Occupational Health
Dr. Anmar Al-Dewachi Ass. Prof. Of Family Medicine MD, M.B.Ch.B, MPH,JHSFMDefinitions
Occupational disease → Disease caused by or resulting from employmentOccupational environment → sum of external conditions and influences which exist at work place and have an effect on the health of working population.The aim of occupational health is to promote and maintain the highest degree of physical, mental and social well-being of workers in all occupations.Occupational Hazards Physical hazards Chemical hazards Biological hazards Mechanical hazards Psychological hazards Occupational diseases: Diseases due to Physical agents Diseases due to Chemical agents Diseases due to Biological agents Diseases due to Mechanical agents Occupational cancers Occupational dermatosis Diseases due to Psychological origin
Diseases due to Physical agents:Heat :either generalized effect as heat hyperpyrexia, heat exhaustion, heat syncope, heat cramps,or local effect burns.Cold :either generalized effect as hypothermia or local effect as frost bite, chilblains Light Dim light → eye strain, occupational cataract, miner's nystagmus.High illumination → blurring of vision and lead to accidents Ionizing radiation: cancer, aplastic anemia, leukemia, infertility, anemia.Ultra violet radiation (arc welding):redness of eyes.Noise occupational deafness.
Diseases due to Physical agents:
Pressure:Exposure to high pressure in divers (diving deep in sea) lead to "Caisson disease" and air embolism.Exposure to low pressure in high altitudes workers → shortness of breath, hypoxia and polycythemia .Electricity Burns, disability and death.Diseases due to chemical agentsGASES → CO, CO2, NH3, N2, HCL, SO2 → GAS POISONING.DUSTS Dust < 5 micron inhaled into the lung → PneumoconiosisInorganic dusts:Coal dust → Anthracosis (Coal Miner's Pneumoconiosis)Silica → SilicosisAsbestos → AsbestosisIron → SiderosisOrganic (vegetable) dusts:Cotton dust → ByssinosisTobacco → TobacossisHay or green dust → Farmers` lungMetals and their compounds → toxic hazards from lead, mercury, cadmium, manganese, beryllium, arsenic, chromium etc.Chemicals → Acids, alkalies, pesticides.Solvents → e.g benzene.
Diseases due to Biological agents: Brucellosis (Malta fever), anthrax, actinomycosis, hydated cyst ,tetanus, leptospirosis, fungal infections etc. Occur in persons working among animals products (hair, wool) and agricultural workers. Diseases due to Mechanical agents: Accidents & fatigue. Occupational cancers: Cancer of skin, lung, bladder etc. Occupational dermatosis: Dermatitis, eczema Diseases due to Psychological origin: Anxiety, depression, industrial neurosis etc.
Prevention of occupational diseases I- Medical measures Pre-placement examination: It is done at the time of employment and includes:- history, thorough physical examination, some investigations as CXR, ECG, GUE, vision testing and special tests for endemic disease. The purpose of pre-placement examination: To put the right man in the right job. Useful as baseline data for future comparison. Periodical examination: The frequency (every month, every year) and content of periodical medical examination will depend upon the type of occupational exposure
Routinely workers are examined once a year. But in certain occupations e.g. lead monthly examinations are indicated. Medical and health care services. Notification of occupational diseases. Supervision of working environment: Frequent visit done by the physician to the factory to know various aspects of the working environment as temperature, lighting, ventilation, humidity, noise, cubic space and air pollution. Maintenance and analysis of records (worker's health record). Health education and counseling
II- Engineering measuresDesign of buildingThe type of floor, walls, height, ceiling, doors , windows, cubic space are all important in the original plan of the building.Good housekeepingIt means work environment approximate to house, it cover good cleanliness, ventilation, lighting, washing …etc.General ventilationVentilation opening must be adequate in the rooms, if dust generated → must be exhaust ventilation system.MechanizationMachine instead of man e.g. hand mixing replaced by machine → to prevent dermatitis
II- Engineering measures Substitution Replacement of a harmful material by a harmless one, orlesser toxicity. Dust control At the point of origin by water sprays as wet drilling of rock. Inclusion of a little moisture in the materials will make the processes of grinding, sieving and mixing comparatively dust-free. Enclosure Enclosing the harmful materials and processes will prevent the escape of dust and fumes into the factory atmosphere e.g. grinding.
II- Engineering measuresIsolationIsolation of the offensive process in a separate building so that workers not directly connected with the operation are not exposed to the hazard (isolation in place or time).Protective devices gas masks, ear plugs, safety shoes, gloves, barrier creams … etc.Research.
Lead poisoning
Lead poisoning is a medical condition caused by increased levels of the heavy metal lead in the body. Types of lead posisoning: 1. Acute lead poisoning from intense exposure to lead over short period of time 2. Chronic lead poisoning from repeated low-level exposure over long period of time. Chronic much more common than acute poisoning.Lead uses and sources
Industrial uses: Glass manufacture, ship building Batteries, printing and potteries In paints (in the past). Plastic manufacturers Rubber product manufacturers Non-occupational sources: Gasoline (thousands of tons of tetraethyl lead every year is exhausted from automobiles). Drinking water from lead pipes. Chewing lead paint on toysMode of absorption
Inhalation Most common route 50-70%. Occur due to inhalation of fumes and dust of lead or its compounds. Ingestion Poisoning by ingestion is less common. Small quantities of lead trapped in upper respiratory tract may be ingested .Lead may also be ingested in food or drink through contaminated hands. Adults absorb about 6 - 10% of ingested lead. Fasting adults absorb more. Children absorb much more lead (30-50% if well fed, and more, if fasting or malnourished). Increased absorption if low Fe, CaSkin only in case of organic lead compounds (absorption through skin) Organic lead has greater affinity for CNS – therefore skin absorption may be SERIOUS.Lead Storage & DistributionRapid turnover soft tissue pool: T1/2 30-40 days; blood, liver, kidney, CNS Slow turnover skeletal pool:T1/2 10-20 years
Distribution of Lead
95% long bones. 4% brain, liver, kidneys. 1% blood. Crosses placenta
Lead excretion
Renal (90%) and biliary (10%)Maximum excretion is ~ 3.5µg/kg/dayIf intake > 3.5 µg/kg/day accumulation will occurLead metabolism and nutrition Low dietary intake of vitamin D, vitamin C, and iron enhance absorption and retention of lead in the body.Body stores:Body stores → 150 – 400 mg in adult. Blood level → < 10 μg/100ml Blood level ↑ to 30 - 40 μg/100ml → clinical symptomsHealth effects of lead exposure
Organs affected by lead poisoning CNS Blood Renal GIT Reproductive Endocrine (including Bp) MusculoskeletalClinical features of lead poisoning
I. Children Early symptom are nonspecific (anorexia, irritability, insomnia……),symptoms slowly intensify over timeNeurological symptomsDevelopmental delay and loss of milestone especially languageHearing lossPeripheral neuropathyEncephalopathyHematological → hemolytic anemiaRenal → lead nephropathyGIT → lead colicII. In adults
The manifestations of lead poisoning can vary from individual to another. Adults with severe lead poisoning (with blood lead levels generally above 80 μg/100ml ) can present with the following:Abdominal pain ("lead colic"), constipation, joint pains, muscle aches, headache, hypertension anorexia, decreased libido, difficulty concentrating and deficits in short-term memory, anemia, nephropathy.A "lead line," a bluish pigmentation seen at the gum-tooth line, is not a very sensitive finding, and is the result of a reaction of lead with dental plaque
A peripheral neuropathy that frequently manifests with extensor weakness or "wrist/ankle drop“Nephrotoxicity can occur in chronic poisoning
Diagnosis: History of lead exposure Clinical examination LAB test Blood lead level (BLL)The main tool in diagnosing and assessing the severity of lead poisoning . The Free Erythrocyte Protoporphyrin (FEP) EP increased when the amount of lead in the blood is high, with a delay of a few weeks . EP levels in conjunction with blood lead levels can suggest the time period of exposure; if blood lead levels are high but EP is still normal, this finding suggests exposure was recent.
EP level alone is not sensitive enough to identify elevated blood lead levels below 35 μg/dL.Due to this and the fact that EP levels also increase in iron deficiency, use of this method for detecting lead exposure has decreased. CBC : basophilic stippling Microcytic hypochromic blood picture Renal function test (urea & creatinine )
Radiology (in children) Radio-opaque lead flecks in the intestinal tract suggesting recent ingestion
Lead lines at the end of growing long bones (seen at end of metaphysis of long bones) in children.
Managment
Reduction or removal from lead exposure is the key first step in treating lead toxicity.Chelation therapy In most cases, removal from exposure is the only therapy needed.Chelation is recommended for individuals with BLL >80 μg/100ml and those with levels between 60 -80 μg/100ml if they have lead-related symptoms.Chelating agents : Promote lead excretion with urineCa-EDTA (Ca ethylene- diamine tetra- acetic acid) DMSA (2,3-dimercaptosuccinic acid)D-penicillamine.Prevention of recurrencePreventive measures
Periodic examination of the workers Substitution Isolation Local exhaust ventilation Personal protection and personal hygiene Health education.Occupational Lung Diseases
Occupational lung diseases (OLD) are caused by the inhalation of dusts, fumes, gases or vapors. Four main categories of OLD can be identified Occupational asthma. Chemical pnemonitis. Pneumoconiosis [fibrotic and non-fibrotic]. Granulomata.Occupational asthma
Occupational asthma (OA) is characterized by airflow obstruction, airway hyperresponsiveness, and airway inflammation that results from a workplace stimulus.Occupational asthma is one of the most common occupational lung diseases in developed countries. 5 - 10% of adult-onset asthma is due to occupational exposure.
Occupations at risk
Animal handlers and veterinarians (animal proteins) Bakers and millers (cereal grains) Carpet makers (gums) Cleaning staff (e.g. detergents , bleach) Electronics workers (soldering resin) Carpenters (wood dust)
Pharmaceutical workers (drugs, enzymes) Seafood processors Spray painters Hair dressers Health care workers (latex and chemicals)
Characteristics of Occupational Asthma
A workplace substance is aerosolized or vaporized Patient has symptoms of asthma, but cough is the most common symptom. Affects only some of those exposed Onset often after symptom-free period of months to years Improvement after removal from work early in course Recurrence of symptoms on re-exposureClinical features
The latency period between exposure to stimuli and development of symptom varies among different stimuli. Rhinitis and conjunctivitis may proceed or accompany asthma symptoms. Cough, dyspnea ,chest tightness , wheezes. The patient report increased symptoms while at work or within several hours of the completion of a shift, and definite improvement on weekends or during vacations.Diagnosis
History and examination Investigations Pulmonary function test PFT Skin test Managements: Stop exposure Treatment of occupational asthma is the same as for non-occupational asthma The prognosis depends upon rapid diagnosis and prompt removal of the worker from further exposure Most patients show incomplete resolution of asthma, even many years following cessation of exposurePneumoconiosis
The term “Pneumoconiosis” group of lung disorders which result from inhalation of dusts. (dust size 0.5 – 3 micron)Many of these dusts give raise to fibrotic reaction in the lung with clinical symptoms.Other group of dusts causes opacities on CXR, but no symptoms. These radiographic changes called Benign PneumoconiosisClassification
Benign pneumoconiosisSiderosis (iron oxide lung)StannosisOther Benign PneumoconiosisFibrotic pneumoconiosisSilicosisAsbestosisCoal Miner’s Pneumoconiosis (anthracosis)Benign pneumoconiosis
Siderosis (iron oxide lung) The most common benign pneumoconiosis. Result from inhalation of iron dust as iron oxide fume in iron and steel foundries during mining and during grinding and welding operation. Stannosis Caused by deposition of tin in the lungs and it is less common than siderosis. The opacities are much denser with hilar L.N due to deposition of tin within them . Other Benign Pneumoconiosis: Calcium, Barium (baritosis), Chromate, Zirconium and Cerium.
Fibrotic pneumoconiosis
Silicosis Disease produced due to inhalation of free silica or silicon dioxide (SiO2). Occupational exposure: works in mining (coal, gold, copper, silver , and lead) Tunneling, stone cutting Pottery and ceramic industry Rock mining and metal grinding The incidence of silicosis depends upon the chemical composition of the dust, size of the particles, duration of exposure and individual susceptibility.The incubation period vary from few months up to 6 years, depending upon the above factors. Clinical features: Insidious onset, they are divided into arbitrary 3 stages which merge into one another. 1st stage: irritant cough, dyspnea on exertion and chest pain. His working capacity is little affected or not affected. 2nd stage: dyspnea with impaired ability to work. 3rd stage: patient is totally incapacitated (signs of RHF). Silicosis is associated with increased risk of Lung cancer &T.B
Prevention
Control of dust: Substitution of the substance if possible. Complete enclosure. Isolation. Wet procedure. Regular cleaning (use of vacuum). Personal protective measures. Regular physical examination of the workers.Asbestosis
Asbestosis specifically refers to the pneumoconiosis caused by inhalation of asbestos fibers. The disease is characterized by slowly progressive, diffuse pulmonary fibrosis. The spectrum of pulmonary disorders associated with asbestos exposure includes : Asbestosis Pleural disease (focal and diffuse benign pleural plaques) Malignancies (non-small cell and small cell carcinoma of the lung as well as malignant mesothelioma)Source of exposure
Mining and milling of the fibers Industrial sources of asbestos (eg, work with textiles, cement, insulation, shipbuilding) Non-occupational exposure to airborne asbestos (eg, regular exposure to soiled work clothes brought home by an asbestos worker, environmental exposure in the neighborhood of industrial sources….)Clinical features
Symptoms are insidious with variable latent period. Dyspnea is the first symptom, which is frequently out of proportion to the clinical signs in the lungsIn advanced cases, there may be clubbing of fingers, cardiac distress , cyanosis , respiratory insufficiency and death.The sputum shows “asbestos bodies” which are asbestos fibers coated with fibrin give rise to golden yellow or brown colorPrognosis → once established; the disease is progressive even after removal of worker from contact. Prevention Use of safer types of asbestos.Substitution.Rigorous dust control.Regular physical examination of the workers (clinical ,CXR, lung function).Health education and stop smoking.Continuing research
Occupational skin diseases
Occupational skin diseases are very common, it responsible for 70% of occupational diseases. Classification of agents causing occupational skin diseases: Mechanical agents : friction, pressure and trauma. Physical agents : Heat, cold, humidity, light, ionizing radiation. Chemical agents : both organic and inorganic chemicals. Biological agents: Viral, bacterial and parasitic agents. Plants and their products: leaves, fruits, dust, and other.Mechanical agents
In the form of cuts, abrasions, repeated trauma → Calluses and blisters.Callus is thickening of the skin in response to repeated trauma, friction or irritation. Blisters result from acute trauma to the skinPhysical agents
Heat :Intertrigo.,Erythema ab igne and burnsCold → frost bite, chilblains.Radiation → burns, dermatitisand cancer (BCC, SCC, melanoma).Electricity → Burns. Erythema ab igne:Occurred in those exposed to furnaces, as cooks, glassblowers and kiln operators and long term exposure to a heating pad. Pathogenesis: Long term exposure to radiant heat to the same area over time produces persistent vasodilatation of the dermal-subcutaneous blood vessels which leads to clinical changes.Clinical Feature
The early stage is an asymptomatic reticulated pattern of the cutaneous blood vessels, which proceed to reticulated pigmentation called poikiloderma. Areas of poikiloderma are prone to SCC and other types of skin cancers.Cold induced skin injuries
Frostnip : The mildest cold-induced injury, characterized by localized paresthesia that resolve with rewarming. There is no permanent tissue damage. Chilblain (Pernio) : is characterized by localized inflammatory lesions that result from acute or repetitive exposure to cold above the freezing point. Lesions are edematous, red, and may be very painful or pruritic. Trench foot (immersion foot) Involves the sympathetic nerves and vasculature of the feet. It resulted from prolonged exposure of the feet to the combination of dampness and cold.Feet were red, edematous, numb or extremely painful, and often covered with hemorrhagic bullae. Frostbite : The most severe form of the localized cold-induced injuries. Frostbite results from the freezing of tissue. The tissue destruction of frostbite is due to both immediate cold-induced cell death and the more gradual development of localized inflammatory processes and tissue ischemia
Chemical agents
Contact Dermatitis:Primary irritants contact dermatitis: Irritants can produce lesions by direct contact to the skin, and this depend on the concentration of substance and the duration of exposure. [e.g. acids, alkaline, dyes, solvents].Allergic contact dermatitis:Cause cell-mediated hyper-sensitivity reaction → Dermatitis.Chemical agents
Occupational acne is caused by several different groups of industrial compounds, including coal tar derivatives, insoluble oils, and chlorinated hydrocarbons Disorder of pigment hyperpigmentation hypopigmentation Hyperpigmentation happened in exposure to heavy metals, organic nitrogen compounds and dyes.
Pathological mechanisms of hyperpigmentations: Exogenous pigment deposition Deposition in skin systemically (silver tattoos in silver worker) Photoeruptions Post inflammatory hyperpigmentation Pathological mechanisms of hypopigmentations: Post inflammatory hypopigmentation Chemical leukoderma (vetiligo)
Vetiligo
Depigmentation of skin without evidence of autoimmune disorder as in true condition.It caused by handling of P-Tri-Butyl Phenol (PTBP) which is used in car industry.stop exposure and give B-complex and steroids → get improvementBiological Agents
DiseasesInfectious Agent
Skin Manifestation
Workers Exposed
Bacterial
Anthrax
Bacillus anthracis
Ulcerated nodular lesion (malignant pustule)
workers with animal skin or hair (wool)
Furuncles
Staph. aureus
Furuncles (boils)
Military and athletes
Fungal
Candidiasis
C. albicans
Intertrigo, paronychia
Military, athletes, and agriculture workers
Dermatophyte(Ringworm)
Tinea species
T. pedis (athletes foot) and T. corporis
Viral
Herpes simplex infection
Herpes simplex-1
H. simplex inf. of fingers (herpetic whitlow)
Health-care workers
Warts
Human papillo v-7
Warts in hands(Butcher’s warts) Meat handlers
AIDS
HIV
Different skin lesions and Kaposi sarcoma
Health-care workers
Parasitic
Cutaneous Leishmaniasis
L. species
Muco-cutaneous ulcer (Baghdad or Delhi boil)
Military, farmers and tropical forest workers
Control and prevention
Pre-selection The workers should be medically examined before employment. Those with an established or suspected dermatitis or liable for skin disease should be kept away from jobs involving a skin hazard 2. Protection Protective clothing when using chemical sprays (insecticides, etc.). Long leather gloves and boots. Barrier creams which must be used regularly and correctly.3. Personal Hygiene: There should be available a plentiful supply of worm water; soap and towels. The workers should be encouraged and educated to make frequently use of these facilities. 4. There should be a periodic medical check-up of all workers for early detection and treatment of occupational dermatitis &If necessary, the affected worker may have to be transferred to a job not exposing him to irritation.
Occupational cancer
Occupational cancer is a serious problem in industry. The sites of body most commonly affected are skin, lung, bladder, and blood forming organs. The risk of exposure is considerably increased in smokers. Occupational cancers are usually reported to account for 1 - 5 % of all human cancers. Characteristics of Occupational Cancer They appear after long exposure. The period between exposure and development of the disease may be as long as 10 - 25 years. The disease may develop even after cessation of exposure.The average age incidence is earlier than that for cancer in general. The localization of the tumors is remarkably constant in any occupation. Lung cancer: Occupational lung cancer has been reported in selected workplace situations. Asbestos, nickel, arsenic, polycyclic aromatic hydrocarbons (PAHs) and radioactive substances as uranium and radon are proved to be lung carcinogens. Whereas, cadmium, beryllium ,glass fibers and ceramic fibers are suspected to be lung carcinogens Prevention is the key to future work-related lung cancers