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OCCUPATIONAL HEALTH Dr. Dalia Abdallah El-ShafeiLecturer of Community & Occupational Medicine

Definition Of Occupational Health: Occupational Health: is defined as the promotion and maintenance of the highest degree of physical, mental and social wellbeing of workers in all occupations (WHO & ILO, 1950 & revised in 1995).

Definition of Occupational MedicineOccupational Medicine is defined as; a branch of preventive medicine with some therapeutic function (Royal College of Physicians, 1978).

It begins as Industrial Medicine then it develops to Occupational Medicine then to Occupational and Environmental Medicine.

Occupational medicine deals with:1- Health promotion for workers and proper prevention and treatment.2- Work environment and its adverse effects on workers health3-Health problems of workers at any workplace

Importance of the discipline More than 2,000,000 people die from work-related accidents or disease every year, equivalent to 1 death every 15 seconds. Progress in bringing occupational health to the industrializing countries is painfully slow. In the poorest countries, there has been no progress at all.

Question 1What are the differences between occupational medicine and clinical medicine?

Differences between Occupational Medicine & Clinical Medicine

Occupational diseaseIt is a disease arising out of or during the course of employment and its cause present in the occupation (e.g. silicosis).

Why its diagnosis is very critical?Worker has the right to receive medical care at the expense of the employer.Worker has the right for paid sick leave.If disability occurs, the worker has the right for compensation.

Some diseases are not specially caused by exposures on job, but they are aggravated by occupational stressors.

so it can be found in the general population (e.g. hypertension).

Work-related disease

Occupational health servicesOccupational health is concerned with physical, mental and social conditions of a worker in relation to his/her work and working environment as well as his/her adjustment to work and the adjustment of work to the worker.

Occupational health team

Occupational physician:

Is the leader of the team who: Designs and implements the occupational health program, Conducts medical examination & biological monitoring, Provides first aid & emergency treatment Supervises the rehabilitative program for disabled workers.

Occupational nurse:

1-Assists the physician in providing medical services 2- Assists in supervising the work environment3- Educates workers 4-Keeps medical records.

Question 2Demonstrate occupational health services and occupational health professionals responsible for providing these services?

Occupational Health Program

Promotion of workers' health

(A) Improvement of the health & working capacity of workers:1- Adequate nutrition either by nutrition education and support as well as prevention and control of parasitic diseases.2- Socioeconomic development through:- Improving workers' income, and proper expending of this income.3- Social welfare through:- Management of family problems.- Making good social relations at work.- Encouragement of sport activities.4- Health education and keeping good medical records.

B) Improvement of work environment:Good sanitation of work place by:- Good design of the machines.- Suitable housekeeping.- Proper lighting and ventilation.- Good control for physical hazards as heat, radiation and noise.- Supplying work place with washing facilities and suitable transportation means.

Prevention of occupational health hazards

a) Medical prevention- Pre-employment medical examination: choose the suitable worker.- Pre-placement examination: done by the occupational physician of the plant to put the suitable worker in the suitable process.- Periodic medical examination : for early detection of any health hazards arises from workplace. Health education about early symptoms and signs of occupational diseasesImmunization of workers and chemoprophylaxis to combat any infectious disease.

a) Medical preventionIn Egypt, the law specifies the periodicity of the examination for workers in each work or job. It is either every 6 months or every 2 years depending on the duration of exposure needed to develop the occupational disease. the workers may be temporally or permanently removed from further exposure or may be advised to continue work.

b) Engineering preventionThrough:-- Mechanization of heavy work process to lighten the physical strain.- Enclosure and segregation of hazardous process.- Good ventilation, lighting and control of other physical hazards at workplace as heat, noise and radiation.

c) Hygienic prevention- Providing good sanitary facilities as washing, changing clothes.- Supplying protective equipment as respirators, protective clothes, and ear muffs or plugs.- Work environment monitoring for detection and evaluation of environmental pollutants.- Ensuring that work legislations are applied and investigation of workers' absenteeism.

3- Control of occupational health hazards

Control - Pre-placement medical examination which provides base line data about workers' health status which will help the occupational physician in detection of any deviation from these data on subsequent periodic medical examination.

Control - Periodic medical examination (screening): by which the occupational disease can be identified in its early stage to prevent progression of the abnormal physiologic condition It includes:a- Survey about history of exposure and any abnormal symptoms or complains.b- Clinical examination. c- Laboratory investigationsd- Biologic monitoring for early detection of any disturbed physiologic function

Control - Early treatment of the diagnosed occupational diseases.- First aid treatment of any occupational injuries.

4- Rehabilitation and compensation of the disabled workers

RehabilitationRehabilitation of disabled workers aims to:- Minimize or prevent the disability.- Retraining the disabled worker for a new job suitable for his new physical and mental capacities.- Compensation of the disabled workers after evaluation of the disability resulted from occupational disease or accident and giving him some privileges.

Occupational Hazards and diseases

Introduction To diagnose an occupational disease, the nature of the worker's occupation and the cause of it must present in the occupation. So, if a worker in a factory of batteries suffered from exposure to lead toxicity (occupational disease), but he works as driver away from exposure to lead, he will not be diagnosed as having an occupational disease as John Stone reported in his book on occupational health.there are 48 occupational diseases in the Egyptian law

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Classification of occupational diseases

(A) Diseased caused by physical agents as1- Exposure to high or low temperature.2- Exposure to noise.3- Exposure to radiation (ionizing and non-ionizing).4- Exposure to vibration.5- Exposure to atmospheric pressure changes.6- Exposure to electricity.

(B) Diseased caused by chemical agents as1- Exposure to toxic metals.2- Exposure to dusts and fumes.3- Exposure to noxious gases.4- Exposure to toxic organic compounds.

(C) Diseased caused by biological agents as1- Parasites.2- Bacteria.3- Viruses.4- Rickettsia.

(D) Diseases caused by psychosocial hazards asExposure to work stress - night work shifts - long working hours .

(E) Diseases caused by mechanical hazards asWrong lifting - wrong movements wrong postures - slippery floor or stairs

(1) OCCUPATIONAL DISEASE DUE TO PHYSICAL AGENTS

Heat disorders

I- Heat disorders1- Systemic disorders:- Heat cramps.- Heat stroke.- Heat exhaustion.2- Skin disorders:- Prickly heat (heat rash).3- Psychoneurotic disorders:- Chronic heat fatigue.4- Eye affection.- Cataract on U.V. rays exposure.5- Heat burn.

Heat crampsExcessive sweating and water intake without salt replacement causing hyponatremia.Clinical picture:- Severe painful cramps in muscles of limbs during work.- Severe spasm at intestinal smooth muscles- Headache, dizziness, body temperature may be normal slightly increased.Treatment of heat cramps:-Prevention by adequate salt intake -Supplementation with salts either oral or intravenous infusion.- Control of hot environment to eliminate or minimize heat hazards.

Heat strokeDisturbance of heat regulating center at brain causing heat retention in body causing hyperpyrexia.Clinical picture:- Abrupt rise of body temperature (40 - 43c).- Flushed hot dry skin.- Delirium, convulsion: may be coma and deathTreatment:- Rapid cooling of body by all possible means.- Removal of patient from the hot environment.- Treat the symptoms by sedatives or stimulants, I.V. saline infusion, O2 inhalation, bed rest.

Heat exhaustionExcessive sweating, salt and water depletion without replacement causing heamo-concentration and hypovolemia and circulatory failure.Clinical picture:- Headache, weakness and fatigue.- Anorexia, vomiting and excessive sweating.- Signs of peripheral circulating failure (pallor - cold moist skin - hypertension - weak rapid pulse).Treatment of heat exhaustion:- Removal of the patient to cool place.- Water and salt replacement.- Treatment of shock.

Heat rash (Miliaria rubra)Due to blocking of sweat gland ducts: sweat retention and inflammatory reactions.Clinical picture:- Raised red vesicles on the affected skin.- Prickling an itchy sensation on exposure to heat.Treatment of heat rash:- Removal to cooler environment.- Skin cleanliness to prevent infections.- Cool showers.- Application of mild drying and soothing lotions.

Question 3Discuss the health effects resulting from exposure to high temperature in a glass factory?

Exposure to noise

2- Exposure to noiseDefinition: Noise is any unwanted or undesirable sound.Auditory field lies between 20-20000 hertz (Hz) or cycles per second. If noise is below the lower level of normal hearing (below 20 Hz) it is called infra sound but if the noise above the upper limit of normal hearing (above 20 kHz) it is called ultrasound.Exposure to noise occurs in the following occupations:- Weaving.- Hammering of metals.- Military exposure due to explosions and shooting.- Building and construction.- Aviation and submarines.

The severity of occupational deafness is related to:

1- The duration of exposure.2- The intensity of the sound.3- The frequency of sound waves.4- The type of noise either continuous noise or impact noise which is more dangerous.5- Personal susceptibility.

Effects of noiseEffects of noise:A) Auditory effect: hearing loss.B) Non auditory effects:1- The heart rate: either increased or decreased depending in the type of noise.2- The respiratory rate: often increased.3- Performance of psycho-motor tasks either adversely or beneficially.4- Deafness is associated with significantly higher rates of mental illness in the community.

Hearing conservationThere are many components to a hearing conservation program including:1- Reduction of noise at source.2- Limit exposure with or without ear protectors.3- Routine monitoring of the place for noise level and the population at work for hearing ability.

Exposure to radiation

3- Exposure to radiationRadiation is the straight line transport of energy through space or matter.Classification of radiation:1- Ionizing radiation: any electromagnetic or particulate radiation capable of producing ions, directly or indirectly when passing through matter.2- Non ionizing radiation: electromagnetic radiation with a wave length not sufficient for ionization.

Types or Products of Ionizing Radiation

or X-rayNeutron

57- Symbols

OH. (hydroxyl radical)H.Radiation Damagewater moleculeg-ray2 OH. H2O2What happens when the water molecule is struck by the gamma ray?

Penetration Abilities of Different Types of Radiation

Alpha ParticlesStopped by a sheet of paperBeta ParticlesStopped by a layer of clothingor less than an inch of a substance (e.g. plastic)Gamma RaysStopped by inches to feet of concreteor less than an inch of leadRadiationSource

NeutronsStopped by a few feet of concrete

a:b:g1:100:10,000

Alpha particles. Alpha particles do not penetrate the dead layer of skin and can be stopped by a thin layer of paper or clothing. If an alpha emitting radioactive material gets inside the body through inhalation, ingestion, or through a wound, the emitted alpha particles can cause ionization that results in damage to tissue. Beta particles. Depending on its energy, beta radiation can travel from inches to many feet in air and is only moderately penetrating in other materials. Some beta radiation can penetrate human skin to the layer where new skin cells are produced. If high enough quantities of beta emitting contaminants are allowed to remain on the skin for a prolonged period of time, they may cause skin injury. Beta emitting contaminants may be harmful if deposited internally. Protective clothing (e.g., universal precautions) typically provides sufficient protection against most external beta radiation.Gamma rays and x-rays (photons). Gamma rays and x-rays are able to travel many feet in air and many inches in human tissue. They readily penetrate most materials. Thick layers of dense materials are needed to shield against gamma radiation. Protective clothing provides little shielding from gamma and x radiation, but will prevent contamination of the skin with the gamma emitting radioactive material. Neutrons. Neutrons also penetrate most materials. They are able to travel many feet in concrete and thousands of feet in air. Thick layers of materials with lots of hydrogen in them (like water or concrete) are needed to shield against neutron radiation. Protective clothing provides no shielding from neutron radiation. Neutrons are not likely to be encountered except in the initial seconds of a nuclear criticality event.

IONIZING RADIATIONMechanism of action:a) Ionization: is to ripe electrons away from atoms and molecules.b) Excitation of molecules.Type:A) Electromagnetic radiation as: X- ray ,Gama rayB) Corpuscular radiation as:* Alpha particles with low power of penetration and great power of ionization.* Beta particles with greater power of penetration.* Neutrons * Protons * Electrons.

Occupational exposure1- Uranium miners and atomic millers.2- Nuclear reactors and atomic energy plant.3- Radiologist.4- Scientists using radioactive materials.

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Clinical pictureA) Acute effect:1- Whole body irradiation: if exposure to doses > 1Gy, acute radiation syndrome will result. It is characterized by prodromal symptoms (nausea, vomiting) and bone marrow depression (leukaemia, anaemia, thrombocytopenia).2- Local irradiation: producing skin reactions according to the dose from mild erythema to tissue necrosis and ulceration.

Clinical pictureB) Chronic effect:1- Chronic radiation sickness.2- Chronic radio-dermatitis: disturbed sensation, focal hyperkeratosis, congestive hyperaemia, painful cracks and ulceration with malignant changes.3- Eye cataract: cataract starts at posterior people of lens capsule.4- Carcinogenic and hereditary harm.

Exposure to atmospheric pressure changes

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4- Exposure to atmospheric pressure changes (Decompression sickness)1- Those working in compressed air that is too rapidly decompressed. (caisson disease)2- Divers who surface too rapidly from depths greater than about 10 meters.3- Crew or paratroopers in aircraft who ascend too rapidly from sea level to heights greater than 5487 meters.

The manifestations of decompression sickness are due to the formation of nitrogen bubbles in the body fluids and in the tissues.The symptoms produced depend upon the site in which the bubbles are formed whilst size and rate of growth of the bubbles determines the severity of the symptoms.

Clinical pictureA) Acute symptoms that is divided into:1- Type I: - Mild or severe limb pain. - Skin mottling or skin irritation.2- Type II: - Paralysis or weakness of the limbs - Tingling or numbness of the limbs. - Vertigo. - Headache. - Dyspnea, chest pain. - Hypotension, coma.B) Chronic symptoms:- Aseptic necrosis of the bones.- Neurological or psychological symptoms.

Prevention and treatment1- Gradual decompression according to the well known standards 2- Use of pressurized airplanes.3- Inhalation of helium/oxygen mixture instead of air by divers to avoid nitrogen narcosis.4- Pre-employment medical examination: Those with chronic sinusitis, otitis media, lung cysts or emphysema must not be employed.5- Periodic medical examination.

Prevention and treatment6- Treatment of decompression sickness: recompressing the patient and reducing the pressure in accordance with a protocol laid down in set of tables.

DISEASE CAUSED BY CHEMICAL AGENTS

Pneumoconiosis(Dusty lung)

Definition: Pneumoconiosis or dusty lung = dust collection in the lung and the lung reaction to its presence.Types of pneumoconiosis:1- Collagenous: - There is fibrosis.- Permanent destruction of the normal alveolar architecture as: silicosis, asbestosis, coal workers pneumoconiosis and Talcosis.2- Non collagenous (benign pneumoconiosis): - Minimal reticular reaction.- Alveolar architecture intact.Such as: Iron oxide: siderosis Tin: stannosisBarium: baritosis Titanium: titanosis

Diagnosis of pneumoconiosis1- Occupational history.2- Clinical picture:a- Symptoms:-The most important is progressive dyspnea.-Melanoptysis in CWP.b- Signs:- Cyanosis- Clubbing- Crepitations.

3- Investigations(a) Chest X- ray: shows lung opacities, ILO classification of lung opacities include:* Small opacities: < 1cm

RoundedIrregularPQRUp to 1.5mmFrom 1.5 3mm From 3- 10mmSTUFine opacitiesMedium sized opacities Coarse opacities

* Large opacities > 1cmA: area of opacity from 1-5 cm2B: combined area of opacity < area of the right upper lobe.C: combined area of opacity > area of the right upper lobe.(b) Pulmonary function: restrictive or obstructive or mixed pattern.(c) Autopsy or biopsy:- Nature of the dust.- The pathological reaction in the lung.

SILICOSISDefinition: it is fibrotic lung disease due to inhalation of dust containing crystalline silicon dioxide (free silica).Workers at risk for silicosis:1- Miners or workers in tunnels.2- Sand blasters.3- Quarry workers.4- Glass workers.5- Ceramic workers.

Pathology1- Acute silicosis: due to inhaled high level of recently fractured quartz causing immediate damage of the alveoli with acute alveolitis then fibrosis.2- Chronic classic silicosis: due to repeated exposure of low level of silica for more than 20 years.- Lung: Discrete fibrotic nodules of 2-3mm, mainly in upper lobes with whorled pattern. These nodules may coalesce together to form massive fibrosis, which may show central ischemic necrosis with cavitation.- Pleura: thickening, fixed, hard with fibrotic nodules.3- Accelerated silicosis: As classic but progress more rapidly.

1- Chronic or classic silicosis: It needs 20 years to develop:- Early stages asymptomatic discovered accidentally on doing chest X-ray.- Progressive dyspnea.- Cough and sputum due to bronchitis.2- Accelerated: As chronic silicosis but progress within shorter period.3- Acute silicosis: It is fatal. It develops in few weeks and progress in 1-3 years only. There is:- Progressive dyspnea.- Massive proteinuria with renal failure.- Respiratory failure and death.

1- History of exposure. 2- clinical picture.3- X- ray is the clue diagnostic tool.a) Chronic silicosis:Small rounded opacities in the upper lung zones.In massive fibrosis: bilateral opacities and there may be cavitation if TB infection occurred.Egg shell calcification when hilar and mediastinal lymph nodes are enlarged and calcified.Bilateral pleural thickening adjacent to pulmonary fibrotic nodules.b) Accelerated: As chronic silicosis but progress more rapidly.c) Acute silicosis: ground glass appearance.1- Pulmonary function tests: (restrictive pattern).

Complications & Management

Complications:1- Tuberculosis silicotuberculosis.2- Respiratory failure.3- Emphysema, bronchitis.Management:1- Removal from exposure.2- Corticosteroid.3- Anti-tuberculosis drugs.4- Treatment of complications.

Prevention of silicosis1- Medical measures:- Pre-employment & Periodic medical examination.2- Engineering measures:- Enclosure of dusty processes.- Substitution of silica by safer material.- Proper ventilation of the work place.3- Hygienic measures:- Work place monitoring for keeping the dust level at its threshold limit value (TLV).- Use of respiratory protective devices.- Avoid smoking.

ASBESTOS RELATED DISEASES

Properties of Asbestos

Asbestos oreNaturally occurring fibrous mineralsGood tensile strengthFlexibleHeat resistantElectrical resistanceGood insulationChemical resistantBecause of these unique properties, asbestos was used extensively in variety of products.

Asbestos fibers

Types of Asbestos- Chrysotile - White asbestos- Amosite - Brown asbestos- Crocidolite - Blue asbestos Most commonly used: Others: Tremolite (sometimes found in vermiculite)ActinoliteAnthophyllite

Uses of AsbestosPipe insulation

Surfacing insulating materials

Reinforcement of materials

Fireproofing

Acoustic and decorative plaster

Textiles

Asbestos insulated pipe

Asbestos insulated boilerGreatly increased during and after World War II in ship insulationUse has greatly declined since the late 1970s

Disorders due to exposure to asbestos1- Asbestosis.2- Hyaline plaques in parietal pleura.3- Malignant mesothelioma of pleura & peritoneum.4- Bronchogenic carcinoma.5- Asbestos warts.6- Cancer larynx.

1- ASBESTOSIS

Asbestosis ExampleJoe Darabant, 1949, covered with chrysotile asbestos fibers. Worked for 30+ years at the Johns-Manville Plant in New Jersey, cutting asbestos shingles and making asbestos block and pipe-covering materials.

Joe, 1989. Forced to retire in 1974 at age 50 from poor health; he died from asbestosis in 1990 at age 66.Photos RAVANESI@2000Asbestosis is a serious chronic, progressive disease that can eventually lead to disability or death in people exposed to high amounts of asbestos over a long period. Asbestos fibers cause the lung tissues to scar; when the scarring spreads, it becomes harder and harder to breathe. Symptoms include shortness of breath, a dry crackling sound in the lungs while inhaling, coughing, and chest pain. This condition is permanent and there is no effective treatment.

Definition: diffuse interstitial pulmonary fibrosis which is usually accompanied by pleural fibrosis and thickening.

Pathogenesis:

Clinical picture & DiagnosisClinical picture:Symptoms: progressive dyspnea.Signs:- Clubbing.- Cyanosis.- Limitation of the movement of the lower chest wall.- Bilateral basal crepitations.Diagnosis:1- History of exposure.2- Clinical picture.

Digital Clubbing

Figure 2-46. Digital clubbing.

Figure 25-2. Chest X-ray of a patient with asbestosis.

Complications & Treatment Complications:1- Cancer lung.2- Respiratory failure due to pulmonary hypertension and core pulmonale.Treatment:1- Corticosteroid may relieve dyspnea.2- Treatment respiratory failure.2- Stop smoking.

2- HYALINE PLAQUES OF PARIETAL PLEURA

HYALINE PLAQUES OF PARIETAL PLEURA- Developed after 10 years.- Not malignant.- Bilateral yellowish well demarcated raised areas of hyaline fibrosis.- X-ray: bilateral linear opacities parallel to ribs.

3- MALIGNANT MESOTHELIOMA

MALIGNANT MESOTHELIOMA- Latent period about 40years.- Most commonly affecting pleura but peritoneum is also affected.- Crocidolite is the most important type involved in this disease.

Photo RAVANESI@2000Mesothelioma ExampleMesothelioma is a rare form of cancer of the pleura, the thin membrane lining the lungs. About 200 cases are diagnosed each year in the U.S. Virtually all cases are linked with asbestos exposure. The cancer is very invasive and spreads quickly, eventually crushing the lungs so that the patient cannot breathe. It is painful and always fatal. It can be caused by very low exposure and is not directly related to the amount inhaled. This cancer may take 30-40 years to develop.

Richard Pankowski, 1986. Diagnosed in 1985 with pleural mesothelioma; died 5 months later at age 36. In college, he worked for less than a year at the Manville Plant in N.J. Father also worked at the plant 30+ years and died from asbestosis. Richards exposure may have begun when he was a child.Tumors protruding through the right rib cage.

4- BRONCHOGENIC CARCINOMA

BRONCHOGENIC CARCINOMA- It is dose dependent.- Smoking is risk factor.- Long thin fibers (crocidolite).- adenocarcinoma type.Preventive measures:1- Engineering:Enclosure, substitution, ventilation, keeping asbestos dust concentration in work place below TLV.2- Hygienic: Personal protective devices. Avoid smoking.3- Medical measures:- Pre-placement examination.- Periodic medical examination.

Lung CancerLung cancer causes the largest number of deaths from asbestos exposure. The risk greatly increases in workers who smoke.

BYSSINOSIS AND RELATED CONDITIONS

BYSSINOSISDefinition: Chronic respiratory disease affecting proportion of workers involved in the manufacture of cotton, flax, hemp, jute & sisal.

Mechanism:1- Mechanical irritation theory:Mechanical irritation of airway epithelial surface by short cotton fibers causes reflex narrowing of airways.2- Pharmacological agent theories:a) Cotton plant contains histamine that cause bronchoconstriction.b) Inhalation of cotton dust will liberate histamine from platelets.c) Release of bronchoconstrictor mediators from polymorph nuclear leucocytes such as: - Slow reacting substance of anaphylaxis. - Leukotriens. - Platelet activation factors.

Mechanism 3- Immunologic mechanism:Massoud & Taylor found that the byssinotic manifestations are due to type III immune complex hypersensitivity reaction.4- Chemotactic theory: chemotaxis of P.N.L.5- Endotoxin activity theory.6- Fungus enzymes.

Pathology: No specific abnormalities in lung and bronchi have been described with byssinosis.

Clinical picture- Byssinosis usually requires 20-25 years to develop.- Symptoms of Byssinosis appear on the first day back to work by chest tightness and breathlessness.- Grading according to severity of symptoms:0: No symptoms.1/2: Occasional chest tightness on the first day of the working week.1: Chest tightness + breathlessness in the first day.2: Chest tightness + breathlessness in the first day and other days.3: As grade 2 + permanent respiratory disability.

Diagnosis1- History of exposure to cotton, flax, hemp.2- Typical manifestations.3- Lung function:- Decline in forced vital capacity in 1st second FEV1(between 5- 10%) during shift.- Decreased forced vital capacity (FVC).- Decreased FEF 25-75%.- Decreased PEFR.- Decreased FEV1/FVC%

Prevention1- Continuous dust conc. measurements in work place.2- Pre-placement examinations: recording history of chest troubles and base line lung function evaluation.3- Periodic medical examination: by measuring FVC and FEV1.4- Treatment of cotton before processing (washing, steaming, treatment with alkali).

TOXIC GASES

Toxic gases Toxic gases can be classified into:1- Simple asphyxiants: the most important gases are nitrogen, methane and carbon dioxide.2- Chemical ashyxiants: the most important gases are:A- Carbon monoxide (Co).B- Hydrogen cyanide (HCN).C- Hydrogen sulphide (H2S).3- Systemically active gases:The most important gases are:A) Arsine (which is a powerful hemolytic agent).B) Stibene (also is a hemolytic agent).C) Phosphine (which is respiratory irritant and neurotoxic).

Toxic gases 4- Irritant gases:A) Upper respiratory irritants:They are highly soluble in water so they dissolved in the upper respiratory tract causing irritation.-Ammonia (NH3) and Sulpher dioxide.

B) Lung tissue irritants:They are less soluble in water so they penetrate deep to lung tissue.- chlorine phosgene - fluorine - nitrogen oxides - ozone

A- Carbon monoxide (Co) toxicity

When you smell an odorless gas,it is probably carbon monoxide.

Sources of incomplete combustion:Furnaces, boilersInternal combustion engine (warehouses, auto plants)

Hazards increased in COLD weather with closed doors & windows

128ANGINACarbon monoxide is the most commonly encountered occupational and environmental agent with cardiotoxic effects. Photograph shows indoor foundry work, where combustion occurring in limited oxygen supply may lead to CO formation.

At risk OccupationsFire fightersGarage mechanicsAircraft refuelersTruck DriversKiln & furnace operatorsForklift operatorsJanitorial staffDisaster relief workersMinersParking garage attendantsAgricultural workers

Chronic exposure to CONYC bridge & tunnel officers

130Aside from acute effects, carbon monoxide likely has chronic effects on the development of coronary artery disease. The most informative studies in this area come from long-term mortality studies of NYC bridge and tunnel officers who had long-term daily CO exposure at work.

CO131

Toxicity:

Acute toxicity: depends on concentration of carboxyhemoglobin in blood.

Chronic toxicity:- Sleep disturbance, headache, memory loss.- Arrythmia, myocarditis.- Impaired autonomic nervous system. 50%Respiratory center depression and death

CO Toxicity Recommendation limits:TLV of CO in respirable air is 50 ppm and TLV of carboxyhemoglobin in blood must not exceed 5g/100g Hb.Prevention and control:- Continuous environmental assessment and keep the concentration below the recommended limit.- Personal protective devices.- Smoking cessation program.Treatment:- Removal from exposure.- 100% O2 using a face mask.- Hyperbaric O2.- Blood transfusion.

B- Hydrogen cyanide (HCN) & Hydrocyanic acid toxicity

HCN & Hydrocyanic acid toxicityUses:1- Fumigant (rodenticide, insecticide).2- Extraction of silver and gold.Mechanism of action:- HCN absorbed through the lung.- Excreted in urine and feces as thiocyanates.- It inhibits cytochrome oxidase enzymes.

HCN & Hydrocyanic acid toxicityToxicity:- Acute: Headache, confusion, nausea, vomiting, rapid weak respiration, convulsions, coma and death.- Chronic: Neurathenia, Psychic alterations, Allergic dermatosis.Treatment: Removal from exposure.- Amyle or Na nitrite inhalation.- Na thiosulfate intravenously infusion.- Recently, Di cobalt EDTA (600 mg intravenously) and Na thiosulfate.

EXPOSURE TO TOXIC METALS

LEADUses:- Manufacture pipes, sheet metals and foil.- In paints, enamels and glazes.Inlet to the body: Through inhalation of dust and fumes. Also, ingestion and absorption through the skin (by organic compounds) may occur.

Metabolism:

A- Distribution in the body:- Bound to RBCs, membranes.- Precipitate in bone, teeth.- Exist in the plasma.B- Excretion:- Almost via the kidney.- Small amount excreted through bile.- Sweat and milk.

Poisoning:

* G.I.T:- Vomiting, diarrhea. - Abdominal colic. - - Constipation.* Nervous system:- Headache. - Psychiatric disturbances.- Tremors. - Mania, loss of weight.* Blood:Disturbance in haemosynthesis.Anemia is due to:- Direct effect on RBCs.- Decreased life span of RBCs.

Prevention & Treatment Prevention: By the triad of:a) Engineering control measures.b) Good industrial hygiene.c) Regular clinical examination and investigation.Treatment of lead poisoning:a) Identification of source of lead poisoning.b) Removal from exposure.c) Chelation therapy for symptomatic patient with blood lead level more than 100 microgram/ dl.d) Chelation is performed under strict medical supervision by giving the patient injections of calcium ethylene dianine tetra acetic acid (Ca EDTA) and/ or oral penicillamine.

ERGONOMICS

Ergonomics The term "ergonomics" is derived from two Greek words: "ergo", meaning work and "nomi", meaning natural laws. Ergonomists study human capabilities in relationship to work demands. It is the application of knowledge as regards human abilities and limitations to the design of tools, machines, tasks etc.

Postureergonomic principles regarding posture:1- All work activities should permit the worker to adopt several different, but equally healthy and safe postures.2- Where muscular force has to be exerted it should be done by the largest appropriate muscle groups available.3- Work activities should be performed with the joints at about mid-point of their range of movement. This applies particularly to the head, trunk, and upper limbs.

The problemIn order to derive the benefits of ergonomic research, we must learn how to observe our bodies in a new way. Any attempt to improve workplace conditions can have only limited success if this issue is ignored.

Risk factors for work- related musculoskeletal disorders1- Repeated exertions2- Lack of balance between rest and activities3- Awkward and extreme postures4- Psychosocial stressors5- Mechanical stressors6- Extreme temperature

How do you know if the worker has a problemThe following symptoms may be found: Tingling Swelling in the joints Decreased ability to move Decreased grip strength Pain from movement, pressure, or exposure to cold or vibrationThese symptoms may not appear immediately because they develop over weeks, months, or years. By then, the damage may be serious.

Thanks