatic individual
within 24 hours of a single exposure to concentrated respiratory irritants.
High-intensity exposure to irritants is one accepted risk factor. Symptoms:
acute extreme shortness of breath, tightness in the chest and wheezing occur
with this problem.

39) Occupational diseases of the eyes criteria for occupational

etiology.
In the diagnosis and treatment of eye injuries and diseases it is most
important to bear in mind the nature of the patient's occupation. For instance,
when one examines a patient who complains of a piece of metal flying into his
eye it is necessary to ascertain whether he was grinding or hammering at the
time of the accident. A grinder gets a superficial corneal foreign body which is
easily removed; but a history of hammering, chipping, boring, or milling, can
make the possibility of an intraocular foreign body. When we treat acute or
chronic conjunctivitis or keratitis it is most important to bear in mind the
likelihood of an occupational cause. Obscure cases of retinitis, retrobulbar
neuritis and ocular palsies, and amblyopia should always make us think of a
possibility of chronic poisoning arising from industrial solvents. The most
important of these poisons are lead, derivatives of benzene, carbon
bisulphide, methyl alcohol, arsenic and its derivatives, carbon tetrachloride,
and trichlorethylene. These and many other toxic substances used in industry
may produce toxic amblyopias, optic neuritis, and ocular palsies. Methyl
alcohol is used as a solvent for shellacs and varnishes, in the preparation of
perfumes, paint removers, as a solvent for aniline dyes, and in toilet materials.
Inhalation of vapour may cause optic neuritis and ocular palsies. Painters
working in closed spaces inhale the fumes of methyl alcohol and among them
optic atrophy has been reported. Lead-poisoning may occur in cornpositors,
plumbers, accumulator makers, makers of lead pipe, and paint grinders. It
causes optic neuritis and ocular palsies. Arsenic is used in the manufacture of

artificial flowers and insecticides, the dyeing industry, pickling, etc. Optic
neuritis was reported. Cosmetics which have some form of arsenic may cause
eczema of the eyelids.
Acute or chronic keratitis: blurring of vision, pain in the eyes, headaches,
lacrimation and a feeling of grittiness. It was found that hydrogen sulfide (H2S)
which is present in the air. This kind of disease appears in workers of sugar
industry and of silk-artificial factories. The largest amount of cases occurs in
winter months when ventilation is poorest.
-Bakers suffer also from blepharitis or conjunctivitis
-Also stone workers or workers in hard metals and sand blasters found to
suffer from chronic keratitis in which cornea shows bilateral shaped scars with
glistening foreign bodies embedded them.
-Industrial poisons like benzene (used in manufacture of garnishes, in dry
cleaning), methyl alcohol (used in perfumes), arsenic (used in cosmetics) and
its derivatives produce toxic amblyopia, optic neuritis and ocular palsies.

40) Laboratory diagnostics of the occupational diseases.

41) Occupational diseases of the skin criteria for occupational
etiology.
An occupational skin disease (OSD) is any skin disorder which is caused by a
person's work. A person's existing skin disorder may also be made much
worse by work activities and such cases are also considered as OSDs. The
commonest type of OSD is dermatitis, an inflammation of the skin. Causes of
OSD are: 1. Irritation. The commonest cause of OSD is irritation of the skin
from contact with substances at work. Strong irritants (such as acids, alkalis or
solvents) cause skin inflammation after a short period of skin contact. Weak
irritants (such as water, detergents, coolants) cause inflammation after
repeated exposures over a longer time. 2. Allergy. Another important cause of
OSD is allergy to substances handled at work. Examples of substances which
can cause skin allergies are cement, metals and resins. Rubber gloves and
boots worn for protection may sometimes paradoxically cause allergy. OSD
usually occurs on the parts of the body which come into contact with work
substances. OSDs occur most frequently on the hands and forearms. Early
signs of OSD include dryness, redness and itch of the skin. If severe, the skin
may become swollen and vesicles may develop. The skin may eventually

become cracked, scaly and thickened. These skin changes often improve when
the worker is away from work, such as during weekends and holidays. Fellow
workers who do the same job may also have similar skin problems. Skin
allergy tests are necessary to determine the cause of the OSD. Installing
devices in work operations, such as local exhaust ventilation, splash guards
and screens.
Disease: Allaergic dermatitis- due to metals, adhesive, cosmetics, drugs with
contact with skin, dyes, other chemical products, food in contact with skin,
other agents, allergic contacts dermatitis, unspecified. Agent: Main causative
agent groups: Antibiotics, Preservatives, Plants and trees, Antiseptics, Rubber
products, Dyes, Glues and bonding agents, Metals. Occupation/industry:
Various occupations in the manufacture and use of each of the causative
agents.
Disease: Irritant contact dermatitis- due to detergents, oils and greases,
solvents, cosmetic, due to drugs in contact with skin, due to other chemical
products, due to food in contact with skin, due to plants, except food, due to
other agents. Agent: Main causative agent groups: Soaps/Detergents,
Solvents, Oils and lubricants, Petroleum products, Acids, Alkalies, Cement,
Metal salts,Slag and glass wool. Occupation/Industry: Various occupations in
the manufacture and use of each of the causative agents.
Disease: Radiodermatitis, Acute radiodermatitis, Chronic radiodermatitisAgents: Ionizing radiation. Occupation/industry: Occupations with exposure to
ionizing radiation from x-ray machines, nuclear reactors etc., work involving
isotopes.
Disease: Acne-Agents: Chloracne: Halogenated aromatic hydrocarbons (ex.
Polychlorinated biphenyls, PCBs). Other chemical-induced acne: Asphalt,
Creosote, Oils, Greases, Pitch, Tar. Occupation/industry: Pesticide and
herbicide industries, work with condensers and transformers Oil refining,
asphalt work.

42) Occupational neoplastic diseases criteria for occupational

etiology.
The etiology of malignant neoplasms of lymphatic and haematopoietic tissue
is largely unexplained, with only a relatively small proportion of cases
attributable to known hereditary or environmental risk factors. Few well

established occupational causes are recognized, but numerous strong

associations with occupations or specific exposures have been observed. It has
been estimated that up to 10% of incident cases of both leukaemia and nonHodgkins lymphoma (NHL) are directly attributable to occupational
exposures. Exposure of ionizing radiation disease type: leukaemia, NHL
industries and occupations: radiologists, nuclear industry. Exposure to
benzene disease types: leukaemina and industries and occupations:
Petrochemical industry, motor mechanics, rubber industry, plastics industry,
shoe and leather workers. Exposures to organic solvents disease types:
leukaemia, NHL and industries and occupations: Rubber industry, plastic
industry, drycleaners and laundry workers, printers, aircraft maintenance
workers, painters, metal workers and toolmakers, welders, petrochemical
workers. Other exposures to electromagnetic fields, pesticides also can result
to leukaemia and NHL at any work involving exposure to livestock, pesticides,
slaughter of animals or electrical utility workers, electricians, telephone line
workers.
Disease: Malignant neoplasm of liver and intrahepatic bile ducts,
Angiosarcoma of liver. Agent: Vinyl chloride monomer. Occupation/industry:
Manufacturing of vinyl chloride, vinyl chloride polymerisation industry.
Disease: Malignant neoplasm of nasal cavity and middle ear, Nasal cavity.
Agent: Hardwood dust, chromium (VI) compounds, nickel compounds.
Occupation/industry: Woodwork, cabinet and furniture makers, chromium
producers, metal plating, dye/pigment manufacturing, nickel smelting and
refining, stainless steel production, manufacture of batteries.
Disease: Malignant neoplasm of larynx. Agent: Asbestos. Occupation:
Asbestos industries and utilizers.
Disease: Malignant neoplasm of bronchus and lung. Agent: Asbestos, arsenic
and its compounds, chromium (VI) compounds, nickel compounds, radon
progeny, silica, soots, bis-(chloromethyl) ether, beryllium, cadmium.
Occupation: Asbestos industries and utilizers, Arsenic mining, copper smelting,
production and use of arsenic pesticides, herbicides and insecticides, tanning,
glassmaking, chromium producers, metal plating, dye/pigment manufacturing.
Disease: Acquired haemolytic anemias, other non-autoimmune, haemolytic
anemias. Agent: Arsenic hydride (asrine), naphtaline, tributyl tin. Occupation:

Electrolytic processes, arsenic minerals processing, Chemical industry,

Manufacture and use of biocides.
Disease: Other aplastic anemias, aplastic anaemia due to other external
agents. Agent: Benzene, ionizing radiation. Occupation: Occupations with
exposure tobenzene ex. use of benzene containing solvents, petroleum
industry, coke ovens Occupations with exposure to ionizing radiation from xray machines, nuclear reactors etc., work involving isotopes.
Disease: Agranulocytosis. Agent: Benzene, ionizing radiation. Occupation:
Occupations with exposure to benzene ex. use of benzene containing solvents,
petroleum industry, coke ovens Occupations with exposure to ionizing
radiation from x-ray machines, nuclear reactors etc., work involving isotopes.

43) Occupational diseases, caused by biological factors classification,

criteria for occupational etiology.
A condition that results from exposure in a workplace to a physical, chemical
or biological agent to the extent that the normal physiological mechanisms
are affected and the health of the worker is impaired.
Biological agents include such organisms as bacteria, viruses, fungus,
parasites, spores and moulds. They may be found in or on soil, water, organic
matter, plants and animals.
Chemical agents can include such things as battery acid, solvents, ammonia
and pesticides.
Physical agents include various forms of energy that may harm a worker, for
example, heat, cold, light, vibration, noise and radiation.
Ergonomic hazards are associated with work such as lifting or moving of
heavy objects and tasks where there is excessive repetitive motion.

Personal protective equipment (PPE) is used to reduce or prevent a

worker's exposure to health and safety hazards. There are many different
types of PPE including respirators, gloves, safety boots, goggles, ear
plugs/muffs, hard hats, chaps and fall arrest devices.
General Responsibilities:

 The employer shall provide information, instruction and supervision to

workers exposed to hazardous biological, chemical or physical agents.
The employer should carry out an assessment of the workplace and
determine the risk that workers will be exposed to hazardous
biological, chemical or physical agents and develop a plan for
controlling worker exposure.
Where workers are exposed to hazardous biological, chemical or
physical agents, and it is not possible to control exposure by means
such as substituting a safer material, or re-designing the work process,
the employer and supervisor should ensure the use of appropriate
personal protective equipment. For chemical agents, the protective
equipment required will generally be identified on either the product
label or material safety data sheet, where available.
The employer should instruct workers on safe handling procedures and
proper personal hygiene techniques to minimize contact with chemical
or biological hazards.
Biological Agents: 1) The employer shall instruct all workers who come into
contact with animals about any transmittable diseases the animals may carry
and how to prevent transmission to themselves, 2) The employer should
encourage workers to have up-to-date tetanus shots.