OCCUPATIONAL HEALTH REFERENCE GUIDE · chemicals including PAH’s, and cigarette smoke is a highly plausible cause of skin irritation and cancers appearing in workers for many industrial

OCCUPATIONAL HEALTH REFERENCE GUIDE

“Patologie wat Waarde Toevoeg”

“Pathology that Adds Value”

CONTENTS


“Pathology that Adds Value”PG

OCCUPATIONAL HEALTH

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EMAIL: [email protected]

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TEL: 021 596 3587

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[email protected]

GENERAL ENQUIRIES

BIOLOGICAL MONITORING

SPECIMEN COLLECTION INSTRUCTIONS

OHS ACT EXTRACTS

FATE OF A CHEMICAL

TABLE 3 SUBSTANCES

TARGET ORGANS

PATHOLOGY SCREEN GUIDELINES

INDUSTRIAL TESTING

AGRICULTURAL TESTING

FOOD HANDLER INFORMATION

DRUG TESTING INFORMATION

ARTICLES & RESOURCES

REFERENCES & HANDY WEBSITES

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VERSION 3, MARCH 2017

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BIOLOGICAL MONITORING



Includes info on:

• Chemical Substances & Metabolites

• Biological Material• Metabolism• Sampling times• Health effects

BIO-MONITORING OHS ACT TABLE 3 TARGET ORGANS GUIDELINES INDUSTRIAL AGRICULTURAL FOODHANDLERS DRUGS ARTICLES

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CHEMICAL SUBSTANCE & METABOLITE

BIOLOGICAL MATERIAL

METABOLISM SAMPLINGTIME

HEALTH EFFECTS



BIOLOGICAL MATERIAL


HEALTH EFFECTS

ACETONEAcetone

It is a ketone, a manufactured chemical and is also found in plants, trees, volcanic gases, forest fires and is a product of body fat breakdown. It is present in vehicle exhaust, tobacco smoke and landfill sites. It is a colourless liquid with a distinct smell and taste. Evaporates easily and is highly flammable. Used as an industrial solvent in resins, lacquers, oils, fats, cotton, cellulose acetate and acetylene. Also used in the paint, lacquer, varnish, rubber, plastics, dyeing, celluloid, photographic and explosives industries and in the manufacture of artificial silk and synthetic leather.

URINE (On Ice).

BEI: 30 mg/g creatinine.

Table 2 substance.

Acetone is highly volatile and may be inhaled in large quantities when it is present in high concentrations. It may be absorbed into the blood through the lungs and diffused throughout the body. May also be absorbed through the skin.

End of shift. Typical symptoms after exposure are narcosis, slight skin irritation & a more pronounced mucous membrane irritation. Exposure to high concentrations produces a feeling of unrest, followed by collapse, stupor, periodic breathing & finally coma. Nausea & vomiting may also occur and are sometimes followed by haematemesis. Ingestion of high levels can result in unconsciousness and damage to the mouth. Skin contact causes irritation.In cases of repeated exposure to low concentrations, headache, drowsiness, vertigo, throat irritation and coughing may occur.

5


BIOLOGICAL MATERIAL


HEALTH EFFECTS


ALUMINIUMAluminium

It is the most abundant metal in the earths crust. Always found combined with oxygen, silicone or fluorine. Light-weight and silvery white in appearance. It is often alloyed with other materials e.g. Copper, manganese, nickel, etc. making it stronger and harder. Used in ship-building for internal fittings and superstructures; the electrical industry for wires and cables; building industry for house and window frames, roofs and cladding; aircraft industry for airframes and aircraft skin; automobile industry for body-work and pistons; light engineering for domestic appliances & office equipment and in the jewelry industry. Sheet aluminium is used in beverage or food containers. Aluminium compounds are used in paints, water treatment, antacids, astringents, food additives, antiperspirants, explosives and fireworks.Occupational exposure occurs in the refining of the primary metal, and in the secondary industries that use aluminium products e.g. aircraft, automotive, metal and welding. Three major steps involved in production. First, extracted with caustic soda from bauxite ore, precipitated as aluminium hydroxide, and converted to aluminium oxide in a calcination process, then the oxide is dissolved in molten cryolite and electrolyzed to yield molten metal. These cells are called pots and the work area is called the pot-room. Casting is the final step where molten aluminium is poured into ingots. Exposure is primarily to aluminium hydroxide and oxide in the initial extraction and purification process, to aluminium oxide and aluminium fluoride in the pot-room (tar-pitch volatiles including PAHs), and to partially oxidized fumes in the foundry.

URINE (On ice).

BEI: 150.0 ug/g creatinine.

Table 2 substance.

Aluminium is found naturally in the environment so you are always exposed to it when eating, drinking water, taking medicines and breathing. Very little gets absorbed into the bloodstream. Most aluminium leaves the body quickly in the faeces. The small amount that enters the bloodstream leaves in the urine. Very little is inhaled from the air and very little can be absorbed by the skin.

Other tests that can be done are Renal function tests (Urea, Electrolytes & Creatinine) and serum Aluminium.

End of workweek.

Body burden: UrinePre shift first day of the week.

High levels may result in respiratory and neurological problems e.g. coughing, abnormal chest x-rays and decreased performance in some CNS testing. Synergism among metal dusts, fine particles, toxic chemicals including PAH’s, and cigarette smoke is a highly plausible cause of skin irritation and cancers appearing in workers for many industrial processes involving aluminium. Workers chronically exposed should undergo regular urine and serum Aluminium testing to exclude any possible accumulation. Any increasing trend is most probably the result of a body burden accumulation effect that must be investigated.

6


BIOLOGICAL MATERIAL


HEALTH EFFECTS


ANILINEP-Aminophenol

It is a solvent and is a clear, slightly yellow, oily liquid with a characteristic odour. Used to make polyurethane foam, agricultural chemicals, synthetic antioxidants, dyes, perfumes, explosives, antioxidant stabilizers for the rubber industry, herbicides and varnishes.

URINE (On Ice).


Table 3 substance.

Aniline damages haemoglobin, decreasing the oxygen carrying capacity of blood. This is known as methaemoglobinaemia.

Other tests that can be done – FBC; Methaemoglobin.

End of shift. It is toxic if ingested, inhaled or by skin contact. Mild skin irritant, cyanosis (purplish blue skin colour), dizziness, headaches, irregular heart beat and convulsions. Direct contact produces skin and eye irritation. Severe poisoning results in anoxia & death. Treatment: remove all traces of Aniline from skin & all contaminated clothing. Methylene Blue treatment is justified for comatose patients with MetHb levels above 60%.

ANTIMONYAntimony

This is a silvery-white metal found in the earths crust. Antimony ores are mined and then mixed with other metals to form alloys or combined with oxygen to form antimony oxide. It does not get used alone as it breaks easily, but when mixed into alloys it is used in lead storage batteries, solder, sheet & pipe metal, bearings, castings, pewter and in the semi-conductor industry to produce diodes & infrared detectors. Also used in anti-protozoan medications (for schistosomiasis) and some veterinary preparations. Antimony oxide is added to textiles and plastics to prevent them from catching fire. Also used in paints, ceramics, fireworks and enamels.

URINE (On Ice).

BEI: 35 ug/g creatinine.

Routes of entry are by inhalation, ingestion and skin contact.

End of shift.End of workweek.At least 3 days exposure.

Inhalation of high levels causes eye and lung irritation and results in heart and lung problems, stomach pains, diarrhoea, vomiting and stomach ulcers. Ingestion of large doses causes vomiting. Can also irritate the skin after contact. Very similar to arsenic poisoning. In small doses, antimony causes headaches, dizziness, depression.

7


BIOLOGICAL MATERIAL


HEALTH EFFECTS


ARSENICArsenic

Arsenic is a naturally occurring element widely distributed in the earths crust. Arsenic is combined with oxygen, chlorine and sulphur to form inorganic arsenic compounds. Used mainly to preserve wood. Organic arsenic compounds are used as pesticides, mainly on cotton fields and orchards.Elemental arsenic is utilised in alloys in order to increase their hardness and heat resistance.

URINE.


(3 day fish free diet prior to collection.)

Table 3 substance.

Occupational exposure to inorganic arsenic compounds is through inhalation, ingestion or skin contact with subsequent absorption.

Target organ – skin.

Other tests that can be done – Liver Functions & FBC.

End of workweek.

Breathing high levels can cause a sore throat / irritated lungs. Ingesting very high levels can result in death. Exposure to lower levels cause nausea, vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, sensation of pins and needles in hands and feet. Low level exposure can cause a darkening of the skin and “warts / corns” on the palms, soles and torso. Skin contact causes redness and swelling. Can increase the risk of skin cancer and cancer in the liver, bladder and lungs. Can cause hair loss.

BENZENEPhenoltt Muconic AcidPhenylmercapturic acid (PMA)

Benzene is a solvent and an aromatic hydrocarbon. It is a colourless liquid with a sweet odour. Evaporates into the air very quickly and dissolves slightly in water. It is highly flammable. It is formed from natural processes and human activities. Used with other chemicals to make plastics, resins, nylon, rubber, lubricants, dyes, detergents and pesticides. Natural sources include volcanic emissions and forest fires. Natural part of crude oil, gasoline and cigarette smoke.

URINE (On Ice).

BEI: Phenol: 50 mg/g creatinine.

Muconic acid: 1.50 mg/g creatinine.

PMA: 45 ug/g creatinine.

BLOOD (2x 4ml EDTA tubes).

Industrial exposure: >50ng/100ml

Phenol = Table 3 substance.

Benzene is metabolized by the liver to phenol & excreted in the urine. Only about 1% of absorbed benzene is excreted unaltered in the urine.

Target organ – bone marrow.

Other tests that can be done – FBC, Liver Functions & Renal Functions.

End of shift.

End of workweek.

Breathing high levels can cause drowsiness, dizziness, rapid heart rate, headaches, tremors, confusion and unconsciousness. Ingestion of high levels in food & drink can cause vomiting, stomach irritation, dizziness, sleepiness, convulsions, rapid heart rate and death. Long-term exposure may result in bone marrow depression and causes anaemia and is associated with leukemia.Muconic Acid is a minor metabolite of Benzene but is a valuable indicator of low level exposure. Sorbic acid which is present in some foods eg. cheese, syrup, dry fruits may be partially transformed to muconic acid. PMA can be done for long-term exposure to petrol fumes.

8


BIOLOGICAL MATERIAL


HEALTH EFFECTS


BROMIDEBromideMethyl Bromide Bromomethane

This is a manufactured chemical and is a colourless gas at room temperature. Occurs naturally in small amounts in the ocean where it is probably formed by algae/kelp. Used as a fumigant to kill pests including rats and insects. Also used as a solvent to get oil out of nuts, seeds and wool and as a soil sterilant for eg. strawberry and almond crops. Also used to prepare golf-courses, particularly to control Bermuda grass.

BLOOD (SST Gel x 2).

Maximum permissible concentration: 50 mg/dl.

Table 2 substance.

Toxic exposure can occur by inhalation or skin absorption. Excretion takes place mainly through the lungs. The remainder is metabolised in the body, and inorganic bromine is excreted in the urine.

Target organs – CNS, eyes, skin, respiratory system.

Other tests that can be done – LFT, Renal functions (UE&C).

End of shift.End of workweek.

Headaches, nausea, weakness. Inhalation of large amounts may lead to a build-up of fluid in the lungs. It could cause muscle tremors, seizures, kidney damage, nerve damage and even death. Swallowing bromide may cause stomach irritation. It is a neurotoxic gas and can cause convulsions, coma, long-term neuromuscular and cognitive deficits. It easily penetrates protective clothing eg. cloth, rubber, leather. Prolonged skin contact causes chemical dermatitis and severe burns.It is an ozone depleting chemical. Methyl Bromide reacts with cysteine on haemoglobin to form an S-methylcysteine adduct which can be increased in exposed workers.

CADMIUMCadmium

It is a metal and is a natural element in the earths crust. Usually found as a mineral combined with oxygen, chlorine or sulphur. All soils & rocks including coal contain cadmium. Does not corrode easily. Used in batteries, pigments, metal coatings and plastics.

URINE.


Table 3 substance.

Cadmium binds to the plasma globulins with accumulation in the kidneys with lesser amounts in the liver.

Target organs – lungs, kidneys and bone.

Other tests that can be done – FBC, LFT and Renal (UE&C). B2 Microglobulin can be done for early detection of nephrotoxicity.

End of workweek.(Not critical).

Breathing high levels severely damages the lungs and can cause death. Also causes throat irritation, metallic taste, cough, chest tightness, chest pain, dyspnoea, chills, sweating, backache, headache and dizziness. Ingesting high levels irritates the stomach causing vomiting and diarrhoea. Long term exposure leads to a build-up in the kidneys and possible kidney disease. Other effects are loss of sense of smell, nose ulceration, shortness of breath, lung damage and fragile bones. The biological half-life of cadmium is about 10-20 years. Cigarette smoking can influence the levels.

9


BIOLOGICAL MATERIAL


HEALTH EFFECTS


CARBON DISULPHIDE2-thiothiazolidine-4-carboxylic acid (TTCA)

Used as a solvent of alkali cellulose, fats, oils, resins and waxes, as well as in the production of viscose rayon, and in the manufacture of optical glass, as a pesticide and in oil extraction.

URINE (On Ice).

BEI: 5.0 mg/g creatinine.

Table 3 substance.

Slow metabolism and excretion with main concentration build- up in the brain.

Target organs – cardiovascular, reproductive and peripheral nervous systems.

End of shift. It is primarily a neurotoxic poison. It begins with weakness, fatigue, headache, sleep disturbances and loss of appetite. Also a slowing of pupillary light reaction, blind spots and narrowing of vision, polyneuritis, motor and sensory disturbances, anorexia, gastritis, anaemia and menstrual disturbances in women.TTCA can be found in cruciferous vegetables - cabbage, cauliflower, broccoli, radish, brussel sprouts.

CARBON MONOXIDECarboxyhaemoglobin

It is found in combustion fumes e.g. produced by cars, trucks, small engines and stoves. Also produced on an industrial scale by the partial oxidation of hydrocarbon gases from natural gas or by the gasification of coal or coke. It is used as a reducing agent in metallurgy, especially for the Mond nickel recovery process, in organic syntheses and in the manufacture of metal carbonyls.

BLOOD.Heparin tube on ice for Panorama or Bloemfontein. If not in these areas, contact your local PathCare Lab to arrange. Fill the tube and do not open it.

BEI: < 8% of haemoglobin.

% Saturation of HB:Non-smokers: 0.5 - 1.5Smokers: 4 - 5 Heavy smokers: 8 - 9Toxic: > 20Lethal: > 50

Table 3 substance.

Decreases the oxygen carrying capacity of blood as the red cells pick up CO quicker than oxygen. If there is a lot of CO in the air, the body replaces oxygen with CO which then blocks oxygen from getting into the body, damaging tissues and resulting in death.

End of shift. Carbon monoxide is absorbed and eliminated unchanged via the respiratory tract. It easily crosses the alveolar capillary barrier and binds to haemoglobin to form carboxyhaemoglobin.Headaches, dizziness, weakness, nausea, vomiting, chest pain & confusion. High levels can cause unconsciousness and death. Long-term exposure causes an increase in haemoglobin and haematocrit. Also results in decreased cardiac function.

10


BIOLOGICAL MATERIAL


HEALTH EFFECTS


CHROMIUMChromium

It is a naturally occurring element (metal) found in rocks, animals, plants, soil, volcanic dust and gases. It is very resistant to wear and corrosion. Found in 3 forms – chromium 0, chromium III and chromium VI. Chromium III occurs naturally while the others are generally produced by industrial processes. It is used for chrome plating, dyes and pigments, leather tanning, wood preserving, stainless steel welding, spray painting, cement production, fuel additives and ceramics. Chromium is also necessary for the metabolism of carbohydrates and fats. In chromium deficiency a condition similar to diabetes is exhibited.

URINE.


Table 3 substance.

Chrome VI is well absorbed through the skin and poorly by the gastro-intestinal tract. Absorbed Cr VI is converted to Cr III (by erythrocytes) and is rapidly taken up by the tissues. About 80% of absorbed chromium is eliminated in the urine. Can also be absorbed through the lungs.

Target organ - lungs, skin, nasal passages.

Other tests that can be done – FBC and RBC Chromium.


Toxic effects are largely due to its highly corrosive nature and solubility. Breathing high levels can cause irritation to the nose e.g. runny nose, nose bleeds and ulcers in the nasal septum and asthma. Ingestion causes stomach upsets, ulcers, kidney and liver damage. Skin contact can cause skin ulcers, “chrome holes” - deep, round holes usually at the base of the nails, the finger-joints, skin between the fingers and the back of the hand, and allergic reactions with severe redness. Occupational carcinogen.

COAL TAR1-Hydroxypyrene

(see also Polyaromatic Hydrocarbons).

It is a brown or black liquid of high viscosity and smells of naphthalene and aromatic hydrocarbons. It is among the by-products when coal is carbonized to make coke or gasified to make coal gas. It is flammable. Used in the process of surfacing roadways. Used in medicated shampoo, soap and ointment as a treatment for dandruff, psoriasis and head lice. Also used in animal and bird repellents, insecticides, pesticides, animal dips and fungicides. Coal tar creosote used in the wood preservation industry.

URINE (On Ice).


Target organs – lungs and skin. End of shift.End of workweek.At least 3 weeks exposure.

Breathing these vapours can cause irritation of the respiratory tract, Eating large amounts of creosote causes a burning in the mouth and throat and stomach pains. Eating large amounts of herbal remedies containing creosote bush leaves may cause liver damage. Large amounts result in severe skin irritation, eye burns, convulsions, unconsciousness and even death. Long term skin exposure can cause cancer.

11


BIOLOGICAL MATERIAL


HEALTH EFFECTS


COBALTCobalt

It is a naturally occurring element found in rocks, soil, water, plants and animals. Used to produce alloys used in the manufacture of aircraft engines, magnets, grinding and cutting tools, artificial hip and knee joints. Also used to colour glass, ceramics and paints. Used as a drier for porcelain enamel and paints. Radioactive cobalt is used for sterilizing medical equipment, radiation therapy for cancer patients and irradiating food. Also part of vitamin B12.

URINE.

BEI: 2.0 - 50.0 ug/g creatinine.

Table 2 substance.

The route of absorption depends on the type of cobalt exposure. Excretion is mainly via the kidneys.

Target organs – cardiovascular, skin.

End of workweek.

Exposure to high levels can result in lung and heart effects (dyspnoea & tachycardia) & dermatitis. Also can cause disturbances in Lipid metabolism.

COPPERCopper

Copper is a metal occurring naturally in rocks, soil, water and air. It is an essential element in plants and animals. Over 75% of copper output is used in the electrical industries. Other applications include water piping, roofing material, kitchenware, chemical and pharmaceutical equipment, and the production of copper alloys. Also used in agriculture to treat plant diseases like mildew, for water treatment and as a preservative for wood, leather and fabrics.

URINE (Must not be frozen).

Proposed BEI: < 50 ug/g creatinine.

Table 2 substance.

Other tests that can be done – Liver Functions.

During shift. Chronic human toxicosis due to copper is found only in those rare individuals who have inherited a particular pair of abnormal autosomal recessive genes who develop Wilson’s disease. Breathing high levels can cause irritation to the nose and throat. Ingesting high levels can cause nausea, vomiting and diarrhoea. Very high doses can damage the liver and kidneys. Drinking water may have high levels if the pipes are made of copper and the water acidic.

12


BIOLOGICAL MATERIAL


HEALTH EFFECTS


CYANIDEThiocyanate(Chronic Exposure)

Cyanide is usually found joined to other chemicals to form compounds e.g. hydrogen cyanide (colourless gas or liquid with a faint, bitter almond odour), sodium cyanide. Some bacteria / fungi and algae can produce cyanide and it is found in some foods / plants e.g. almonds, lima beans, spinach, cassava roots.Used in electroplating, steel hardening, extraction of gold and silver from ore, fumigation of fruit trees, ships, warehouses etc. Manufacture of stainless steel. Used in photography and the making of blueprints; in the manufacture of pigments, metallurgy; organic chemical production and the manufacture of plastics.It is the main metabolite of cyanide, acrylonitrile and hypotensive agent nitroprusside.

CyanideHydrocyanic acidAcute Exposure after inhalation of cyanide gas or after cyanide ingestion. It is present in fumigants, insecticides, metal polishes, electroplating solutions, fumes from burning urea foam and cyanogenic foods.

URINE (On Ice).

Reference limits for Urine Thiocyanate:

Non-smokers: 1.5 - 12.9 mg/L.

Smokers: 1.5 - 16.5 mg/L.

Pre-exposure levels are advisable to identify smoking and dietary influences.

BLOOD (2x4ml EDTA tubes).

Reference Limits:

Asymptomatic: < 200ug/L.Toxic: 500 - 1000ug/L.Stupor: 1000 - 2500ug/L.Potentially lethal: > 2500ug/L.

Table 2 substance.

Cyanide enters the body by inhalation of vapours or dust containing cyanide compounds. Also through ingestion of food or water containing cyanide. Cyanide combines with the 2% of methaemoglobin normally present. Cyanide ions are gradually released from its link with cytochrome oxidase or methaemoglobin and converted to thiocyanate ions and excreted in urine, part of it is exhaled unchanged.

End of shift.

End of shift.

Cyanide as vitamin B12 (cyanocobalamin) is needed as part of a healthy diet to prevent anaemia. The cyanide ion of soluble cyanide compounds is rapidly absorbed from all routes of entry - respiratory and gastrointestinal tracts, as well as through unbroken skin. Cyanide inhibits cytochrome oxidase, which prevents the uptake of oxygen by the tissues, resulting in dizziness, weakness and permanent mental and motor impairment. Exposure to high levels for a short period harms the central nervous, respiratory and cardiovascular systems. Brief exposures at lower levels result in rapid, deep breathing, shortness of breath, convulsions and loss of consciousness. These short terms effects go away with time as cyanide does not stay in the body. Skin contact can cause skin irritation and ulcerations. Thyroid gland enlargement can occur. Normal blood pressure with rapid pulse is usual in mild cases. About 80% is detoxified by liver enzymes and converted to thiocyanate and excreted in the urine.Exposure to toxic levels causes a rapid onset of symptoms - flushing, headache, tachypnoea, dizziness and respiratory depression which rapidly progresses to coma and death.

13


BIOLOGICAL MATERIAL


HEALTH EFFECTS


DICHLOROMETHANEMethylene ChlorideDichloromethane

It is a colourless liquid with a mild, sweet odour. Does not occur naturally. Used as an industrial solvent for oils, fats, waxes, bitumen, cellulose acetate and esters, as a paint stripper and degreaser, sometimes mixed with petroleum naphta and tetrachloroethylene, especially for the cleaning of electric motors, also used in the manufacture of photographic film. It is an halogenated hydrocarbon.


Maximum permissible concentration :0.05 mg/100ml.

Table 1 substance.

Easily absorbed by the lung.Converted to carbon monoxide (carboxyhaemoglobin) in the blood or formic acid in the urine.

End of shift. The principal toxic action of dichloromethane is exerted on the CNS as a narcotic, or in high concentrations as an anaesthetic ranging from severe fatigue to light-headedness, drowsiness and even unconsciousness. The narcotic effects cause loss of appetite, headache, giddiness, irritability, stupor, numbness and tingling of the fingers and toes. Can become less attentive and less accurate with hand-eye co-ordination. Skin contact causes burning and redness. Prolonged exposure to lower narcotic concentrations may produce a shortness of breath, a dry non-productive cough with pain and possible pulmonary oedema. May also cause haematological disturbances e.g. reduced erythrocytes and haemoglobin levels as well as engorgement of the brain blood vessels and dilatation of the heart.

DIMETHYLFORMAMIDEn-Methyl-formamide

It is a colourless, volatile water-soluble liquid with a faint ammonia-like odour. It is an organic solvent used in acrylic fibre spinning; chemical manufacturing and pharmaceutical production. Also present in textile dyes and pigments; paint stripping solvents; printing and adhesive formulations.

URINE (On Ice).

BEI: 30mg/g creatinine.

Table 3 substance.

It is readily absorbed through the skin, inhaled or ingested.

Target organs: eyes, skin, respiratory system, liver, kidneys and cardiovascular system.

End of shift. Skin & eye irritation. Nausea, vomiting, abdominal pain, constipation, headache and dizziness. This compound is readily absorbed through the skin. Is known to be toxic to the liver, also causes skin problems and alcohol intolerance. The half-life is about 12 hours.

ETHYL BENZENEMandelic Acid

It is a colourless, flammable liquid that smells like gasoline. Found in natural products e.g. coal tar, petroleum. Also found in inks, insecticides and paint. Used primarily to make styrene. Other uses are as a solvent & raw material for production of cellulose acetate, diethyl benzene and synthetic rubber. It is a minor component of gasoline & aviation fuels.

URINE (On Ice).

BEI: 1500 mg/g creatinine.(1.5 g/g)

Table 3 substance.

Inhalation is the most important route of absorption and accumulates in the intestine, liver, kidney and fat.

70% of Ethyl Benzene is eliminated in the urine.



Respiratory, eye and mouth irritation. Symptoms are followed by narcosis, cramps & death due to respiratory centre paralysis. Breathing high levels can cause dizziness, throat and eye irritation. Kidney, blood and testicular effects. Similarly to other hydrocarbons, ethylbenzene vapours may cause central nervous system effects such as headaches, memory loss, fatigue, etc. Prolonged and repeated skin contact may cause dermatitis, reddening of skin, hair loss and chapped appearance, due to its defatting action.

14


BIOLOGICAL MATERIAL


HEALTH EFFECTS


FLUORIDEFluoride

Fluorine is a naturally occurring, pale yellow-green gas with a sharp odour and is an essential trace element. Combines with metals to make fluorides e.g. sodium fluoride, calcium fluoride and hydrogen fluoride. Used to make chemical compounds, used for etching glass. Used in mining, production of steel, chemicals, ceramics, lubricants, dyes, plastics and pesticides. Also added to drinking water and dental products.

URINE (On Ice).

BEI: 3mg/g creatinine prior to shift.

Or

10mg/g creatinine at end of shift.

Table 3 substance.

Organic fluorides are metabolized and release fluoride ions into the body. Absorbed fluorides are deposited mostly in the bone. Soluble fluoride is taken up by the blood and rapidly distributed to the whole body. The kidney is the major route of elimination.

Target organs: Kidneys, bone.

End of shift or pre-shift.

Small amounts prevent tooth cavities but high levels can be harmful, causing denser bones which can become brittle. Can be very irritating to skin, eyes and respiratory tract. Ingestion can cause severe burning and or perforation of the digestive system which may lead to death.The skin does not constitute a route of absorption except in the case of burns caused by hydrofluoric acid.

FORMALDEHYDEFormic Acid

Formaldehyde is a colourless, strong-smelling flammable gas, also known as methanol, methylene oxide, oxymethyline and methylaldehyde. Widely used to manufacture building materials, fertilizer, paper, plywood and urea-formaldehyde resins. Also used in plastic production, photographic industry, in dyeing, in the rubber, artificial silk and explosives industries. It is also a powerful antiseptic, germicide, fungicide and preservative, especially in the fish canning industry. Incomplete combustion, cigarette smoking, burning wood, kerosene and natural gas also release formaldehyde.

URINE (On Ice).

BEI: 80.0 mg/g creatinine (methanol).

The BEI cannot be adequately assessed due to too many variables.

Table 1 substance.

Formaldehyde probably combines rapidly with cellular constituents in all exposed tissues, including the mucous membranes of the respiratory tract. It is known to be oxidized to formic acid in erythrocytes and in the liver, and this metabolite is further oxidized to carbon dioxide and water. A portion of the formic acid produced by the metabolism of formaldehyde is excreted in urine.

Other tests that can be done - FBC & LFT.

End of workweek.

Formaldehyde vapour causes mild irritation of the mucous membranes of the eyes and respiratory passages at a level of 2-3 ppm, while levels of 10-20 ppm result in moderate to severe irritation after only a few minutes. Lacrimation, cough, inflammation of the bronchi, pulmonary oedema and death have resulted from exposure to very high concentrations of the chemical. Direct contact with formalin may produce dermatitis. Carcinogenic. Ingestion of food containing formic acid or its precursors is an important influencing factor. Precursors encountered in industry include methanol, halo-methanes and acetone.

15


BIOLOGICAL MATERIAL


HEALTH EFFECTS


n-HEXANE2,5 hexanedione

It’s a saturated aliphatic hydrocarbon (alkane), a colourless, volatile liquid with a slightly disagreeable odour. Highly flammable. A solvent in grease-removing fluids, glue, cements, adhesives for production of footwear, handbags, suitcases, etc. Retreading of car tyres, extraction of vegetable oils. Solvent for colours in graphic art.It is a widespread environmental pollutant.

URINE (On Ice).


Table 3 substance.

2,5 Hexanedione is the metabolite of n-hexane and is excreted in the urine. Absorbed by inhalation or through the skin.

End of shift. The effects fall into 2 classes – irritation of skin and mucous membranes and post absorption effects. Redness, oedema, vesicles, burning sensation, dizziness, vertigo, convulsions & narcosis if exposed to very high concentrations. Chronic effects manifest in the nervous system. Initial symptoms are most often a dorsal extension of the foot. Tactile and thermal hyposthenia of the legs. In serious cases of intoxication, degeneration of the visual nuclei & the tracts of hypothalamic structures were seen. The course of the disease is generally very slow. Recovery is generally complete, but a diminution of the tendon reflexes, particularly the Achilles tendon, may persist. The excretion of n-hexane metabolites significantly decreases in cases of simultaneous exposure to MEK or toluene.

ISOCYANATESToluenediamine Toluenediisocyanates

Isocyanates are highly reactive, low molecular weight chemicals. Widely used in the manufacture of flexible and rigid foams, fibres, coatings, paints, varnishes, elastomers, and are increasingly used in the automobile industry, autobody repair, and building insulation materials. Spray-on polyurethane products containing isocyanates have been developed for a wide range of retail, commercial, and industrial uses to protect cement, wood, fibre-glass, steel and aluminium, including protective coatings for truck beds, trailers, boats, foundations and decks. The most widely used compounds are di-isocyanates, which contain two isocyanate groups and poly-isocyanates. The most commonly used di-isocyanates include methylene diphenyl di-isocyanate (MDI), toluene di-isocyanate (TDI) and hexamethylene di-isocyanate (HDI).

URINE (On Ice).

BEI: not available.

Not industrial exposed: < 3.6 ug/g creatinine.

Table 1 substance.

If isocyanate asthma is suspected then specific Rast tests can be done - Rast TDI K75, Rast MDI K76 and Rast HDI K77.

End of shift. Isocyanates are powerful irritants to the mucous membranes of the eyes, gastrointestinal and respiratory tracts. Direct skin contact can also cause marked inflammation. Isocyanates can also sensitize workers, making them subject to severe asthma attacks if they are exposed again. Death from severe asthma in sensitized subjects has been reported. Workers exposed to isocyanates can experience persistent or recurring eye irritation, nasal congestion, dry or sore throat, cold-like symptoms, cough, shortness of breath, wheezing or chest tightness. Preventing exposure is a critical step. Engineering controls e.g. closed systems and ventilation should be the principal method for minimizing exposure. Worker isolation, personal protective clothing and equipment may also be necessary. Early recognition of sensitization and prompt elimination of exposures is essential to reduce the risk of long-term or permanent respiratory problems for workers.

16


BIOLOGICAL MATERIAL


HEALTH EFFECTS


ISOFLURANEENFLURANEMETHOXYFLURANEFluoride

Clear, colourless, mobile liquid with a characteristic pungent odour. Soluble in water. Heavier than air and may accumulate in lowered spaces causing a deficiency of oxygen. They are fluorinated, chlorinated, halogenated hydrocarbon group of volatile anaesthetic ethers. Intended for vaporization and administration by inhalation. At low concentrations the inhaled vapour is used to provide analgesia in conscious patients or in patients undergoing anaesthesia. Produce flouride ions.

URINE (On Ice). Table 2 substance although Fluoride is a Table 3 substance.

As much as 50-70% of the absorbed dose is metabolized by the liver to free fluoride, oxalic acid, diflouromethoxyacetic acid and dichloroacetic acid. Diffuses into fatty tissues and is released slowly from this reservoir. 20% of methoxyflurane is recovered from exhaled air while urinary excretion of organic fluorine, fluoride and oxalic acid accounts for +-30%. Used with caution in patients with renal disease.

Routes of exposure are inhalation and ingestion.

Target Organs: eyes, skin, respiratory system, kidneys and CNS.

End of shift.End of workweek.Minimum of 5 days exposure.

Inhalation causes cough, sore throat, dizziness, weakness, drowsiness, headache, irritation of eyes, skin and respiratory tract, abdominal pain, nausea, vomiting and convulsions.Reduces pain sensitivity and relaxes muscles. Affects kidneys and liver. Nephrotoxic. Can cause retrograde amnesia.

ISOPROPANOLIsopropyl alcoholAcetone

It is found in a variety of solvent and cleaning products, often in combination with methanol, ethylene glycol or ethanol.

URINE (On Ice).


This is rapidly absorbed and distributed throughout the body after inhalation or ingestion. The main metabolite is acetone.

End of shift. See Acetone.

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BIOLOGICAL MATERIAL


HEALTH EFFECTS


LEADSolid lead (Inorganic)

Lead is a naturally occurring bluish-gray metal found in small amounts in the earth’s crust. Can be found in all parts of our environment. Most of it comes from human activities including burning fossil fuels, mining, and manufacturing. Used in production of lead paints, batteries, pigments, ammunition, metal products (solder and pipes), lead smelting and refining, shipbuilding, ceramics and glass industry, X-ray shields, making motor vehicle bodies, repairing vehicle bodies containing lead, small bore rifle shooting, printing. Because of health concerns, lead in gasoline, paints and ceramic products, caulking, and pipe solder has been dramatically reduced in recent years. Lead does not break down but the compounds are changed by sunlight, air and water.

Lead alkyls(Organic / fumes)

Tetra-alkyl lead and tetra-methyl lead are liquid compounds of lead, which are miscible in all proportions with gasoline (and other organic solvents), and are used as “antiknock” ingredients in gasoline as fuel for the internal combustion engine. Found at oil refineries, oil transport terminals and tanker repairs. Filling petrol-driven vehicles at service stations.

BLOOD (Trace element K2 EDTA tube - royal blue top).

Blood Lead: Female : (capable of procreation) < 35 ug/dl.Male: < 40 ug/dl.

Repeat at these intervals:< 20 ug/dl - 12 mths.20-39 ug/dl - 6 mths.40-59 ug/dl - 3 mths.> 60 ug/dl - at the discretion of the designated OH Officer.

Toxic Levels:>60 ug/dl - Since 30/06/2005.

Females who are capable of procreation should have blood lead measurements carried out at 3 monthly intervals.

URINEUrinary lead: Female (capable of procreation): <65.0 ug/l.Male: <130.0ug/l.

Repeat at these intervals:<120 ug/l - 6 weeks.120-149 ug/l - 1 week.>150 ug/l - at the discretion of the designated OH Officer.

Occ. Health & Safety Act 1993.Lead Regulations 2001. (Government Gazette Vol 440 no 23175 28/2/02 no 7292).

Lead can be breathed in when dust, fumes or vapour containing lead are in the air and inhaled. Also ingested from contaminated clothing, hands, beard, contaminated food or beverages. Can also be absorbed through the skin. Target organs are the eyes, GI tract, CNS, kidneys and brain. A certain amount may be absorbed in the air passages, but the main portion is taken up by the pulmonary bloodstream. More than 90% of the lead in the blood will be held by the erythrocytes. Excretion takes place both in urine and faeces. Lead in faeces is derived mainly from non-absorbed lead; lead in urine is therefore a much better measure of absorption.Half life of lead in blood = 25 days, in soft tissue = 40 days, bone = 25 years.

Other tests that can be done – Haemoglobin, FBC & ESR; Renal Functions; LFT.

During shift.

(Baseline blood lead and Hb levels done within 14 days of comencing emploment Repeated after 3 months and 6 months).

During shift.

(Done 6 months after employment commences).

Symptoms of poisoning are abdominal pain, constipation, vomiting, tiredness, nerve tingling, arthralgia, loss of weight. Severe symptoms include anaemia, forgetfulness, decreased performance, irritability, headache, kidney damage, sterility, miscarriages, damage to the foetus, colic, peripheral nerve damage e.g. wrist drop, raised BP. Unborn children can be exposed through their mothers. Harmful effects include premature births, smaller babies, decreased mental ability, learning difficulties and reduced growth. In men this can damage the organs responsible for sperm production. Organic lead intoxication symptoms are: Mild - insomnia, lassitude, nervous excitation, lurid dreams, tremor, spasmodic muscular contractions, bradycardia, hypothermia. Severe – complete disorientation, hallucinations, facial contortions, seizures, coma, death. Low Hb levels can confirm a chronic excess lead exposure if other causes for a decreased Hb have been excluded.

18


BIOLOGICAL MATERIAL


HEALTH EFFECTS


MANGANESEManganese

It is one of the most abundant elements in the earth’s crust and is found in soil, rocks, water & biological materials. It is an essential trace element and is necessary for good health. Found in several food items e.g. grains, cereals, tea. Also found in pesticides; fungicides and fertilizers. Main uses are – in the production of steel; as an alloying agent for special steels, aluminium and copper; in the manufacture of dry cell batteries; welding rods; glass manufacturing; colouring agent in bricks and pottery; manufacture of fireworks and matches; for the production of manganese chemicals e.g. potassium permanganate.

URINE (On ice).

BEI: < 10.0 ug/L.

BLOOD(Trace element K2 EDTA tube - Royal blue top).

BEI: 6.1 - 23.0 ug/L.

BAT: 20 ug/L.

Table 2 substance.

In occupational exposure absorbed mainly by inhalation. May also enter the GIT with contaminated food and water. After absorption it is rapidly eliminated from the blood & metabolized mainly by the liver and excreted in the bile. It preferentially accumulates in mitochondrial rich tissue & also penetrates the blood-brain barrier & the placenta. The elimination half-life is 40 days.

Other tests that can be done – Iron, FBC, Liver functions.

End of shift. Asthenia; anorexia; headache; vertigo; somnolence; indifference; apathy; emotional & behavioural disorders; cramps; back pain. Speech becomes slow & irregular. Increased tonus of facial muscles. Gestures are slow and awkward. Inability to run and walk backwards. Muscular rigidity with a slow spasmodic unsteady gait. Tremors. Sometimes also vasomotor disorders with sudden sweating; pallor or blushing. Iron deficiency anaemia increases the uptake of manganese. A urine manganese exceeding 10 ug/L should be followed up by a blood manganese analysis. Any worker with a blood manganese level >6.1 ug/L must be monitored on a regular basis. Any increasing trend must be investigated and mediated before any irreversible neurotoxic damage ensues.

19


BIOLOGICAL MATERIAL


HEALTH EFFECTS


MERCURYMercury

Mercury is a non-essential, volatile liquid metal that occurs naturally in the environment in several forms. It is mined as mercuric sulfide. The metal form is a shiny silver-white liquid. Combined with other elements e.g. chlorine, sulphur or oxygen, inorganic mercury compounds or “salts” are formed. These are mostly white powders or crystals. In a chemical bond with carbon, organo-mercurial compounds are formed e.g. methyl mercury. The mercury portions of these do not break down but the form of mercury can change. Metallic mercury is used in thermometers; dental fillings; batteries; laboratory apparatus; instrumentation e.g. vacuum pumps; production of chlorine gas and caustic soda. Also used to extract gold from ore. Inorganic salts of mercury are used as topical disinfectant agents; medicinal products; pigments in paint; fungicides.Organic / Methyl mercury is found in fish and sea mammals.

Inorganic Mercury : URINE.


Methyl Mercury:BLOOD.

(Trace element K2 EDTA tube - Royal blue top).

BEI: 2.0 ug/100 ml.

(Recommendation - urine mercury levels repeated 3 monthly in cases of exposure.)

Blood mercury levels done for organic phase and acute exposure.

Table 3 substance.

Organic mercury is rapidly distributed by blood & is mainly carried by the red blood cells. It accumulates in the liver & kidneys & is decomposed into inorganic mercury. Methyl mercury is concentrated in the CNS especially the grey matter and is excreted in the bile, breast milk and hair strands. A large part is re-absorbed in the intestines. Excretion is slow – 1% of body burden excreted daily – biological half-life of 70 days. Inorganic mercury exists for a short time in metallic form and is rapidly oxidized to mercury ions which fix to proteins. Excreted mainly through the colon and kidneys. Biological half-life is about 60 days.

Other tests that can be done – LFT; FBC; Renal Functions; Urinalysis.

Inorganic Mercury: Prior to shift.

Organic /Methyl Mercury:End of shift. End of workweek.

Exposure occurs when working or living near industries using or producing mercury; living near hazardous waste sites, municipal incinerators, sewage treatment plants; suckling infants; tobacco smoking; eating contaminated fish or shellfish; eating grain treated with mercury compounds; eating food grown in contaminated soil (plants take up inorganic mercury); drinking contaminated water and absorbing vapours from dental fillings.

Acute poisoning - pulmonary irritation; renal insufficiency; digestive disorders with a metallic taste in the mouth; ulcers of buccal mucosa; vomiting; diarrhoea; proteinuria; allergic contact dermatitis and skin irritations. Chronic poisoning – main target organ is the CNS. Renal tubular damage with proteinuria or nephrotic syndrome. A characteristic tremor occurs beginning in the fingers, eyelids, lips or tongue. Severe gingivitis where teeth may fall out. Irritability, staccato speech, insomnia, quick temper, depression, constrictions of visual fields, hearing impairment. Chronic seizures may occur. Severe behavioural and personality changes. Memory loss, increased excitability, delirium and hallucinations may also occur.

METHAEMOGLOBINMethaemoglobin

This is a form of the oxygen-carrying protein haemoglobin which is unable to carry oxygen. It is bluish chocolate-brown in colour.

BLOODHeparin tube on ice. Done at Panorama. If not in this area, contact your local PathCare Lab to arrange.Must reach the lab within 4 hours.

Reference Limits:0.4 – 1.5 %.

Table 3 substance.

Other tests that can be done – arterial blood gases.

During shift.

Or

End of shift.

Methaemoglobinaemia arises from the excessive conversion of haemoglobin to methaemoglobin. This occurs when Hb is oxidized at a rate exceeding the normal enzymatic capacity. Numerous agents responsible for this e.g. aniline, benzocaine, nitrates, nitrophenol, primaquine. Can also be due to a congenital enzyme deficiency. Characterised by cyanosis in the absence of cardiac or pulmonary disease. Symptoms related to impaired oxygen delivery include headache, weakness, tachycardia, breathlessness. Concentrations > 50% result in severe hypoxaemia and CNS depression. Treated with oxygen, methylene blue and in severe non-responding cases – exchange transfusion / hyperbaric oxygenation.

20


BIOLOGICAL MATERIAL


HEALTH EFFECTS


METHANOLFormic Acid(occupational exposure)Methanol(poisoning by ingestion)

It is a colourless, flammable liquid soluble in water. Methyl alcohol is the starting material in the manufacture of many chemical products. 40% used for the production of formaldehyde which is then used to make phenolic, urea, melamine and acetal resins. It is a solvent for inks, dyes, resins and adhesives. It is used in the manufacture of photographic film, plastics, textile soaps, wood stains, coated fabrics, shatterproof glass & waterproofing formulations. Ingredient of paint & varnish removers, dewaxing preparations, embalming fluids & anti-freeze mixtures.It is an aliphatic alcohol, a non drinking type of alcohol.

Methanol Exposure – Formic acid:URINE (On Ice).

BEI : 80mg/g creatinine.

Methanol Poisoning:BLOOD (2 x Grey top tubes on ice).

Normal: < 0.05 mmol/L.Toxic: > 6.24 mmol/L.

Table 3 substance.

Absorbed by all routes (inhalation, ingestion, dermal) and metabolized to formic acid. The formic acid elimination rate is reduced by the ingestion of ethanolic beverages.

Before shift at End of workweek.

End of workweek.

Severe poisoning following ingestion causes blindness as a result of optic nerve degeneration and retinal changes. Breathing and cardiovascular functions depressed. Exposure to methyl alcohol vapours causes irritation of mucous membranes; headache; ringing ears; vertigo; insomnia; dilated pupils; clouded vision; nausea; vomiting; colic. May also cause skin injuries due to irritant / solvent action.

Blood Methanol concentrations in excess of 14mmol/L are an indication for haemodialysis as is deepening of acidosis.Methanol is a natural constituent of blood, urine and expired air. It is probably formed by the activites of intestinal microflora or by other enzymatic processes. Also exposed through alcoholic beverages, fruit juices or the use of aspartame as an artificial sweetener. Degradation of natural pectin in the colon also forms methanol.

METHYL CHLOROFORM1,1,1 TRICHLOROETHANETrichloroacetic Acid (TCA)TrichloroethanolTrichloromethane

It is a synthetic chemical, a chlorinated hydrocarbon and has a chloroform-like odour. It is a colourless, volatile liquid. Used principally for cold-cleaning, dip-cleaning and bucket-cleaning of metal for the removal of grease, oil and wax. Also for dry cleaning, in the textile industry, printing inks, correction fluid, household products e.g. spot cleaners, glues and aerosols.

URINE (On Ice).

BEI: TCA 7 mg/g creatinine.


Normal range: 0.0ug/100ml.

Table 3 substance.

Rapidly absorbed through the lungs and GIT. Mainly eliminated unchanged with the expired air and to a limited extent in urine as trichloroethanol and trichloroacetic acid.


First clinical manifestation of over-exposure is a functional depression of the CNS starting with dizziness, in-coordination, impaired Romburg test, anaesthesia and respiratory arrest. Can cause conjunctivitis. Prolonged skin contact causes transient erythema and irritation. It lasts in the air for +- 6 years and affects the ozone layer. Possible carcinogen.

21


BIOLOGICAL MATERIAL


HEALTH EFFECTS


METHYL-ETHYL-KETONEMEK(2-butanone)

Ketones are produced in industry by catalytic dehydrogenation or oxidation of secondary alcohols; usually obtained by hydration of olefins in the petrochemical industry. Produced mainly for use as solvents in the production of plastics, artificial silk, explosives, cosmetics, perfumes, pharmaceuticals, dyes, resins, gums, tars, waxes and fats. For the extraction of lubricating oils. Also used in the manufacture of acrylic and vinyl surface coatings. Ketones are flammable, volatile, colourless and soluble in water.

URINE (On Ice).


(New reference range with effect from 01/07/08).

Table 3 substance.

Absorbed by all routes but inhalation is the primary route for occupational exposure. Usually rapidly excreted in the urine & expired air.

Other tests that can be done – LFT; Renal Functions.

End of shift. Ketones possess narcotic properties when inhaled in high concentrations. At lower concentrations they can provoke nausea and vomiting, irritating to the eyes and respiratory system. Also skin irritant causing dermatitis . Can cause peripheral neuropathy.

METHYL-ISO-BUTYL-KETONEMIBK

It is a colourless liquid with a mild, pleasant odour. Used mainly as a solvent for protective coatings, lacquers and varnishes. Also a raw material for producing anti-oxidants. Used in the production of paints and pesticides.

URINE (On Ice).


Table 3 substance.

Main route is inhalation. A small amount is excreted unchanged by the kidneys. Absorbed MIBK is basically eliminated from the system within 90 minutes.

End of shift. Inhalation causes irritation of the eyes and nose. High concentrations cause anaesthesia and CNS depression. Skin dries out with contact and may result in dermatitis.

METHYL-N-BUTYLKETONE2,5 Hexanedione(2-hexanone)

This ketone is manufactured from acetic acid and ethylene reacting under the influence of a catalyst and pressure. Mainly used in the lacquer industry. One of the metabolites is 2,5 hexanedione. See above under n-Hexane.

URINE (On Ice).

BEI: 5.0mg/g creatinine.

See above under n-Hexane. End of workweek.

See above under n-Hexane.Causes peripheral neuropathy.

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BIOLOGICAL MATERIAL


HEALTH EFFECTS


NICKELNickel

Nickel is a very abundant natural element. Pure nickel is a hard, silvery-white metal. Combined with other metals e.g. iron, copper, chromium and zinc to form alloys. Most nickel used to make stainless steel. Also used in electro-plating; in the manufacture of acid-resisting and magnetic alloys and magnetic tapes; in casting operations for machine parts; as a catalyst in the hydrogenation of fats and oils; in synthesis of acrylic esters, in coinage; in Ni-Cd batteries; in paint pigment; in ceramics and glass.

URINE.

NO BEI.

Non-occupational exposure:< 2ug/g creatinine.

Any value greater than 3 times this value should be repeated as soon as possible.

Soluble Nickel:Proposed BEI: 30ug/g creatinine.

Table 1 substance.

In occupational exposure inhalation is the main route of absorption. The absorption rate is greatly dependent on the solubility of the compound. Sparingly soluble compounds are highly retained in the lungs and lymph nodes.

Other tests that can be done – lung function tests, sputum cytology, whole blood nickel.

End of shift. Most common harmful health effect is an allergic reaction – a skin rash at the site of contact. Can cause asthma. Can also cause headache, vertigo, nausea, vomiting, rhinitis, sinusitis, chronic bronchitis and reduced lung function. Ingestion causes stomach ache. Carcinogenic.

Nickel rich foods eg. chocolate, nuts, beans, porridge oats.

The concentrations of nickel in plasma and urine are good indicators of recent exposure to metallic nickel & its soluble compounds. It is not a cumulative toxin with almost all being excreted in the urine.

23


BIOLOGICAL MATERIAL


HEALTH EFFECTS


ORGANOPHOSPHATESRBC Cholinesterase = acetyl cholinesteraseSerum Cholinesterase = pseudo cholinesterase

Organophosphorus compounds are widely used in agriculture as pesticides for the control of insect pests (insecticides), acarids, nematodes, plant diseases (fungicides), weeds (herbicides). Used to control pests on fruit trees, vegetable crops, ornamental plants, cotton and cereal crops, tree nurseries and to destroy flies, gnats, parasites on domestic animals.

RBC: (4ml EDTA tube).Keep cool. Do not centrifuge the specimen. Tested within 5 days.

This test is done to establish the individual’s baseline before spraying commences.

Reference range:• 6021-9165 IU/L.

If 15-25% below baseline:• Repeat test.

If 25-30% below baseline:• Repeat test.• Re-evaluate safety

precautions.

If 30% or more:• Remove from

exposure & investigate safety conditions.

SERUM: (SST Gel tube).

This test is done to establish acute exposure during spraying. Should this result be lower than the baseline, it is an indication of cholinesterase inhibition.

Reference range: 4.62 - 11.50 kU/L.

Table 3 substance.

Organophosphates are rapidly absorbed through the mucous membranes of the digestive tract, the respiratory system and the skin, and are conveyed by the blood to various body tissues. Certain compounds are active cholinesterase inhibitors, others are transformed into such inhibitors after absorption in tissues, mainly in the liver by oxidation.

Target organ: CNS.

Other tests that can be done – FBC, Hb.

RBC:Baseline: Before spraying ie no exposure for 30 days. Follow up after 30 days of exposure.

SERUM:During spraying + symptoms of acute poisoning.

Workers involved in the manufacture, formulation, preparation, packaging, transport, storage, mixing and application will have the highest exposure.

Acute exposure: sweating, constricted pupils, lacrimation, excessive salivation, wheezing, cramps, vomiting, diarrhoea, tenesmus, bradycardia, fall in blood pressure, blurred vision, urinary retention, weakness, cyanosis, elevated blood pressure, anxiety, restlessness, ataxia, convulsions, insomnia, coma, Cheyne-Stokes respirations, respiratory and circulatory depression

Chronic exposure: headaches, weakness, feeling of heaviness in the head, decline of memory, quick onset of fatigue, disturbed sleep, loss of appetite, disorientation, trembling, neuritis, paresis, increased secretion of saliva, sweet, tears and mucus.

RBC: Causes of decreased levels: Carbamates, organophosphates, megaloblastic anaemia, myasthenia gravis on treatment.Causes of increased levels: sickle cell anaemia.

Serum: Causes of decreased levels: Organophosphates,; carbamates; steroids; contraceptives; lithium; hepatitis; cirrhosis; CCF; MI; PE; chronic renal disease; late pregnancy and malnutrition.Causes of increased levels: Hyperthyroidism; DM; pernicious anaemia; alcoholism; nephrotic syndrome and haemolysis.

24


BIOLOGICAL MATERIAL


HEALTH EFFECTS


PARAQUATParaquat

Most common quick acting non-selective herbicide which destroys green plant tissue. Does not harm bark. Used for weed control in fruit orchards, plantation crops e.g. coffee, cocoa, coconut, rubber, bananas and forestry. Used as a desiccant for e.g. pineapples. Applied after harvest to accelerate the drying out process and enabling plants to be burnt after 3-5 weeks compared to 13 weeks after cutting and natural drying. Very toxic.

URINE (On Ice). Table 2 substance.

Occupational exposure through skin.

Target organs – lungs.

End of workweek.

Causes pulmonary oedema and other lung damage leading to fibrosis. Affects skin, eyes, nose and finger nails.

PARATHIONRBC Cholinesterase

Parathion is the leading product of a group of insecticides – organophosphorus pesticides. Identified by the ability to inhibit the action of cholinesterase enzymes. It is highly toxic and is sold only to professional agriculturalists and farmers. See above under Organophosphates.

BLOOD (4ml EDTA tube). Table 3 substance.

Enters the body by any route – ingestion, inhalation and easily absorbed by the skin.See above under Organophosphates.

See above under Organo-phosphates.

Affects the CNS by inhibiting cholinesterase enzymes which causes excessive, continuous stimulation of those muscles and glands which are activated by acethylcholine. Symptoms include headaches, fatigue, giddiness, nausea, sweating, blurred vision, tightness in chest, abdominal cramps, vomiting and diarrhoea. In advanced poisoning – difficulty in breathing, tremors, convulsions, collapse, coma, pulmonary oedema and respiratory failure can occur.

PENTACHLOROPHENOLPentachlorophenol (PCP)

It is a manufactured chemical which is a restricted use pesticide (fungicide) and used as a wood preservative for utility poles, railroads and wharf pilings.

URINE (On Ice).


Table 3 substance.

Main routes of exposure are the respiratory tract and the skin and excreted in the urine.

Pre shift at end of workweek.

Exposure to high levels cause body cells to produce excess heat, causing high fever, profuse sweating and difficulty breathing. High temperature can cause injury to various organs and tissues. Liver effects and damage to the immune system. Possibly carcinogenic.

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BIOLOGICAL MATERIAL


HEALTH EFFECTS


PERCHLOROETHYLENETrichloroacetic AcidTetrachloroethylene

It is a manufactured chemical and is a non-flammable, high boiling solvent for oils, fats, waxes, gums, resins, bitumen pitch, halogens, dyes, rubber and others. It evaporates easily and has a sharp sweet odour. Used as a dry-cleaning agent. It is a halogenated hydrocarbon. See also Trichloroethylene.

URINE (On Ice).


Table 3 substance.

Inhalation is the main route. Stored in the body fat and slowly released into the bloodstream.Pulmonary uptake increases with the duration of exposure.


End of workweek.

High concentrations can cause dizziness, headache, sleepiness, confusion, nausea, difficulty in speaking and walking, unconsciousness and death. Skin irritation may result from repeated / extended skin contact. Potential carcinogen.

PHENOLPhenol

It is a manufactured chemical and a natural substance. It has a distinct odour that is sickeningly sweet and tarry. Used in the production or manufacture of asbestos goods, bakelite, drugs e.g. antiseptic lotions and throat lozenges, explosives, fertilizers, illuminating gas, paints, paint removers, perfumes, rubber, textiles, wood preservatives, synthetic resins. It finds extensive use in the petroleum, paper, leather, soap, toy, tanning, dye and agricultural industries. It is a major metabolite of benzene.

URINE (On Ice).

BEI:250 mg/g creatinine.

Table 3 substance.

Readily absorbed through the skin and inhalation. Phenol vapours readily absorbed into the pulmonary circulation. It is rapidly excreted in the urine within 48 hours of exposure in the form of conjugates with glucuronide and sulphate.

Target organs – eyes, skin, respiratory system, blood, CNS, bone marrow.

Other tests that can be done – LFT, Renal Functions and FBC.

End of shift. Short term exposure can cause respiratory irritation, headaches, burning eyes, dizziness, nausea, cyanosis, bone marrow depression. Skin exposure to high amounts causes skin burns, liver damage, dark urine, irregular heartbeat. Ingestion causes internal burns. Establish a baseline phenol prior to exposure. Exposure to other chemicals can affect Benzene metabolism.

26


BIOLOGICAL MATERIAL


HEALTH EFFECTS


PLATINUMPlatinum

Malleable silvery white metal found in the earths crust. Has exceptional catalytic properties and is used in the chemical and petroleum industries. Used as a catalyst in fuel cells for generation of electricity. Has a high melting point and is resistant to corrosion. Used for laboratory equipment and to protect ship hulls and propellers. Also used in glassmaking, production of fibreglass and jewellery. Used for dental and neurological prostheses and electrodes. Platinum drugs appear to be active against a wide range of tumours in animals and in man.

URINE (On ice).

Reference Range: <4.0 ug/g creatinine.

Table 2 substance.

Main route of absorption is through inhalation.

End of shift. Causes eye irritation, sneezing, runny nose, cough, wheeze, itching and contact dermatitis. Can develop asthmatic symptoms with tightness of chest and shortness of breath.

POLYAROMATIC HYDROCARBONS (PAH)1-Hydroxypyrene

This is a group of over 100 different chemicals formed during the incomplete burning of coal, oil and gas, garbage or other organic substances e.g. tobacco, charbroiled meat. Some are manufactured and are colourless, white or pale yellow-green solids. Found in coal tar, crude oil, creosote and roofing tar. Some used in medicines, to make dyes, plastics and pesticides. Used for paving roads (bitumen). Also used to waterproof boats. Thin bitumen plates used in computers and dishwashers for sound insulation. Found in high concentrations in coke ovens; aluminium reduction plants, steel industry and creosote impregnating plants.

URINE (On Ice).


Inhalation of contaminated air e.g. wild fires or eating grilled foods. Absorption by inhalation and small quantities through skin. Oxidized and converted into water soluble compounds and eliminated in the urine.

End of shift.End of workweek.At least 3 weeks exposure.

Acute exposure causes nausea, metallic taste in mouth, eye irritation and giddiness. Repeated exposure causes decreased BP, raised pulse, anxiety and tremors. Also a skin irritant. Carcinogen. Exposure to PAH through diet can influence the urine PAH creatinine ratio.

27


BIOLOGICAL MATERIAL


HEALTH EFFECTS


POLYCHLORINATED BIPHENYLPolychlorinated Biphenyl

PCB’s are mixtures of up to 209 chlorinated compounds. No known natural sources. Either oily liquids or solids that are colourless to light yellow. Some can exist as a vapour. No known smell or taste. Used as coolants and lubricants in transformers, capacitors and other electrical equipment as they don’t burn easily and are good insulators. Also as plasticisers for plastic materials, adhesives for waterproof wall coatings, carbonless copy paper, impregnated citrus fruit wrapping paper, fire retardant. Found in old fluorescent lighting fixtures, hydraulic oils, old tv’s and fridges. Do not readily breakdown so may remain in environment for a long time. PCB’s enter air, water and soil during manufacture, use and disposal, from accidental spills and leaks during transport, from hazardous waste sites, leaks from old transformers. Can travel long distances in the air. Taken up by marine organisms.

BLOOD (2 x 4ml EDTA tubes).

BEI: not available.

Not industrial exposed:1.8 - 3.8 ug/L.

Table 2 substance.

Absorbed through inhalation, skin absorption, ingestion, eye contact. In industry skin absorption the most important route. Highly lipophilic and distributes mainly to fat. Can be found in breast milk.

Target organs – skin, eyes, liver, reproductive system.

Other tests that can be done – LFT, Lipogram.

During exposure.

Skin & mucous membrane changes, swelling of the eyelids, burning of the eye, excessive eye discharge, burning sensation and oedema of face and hands, simple erythematous eruptions with pruritis, acute eczematous contact dermatitis, hyperpigmentation of skin and mucous membranes, discolouration of finger nails and thickening of the skin. Irritation of the upper respiratory tract frequently seen. Digestive symptoms such as abdominal pain, anorexia, nausea, vomiting, jaundice. Can cause liver damage and reproductive impairment. Potential carcinogen.

STYRENEMandelic acid & Phenylglyoxylic acid

Is a synthetic chemical, a colourless liquid that evaporates easily and has a sweet smell. Used to make rubber, plastic insulation, fibreglass, pipes, auto parts, food containers and carpet backing. Most of these contain styrene linked together in a long chain called polystyrene. Low levels of styrene also found in fruits, vegetables, nuts, beverages and meats. Styrene vapours from building materials, cigarette smoke, photocopy machines, auto exhaust and hazardous waste sites.

URINE (On Ice).

BEI: Mandelic acid:Pre - 300mg/g creatinine.Post - 800mg/g creatinine.

BEI: Phenylglyoxylic acid:Pre - 100mg/g creatinine.Post - 240mg/g creatinine.

Table 3 substance.

Absorbed through the lungs and skin. Rapidly metabolised to mandelic acid & to a lesser extent phenylglyoxylic acid & excreted in the urine.

End of shift.

Or

Pre-shift + End of shift.

Inhalation of high levels can cause CNS effects e.g. changes in colour vision, tiredness, feeling drunk, slowed reaction time, concentration problems, and balance problems. Also causes acute mucous membrane irritation of the eyes, nose and throat. Skin contact can burn and cause fissured dermatitis. Haematological changes (esp. leucopenia & lymphocytosis) can occur. Ovulation & menstruation disorders have been observed. Possible carcinogen. Mandelic acid & Phenylglyoxylic acid are not detected in the urine of non-exposed individuals.

28


BIOLOGICAL MATERIAL


HEALTH EFFECTS


TETRACHLOROETHYLENETetrachloroethyleneTrichloroacetic acid

See above under Perchloroethylene. It is a halogenated hydrocarbon.

URINE (On Ice).



Normal range: <2ug/100ml.

See above under Perchloroethylene.

End of workweek.

See above under Perchloroethylene and Tricholoroethylene.

TOLUENEHippuric Acid & Ortho-cresol

It is a clear, colourless liquid with a distinctive smell. Flammable. Occurs naturally in crude oil and in the tolu tree. Produced in the process of making gasoline and other fuels from crude oil and making coke from coal. Used to make paints, thinners, nail polish, lacquers, adhesives, rubber and in some printing and leather tanning processes. Solvent for oils, resins, rubber, coal, tar, asphalt, pitch, cellulose paints & varnishes. Also used in cleaning products, handy crafts, dyes and benzene manufacture.

URINE (On Ice).

BEI : Hippuric Acid:2.5 g/g creatinine.

BEI: O-cresol: 1.0 mg/g creatinine.


BEI: End of shift: 10.0mg / 100ml.

Prior to last shift of week:0.5mg / 100ml.

Table 3 substance.

Absorbed mainly through inhalation and to a lesser extent the skin. Spreads through the different tissues in different amounts depending upon their perfusion & solubility characteristics. Then oxidised to its lateral chain in the liver microsomes. 68% of toluene is excreted in the urine via the kidneys as hippuric acid & small amounts as o-cresol. Obese subjects retain more toluene than thin persons. The same liver enzyme system oxidizes toluene, styrene and benzene. These substances tend to inhibit each other. Hippuric acid also found in fruit and vegetables as benzoic acid.

Other tests that can be done – FBC, LFT, Renal Functions.

End of shift. Irritation of the mucous membranes of the eyes, nose and throat, euphoria, headaches, vertigo, nausea, loss of appetite, alcohol intolerance, tiredness, weakness and memory loss. Skin contact can cause irritation and a feeling of ‘pins and needles’. These symptoms appear at the end of the day, and are more severe at the end of the week, and become less or disappear during the weekend or on holiday. High levels can affect the kidneys.

Blood toluene levels can increase after large doses of alcohol.

29


BIOLOGICAL MATERIAL


HEALTH EFFECTS


TRICHLOROETHYLENE (TCE)Trichloro-Compounds, Trichloroacetic Acid & Trichloroethanol

It is a non-flammable colourless liquid with a sweet odour and a sweet burning taste. Used mainly as a solvent to remove grease from metal parts. Also an ingredient in adhesives, paint removers, correction fluids and spot removers.

URINE (On Ice).

BEI: Trichloro-compounds:300 mg/g creatinine.

BEI: Trichloroacetic acid:100 mg/g creatinine.

BEI: Trichloroethanol;150 mg/g creatinine.


BEI: 500 ug/100 ml.

Table 3 substance.

Inhalation is the main route of absorption. The majority of the absorbed trichloroethylene is metabolised mainly into trichloroacetic acid & trichloroethanol, which are eliminated in the urine. The non-metabolised portion of trichloroethylene is exhaled.

Other tests that can be done – LFT.


Powerful narcotic action exacerbated by ethanol. The CNS is the main target organ with the main symptoms being irritability, headache, drowsiness, dizziness, blurred vision, nausea, vomiting and cardiac arrhythmias. Causes Intolerance to alcohol - drunkenness after consumption of small quantities of alcohol. Skin blotches occur due to vasodilation - “degreasers flush”.

Workload during exposure increases the uptake of TCE and therefore increases the blood concentrations.

TRINITROTOLUENE (TNT)2.4 & 2.6 Dinitroaminotoluene

Toluene is nitrated with a mixture of sulphuric and nitric acids in a multistage process to produce TNT in the form of a dark yellow oily liquid. The finished product can be in the form of flakes, a crystalline powder , a slab or biscuit and a crushed flake. Used as a military and industrial explosive.

URINE (On Ice).

BEI: <10mg/L.

Not tabled.

Entry into the body by skin absorption, inhalation or ingestion.

Other tests that can be done – LFT, urinalysis.

End of workweek.

Exposure causes irritation of the digestive tract - gastritis may occur with nausea, vomiting & epigastric pain not related to meals; toxic jaundice, aplastic anaemia and cataracts. A common sign of absorption is orange staining of the hands, arms and face; dermatitis is relatively uncommon although TNT has been known to cause papular eruption on exposed skin, with oedema & subsequent desquamation.The formation of methaemoglobin in the blood (lilac colouring of the lips and earlobes, breathlessness, nausea, lassitude and retrosternal constriction) is not uncommon and is an indication for the temporary removal from exposure.

TURPENTINETrichloroethyleneEthyl BenzeneXylene

See above under the individual substances.

URINE (On Ice). See individual substances. End of shift.End of workweek.

Turpentine oils have a pronounced irritant effect on mucous membranes and skin leading to bullous dermatitis and can produce sensitization. Can cause turpentine eczema. Inhalation of high concentrations causes pronounced respiratory irritation. Ingestion causes central spasm and irritation of intestine and uro-genital tract. Skin absorption can cause kidney damage. If swallowed, liquid paraffin should be given to minimize GIT absorption.

30


BIOLOGICAL MATERIAL


HEALTH EFFECTS


VINYL CHLORIDEChloroethyleneThiodiglycolic acidThiodiacetic acid

Colourless gas, burns easily and is not stable at high temperatures. Has a mild sweet odour. A manufactured substance that does not occur naturally. Used to make PVC (polyvinyl chloride). PVC used to make a variety of plastic products e.g. pipes, wire & cable coatings, packaging materials, vehicle upholstery, and plastic kitchenware.

URINE (On ice).

Reference Range: <2.0mg/L.

Table 1 substance.

Absorbed by the lungs and transformed and excreted in various ways depending on amount accumulated. Can be eliminated unchanged by exhalation. The rest is metabolized in the liver and passes into the urine as thiodiglycolic acid.

Target organs are the liver, kidney, lung, spleen, CNS and blood.

Other tests that can be done – LFT, FBC, Renal Functions.

End of shift. Inhalation causes dizziness, sleepiness, unconsciousness and at very high levels – death. Can cause permanent liver enlargement and damage, immune reactions, nerve damage e.g. Raynauds, liver cancer. Ingestion can occur if contaminated water is used. Skin absorption can also occur when handling vinyl products, contaminated soil or bathing in contaminated water.Human carcinogen.

XYLENEMethylhippuric Acid

This is a colourless sweet smelling liquid. Flammable. Occurs naturally in petroleum and coal tar. Used as a solvent in the printing, rubber and leather industries. Also used as a cleaning agent, a thinner in paints & varnishes. Used as a high octane in aviation fuels, in the synthesis of dyes & in the production of phthalic acids.

URINE (On Ice).

BEI: 1.5 g/g creatinine.

Table 3 substance.

Rapidly absorbed from the lungs, metabolized & excreted in the urine.

Other tests that can be done – FBC, LFT.

End of shift. High levels can cause headaches, lack of muscle co-ordination, dizziness, confusion, changes in sense of balance. Can also cause irritation of skin, eyes, nose and throat; difficulty in breathing; delayed reaction time; memory difficulties; stomach discomfort; sweetish taste in mouth; nausea; loss of appetite and a strong thirst.

ZINCZinc

This is one of the most common elements found in the earths crust. Found in air, soil, water and in all foods. It is a bluish-white shiny metal. Used as a coating to prevent rust (galvanizing), dry cell batteries, mixed with other metals to make alloys e.g. brass and bronze. Zinc compounds used to make paint, rubber, dyes, wood preservatives and ointments. It is also an essential dietary element. Zinc metal used in the auto industry, electrical equipment, hardware and toys.

URINE.

Reference Range:<0.9 mg/g creatinine.

Table 2 substance.

Absorbed via the respiratory and gastrointestinal routes. Inhalation of zinc fumes is the main route of occupational exposure. Excreted mainly via faeces.

During shift. Ingestion of large amounts can cause stomach cramps, nausea, vomiting, anaemia and decrease in good cholesterol levels. Inhaling large amounts can cause metal fume fever. High levels in blood means high zinc consumption and or high exposure. Skin contact can cause nasal ulcerations and dermatitis.

31



SPECIMEN COLLECTION INSTRUCTIONSBIO-MONITORING OHS ACT TABLE 3 TARGET ORGANS GUIDELINES INDUSTRIAL AGRICULTURAL FOODHANDLERS DRUGS ARTICLES

32



PLEASE NOTE:Urine specimens marked as “On Ice” on above list to be transported on ice packs. Please contact Special Operations on 021 596 3587 to arrange if these are required. If transported for longer than 6 hours, please freeze the urine specimens.

URINE SPECIMEN COLLECTION INSTRUCTIONS:• The employees should be encouraged to drink a cup of tea or similar about an hour before the time, without emptying

their bladders until the time of specimen collection.• The specimen jar must be filled to the top and closed tightly.• The specimens must be collected at the end of the work-week (after 14h00 on Thursdays - Fridays) / end of shift (after

14h00 or after a minimum of 6 hours exposure) / pre-shift (before commencing work) or according to the relevant pre-arranged times.

• The name of the employee to be written on the specimen jar. • Ensure that the specimen jar is closed tightly and placed upright in the cooler box immediately.• Please complete the forms provided. Record the names, date of birth, authorisation or order

number (if required) and the clock or ID numbers (whichever you require) and then place the forms into the specimen bag provided and place on top of the containers in the cooler box.

• Collection of the specimens can be done directly with the Transport Division on 021 596 3669. If the specimens have not been collected by 16h30, please contact us.

• If the cooler box has been left overnight for the night shift workers: please phone us in the morning to arrange collection of the cooler box.

• Please contact Special Operations (021 596 3587) if you have any queries.

SPECIMEN COLLECTION INSTRUCTIONS


33



EXTRACTS FROM THE OHS ACTBIO-MONITORING OHS ACT TABLE 3 TARGET ORGANS GUIDELINES INDUSTRIAL AGRICULTURAL FOODHANDLERS DRUGS ARTICLES



BIO-MONITORING OHS ACT TABLE 3 TARGET ORGANS GUIDELINES INDUSTRIAL AGRICULTURAL FOODHANDLERS DRUGS ARTICLES 34

DEFINITIONS:

BEI - biological exposure index: is a reference value intended as a guide-

line for the evaluation of potential health hazards as listed in Table 3 of

Annexure 1 hereby as revised from time to time and listed in the Govern-

ment Gazette;

HCS - hazardous chemical substance: means any toxic, harmful, corrosive,

irritant or asphyxiant substance, or a mixture of such substances for which

(a) an occupational exposure limit is prescribed; or

(b) an occupational exposure limit is not prescribed; but which creates a

hazard to health;

Assessment of potential exposure5. (1) An employer or self employed person shall after consultation with

the relevant health and safety representative or relevant health and safety

committee, cause an immediate assessment to be made and thereafter at

intervals not exceeding two years, to determine if any employee may be

exposed by any route of intake.

(2) The employer shall inform the relevant health and safety representative

or relevant health and safety committee in writing of the arrangements

made for the assessment contemplated in sub-regulation (1), give them

reasonable time to comment thereon and ensure that the results of the

assessment are made available to the relevant representatives or commit-

tees who may comment thereon.

(3) When making the assessment, the employer or self employed person

shall keep a record of the assessment & take into account such matters as:

(a) the HCS to which an employee may be exposed;

(b) what effects the HCS can have on an employee;

(c) where the HCS may be present and in what physical form it is likely to

be;

(d) the route of intake by which and the extent to which an employee can

be exposed; and

(e) the nature of the work, process and any reasonable deterioration in, or

failure of, any control measures.

(4) If the assessment made in accordance with sub-regulation (3) indicates

that any employee may be exposed, the employer shall ensure that moni-

toring is carried out in accordance with the provisions of regulations 6 and

7 and that the exposure shall be controlled as contemplated in regulation 10.

(5) An employer shall review the assessment required by sub-regulation (1)

forthwith if:

(a) there is reason to suspect that the previous assessment is no longer

valid; or

(b) there has been a change in a process involving an HCS or in the

HAZARDOUS CHEMICAL SUBSTANCES REGULATIONS 1995 (R1179)




methods, equipment or procedures in the use, handling, control or pro-

cessing of the HCS, and the provisions of sub-regulations (2) and (3) shall

apply.

Medical surveillance7. (1) An employer shall ensure that an employee is under medical surveil-

lance if:

(a) the employee may be exposed to a substance listed in Table 3 of

Annexure 1;

(b) the exposure of the employee to any substance hazardous to his or her

health is such that an identifiable disease or adverse effect to his or her

health may be related to the exposure, there is a reasonable likelihood

that the disease or effect may occur under the particular conditions of

his or her work and there are techniques to diagnose indications of the

disease or the effect as far as is reasonably practicable; or

(c) the occupational health practitioner recommends that the relevant em-

ployee should be under medical surveillance in which case the employer

may call on an occupational medicine practitioner to ratify the appropriate-

ness of such recommendation.

(2) In order to comply with the provisions of sub-regulation (1) the employer

shall, as far as is reasonably practicable, ensure:

(a) that an initial health evaluation is carried out by an occupational health

practitioner immediately before or within 14 days after a person commenc-

es employment, where any exposure exists or may exist, which comprises:

(i) an evaluation of the employees medical and occupational history;

(ii) a physical examination; and

(iii) any other essential examination which in the opinion of the occupation-

al health practitioner is desirable in order to enable the practitioner to do a

proper evaluation.

(b) that subsequent to the initial health evaluation contemplated in para-

graph (a) the relevant employee undergoes examinations as contemplat-

ed in paragraph (a)(ii) and (iii), at intervals not exceeding two years, or at

intervals specified by an occupational medical practitioner.

(3) An employer shall not permit an employee who has been certified unfit

for work by an occupational medicine practitioner to work in a workplace

or part of a workplace in which he or she would be exposed: Provided

that the relevant employee may be permitted to return to work which will





expose him or her if he or she is certified fit for that work beforehand by

an occupational medicine practitioner.

(4) The employer shall record and investigate the incident contemplated in

subregulation (3) in compliance with regulation 8 of the General Adminis-

trative Regulations.

ANNEXURE 1HAZARDOUS CHEMICAL SUBSTANCES GUIDELINESPrevention and control of exposure

1. Exposure of employees to substances hazardous to health should be

prevented or, where this is not reasonably practicable, adequately con-

trolled. This is a fundamental requirement of the Regulations for Hazard-

ous Chemical Substances (HCS), 1995. Exposure can occur by inhalation,

ingestion or absorption through the skin, but inhalation is usually the main

route of entry into the body.

Tables 1 and 2 of Annexure 1 list the occupational exposure limits, which

should be used in determining the adequacy of control of exposure by

inhalation, as required by the HCS Regulations.

2. The advice in this document should be taken in the context of the

requirements of the HCS Regulations, especially regulation 5 (Assessment

of potential exposure), regulation 10 (Control of exposure), regulation 12

(Maintenance of control measures) and regulation 6 (Air monitoring). Sub-

stances hazardous to health are defined in regulation 1. There is separate

legislation for lead and asbestos and these substances are not covered in

detail in this document. This document also does not apply to exposure

below ground in mines or exposure to micro-organisms.

3. Adequate control of exposure (when prevention is not reasonably prac-

ticable) should be achieved by one or more of a range of control measures

described in regulation 10 of the HCS Regulations. Control by personal

protective equipment should be applied only when other means are not

reasonably practicable.

4.2 Biological monitoring of exposure4.2.1 Objectives

Biological monitoring of exposure can be divided into two types of testing:

(a) Biological monitoring: Measures the biochemical concentrations of

HCS’s and/or their metabolites in biological samples of exposed individu-

als, e.g. blood lead for inorganic lead exposure, or urinary arsenic for

inorganic arsenic exposure. The aim is to measure the degree of absorp-

tion into the body by measuring indicators in representative biological

samples, typically urine or blood (usually not related to the target organ).(b) Biological effect monitoring: Determines the intensity of biochemical or physiological change due to exposure, e.g. red cell cholinesterase for exposure to organosphosphate pesticides.





4.2.2 Uses of biological monitoring

Biological monitoring tests are indices of an individual’s exposure and they

may be a useful tool for the occupational health and safety team. They

give information on the overall level of exposure, regardless of whether an

HCS has been absorbed by the respiratory, oral, or cutaneous route. Cu-

taneous absorption can play a significant role in the case of some organic

compounds. The amounts absorbed through the skin may be comparable

to or even higher than those absorbed via the respiratory tract. Where

appropriate, environmental control measures may thus be supplemented,

with biological monitoring. Knowledge of the real individual exposure,

permits targeted applications of preventive measures.

4.2.3 Important considerations in biological monitoring

(a) In choosing a test to meet the above objectives, it is important to have

an understanding of the relationship between environmental exposure

and the concentration of an HCS in biological samples. This includes an

understanding of the principles of absorption, biotransformation, distribu-

tion and excretion of an HCS.

(b) In addition, there should be analytical methods available of sufficient

sensitivity and specificity to detect concentrations of the substance in

urine, blood or exhaled air in the range likely to be encountered in

industry.

(c) The HCS’s listed in Table 3 of Annexure 1 are those for which the above

criteria have a reasonable chance of being met.

4.2.4 Biological Exposure Indices (BEIs)

BEI’s are reference values intended as guidelines for the evaluation

of potential health hazards in the practice of industrial hygiene. A BEI

represents in theory the level of an HCS or metabolite most likely to be

observed in a specimen collected from a healthy worker who has been

exposed to an HCS to the same extent as the worker with inhalation ex-

posure to an OEL-TWA. BEI’s do not represent a sharp distinction between

hazardous and non-hazardous exposures. For example, owing to biologi-

cal variability, it is possible that an individual’s measurements can exceed

the BEI without incurring an increased health risk. Conversely, there may

be some susceptible individuals who may be harmed at effects below the

BEI.

If measurements in specimens obtained from a worker on different occa-

sions persistently exceed the BEI, or if the majority of measurements in

specimens obtained from a group of workers at the same workplace ex-





ceed the BEI, the cause of the excessive values must be investigated and

proper action be taken to reduce the exposure. BEI’s apply to eight-hour

exposures, five days a week. However, BEI’s for differing work schedules

may be extrapolated on pharmacokinetic grounds. BEI’s should not be

applied either directly or through a conversion factor, in the determination

of safe levels for non-occupational exposure to air and water pollutants,

or food contaminants. The BEI’s are not intended for use as a measure of

adverse effects or for diagnosis of occupational illness.

4.3.1 Objectives

(a) The principle of general medical screening is to detect a disease at

an early sub-clinical or pre-symptomatic stage in order to take action to

reverse these effects or to slow progression of the disease. The abnor-

malities sought, include patho-physiological or histo-pathological changes.

Such tests are well established in general preventative medicine, e.g. PAP

smears for cervical cancer, cholesterol screening, faecal occult blood for

lower bowel cancer, etc.

(b) In medical surveillance in industry one is interested not only in detect-

ing adverse effects in the individual, but also in the implication of the

findings for the effectiveness of workplace control measures. Medical

surveillance is thus directed not only at early adverse effects but also at

established disease.

4.3.2 Types of examination

(a) The number of validated screening tests with regard to HCS’s is smaller

than in general preventive medicine, but is likely to grow in the future.

Examples of subclinical tests include urinary cytology for bladder cancer

among workers exposed to potential bladder carcinogens, or full blood

counts for employees exposed to an HCS toxic for the blood-forming

organs.

(b) Medical surveillance may include simple clinical examination, such as

examination of the skin of employees exposed to contact irritants or aller-

gens, or of the nasal septum of employees exposed to chromates.

(c) Chest X-rays for silicosis are an example of screening for irreversible

(although potentially progressive) disease. Lung function testing is well

established as a non-specific test for the possible effect of respiratory

irritants, sensitisers and fibrogenic agents.

4.4 Designing and implementing a programme of medical surveillance4.4.1 The following steps should be included in any programme:

(a) Risk assessment to determine the potential exposure to and routes of

absorption of an HCS, as required by regulation 5.

(b) Identification of target-organ toxicity, so as to direct medical

screening.

(c) Selection of appropriate tests and testing schedule. Tests should

have the desirable operating characteristics of high sensitivity, specificity,

reliability and predictive value. The frequency of testing is laid down in





general terms by regulation 7(2) , but should in any case be based on an

understanding of the nature of the hazard and the natural history of any

adverse effects.

(d) Development of action criteria. These are provided for some HCS’s

in the form of BEI’s in Table 3 of Annexure 1. Criteria for interpreting

lung function testing have also been published in the medical literature.

However, in many cases, the occupational health practitioners will have to

develop pragmatic criteria in the context of the specific workplace.

(e) Standardisation of test process. Quality control needs to be exercised

both in the testing site and in the laboratory contracted to carry out anal-

yses. Consistency over time should be sought so as to make longitudinal

measurements comparable.

(f) Ethical considerations. Information and training of employees as

required by regulation 3(1) should include the rationale for doing medical

surveillance, and the consequence of abnormal findings. An employee

must be notified of the results and interpretation of his/her tests and any

recommendations made. The confidentiality of personal medical records is

laid down by regulation 9.

(g) Determination of employee’s fitness to remain in that job. [Regulation

7(3)]. Results may be compared against the action criteria (BEI if relevant),

and preferably also the employees previous results to determine whether

individual action needs to be taken. Action may include repeating the test,

further medical examination, removal of the employee from further expo-

sure, and notification of the employer. Co-operation of employees can be

best secured by a policy of protection of conditions of service in case of

medical removal from a particular job.

(h) Evaluation of control. An abnormal finding in an employee, or a pat-

tern of findings in a group of employees, may point to inadequate primary

control of exposure. In such cases the employer needs to be notified of

such details of the medical findings as are necessary to evaluate the work-

place problem and take remedial action.

(i) Record keeping. This includes both medical records and exposure

information for every employee. While the employer is responsible for

record keeping in terms of regulation 9, the contents of personal medical

records may be accessible to the occupational medicine practitioner, the

employee, and any person nominated by the employee in writing.





4.4.2 The onus is on the occupational health practitioner carrying out medical surveillance to be familiar

with the latest scientific information regarding the HCS and tests that might be useful. The aim should

be to design a programme that is rational, ethical and effective. This may have to be done in the face of

incomplete information of uncertainty regarding exposures, toxicity and test performance.





Exposure in mines33. The HCS Regulations and the occupational exposure limits in this publication do not apply to exposure to substances hazardous to health in mines.

Lead and asbestos34. Work with asbestos or lead is not subject to the HCS Regulations. The exposure limits for various types of asbestos and lead are specified in the As-

bestos Regulations and the Lead Regulations.

Pesticides35. Substances used as active ingredients in pesticides are listed under their chemical names and/or their common (ISO) names. These names may some-

times be used as parts of the names of proprietary pesticide formulations. In all cases the exposure limit applies to the specific active ingredients and not

to the formulation as a whole.

Sensitisers41. Certain substances may cause sensitisation of the respiratory tract if inhaled or skin contact occurs. Respiratory sensitisers can cause asthma, rhinitis,

or extrinsic allergic alveolitis. Skin sensitisers cause allergic contact dermatitis. Substances which cause skin sensitations are not necessarily respiratory

sensitisers or vice-versa. Only a proportion of the exposed population will become sensitised, and those who do become sensitised, will not have been

identified in advance. Individuals who become sensitised may produce symptoms of ill health after exposure even to minute concentrations of the sensitiser.

Other factors44. Working conditions which impose additional stress on the body, such as exposure to ultra-violet radiation, high temperatures, pressures and humidity

may increase the toxic response to a substance. In such cases, specialist advice may be necessary to evaluate the effect of these factors.


42



FATE OF A CHEMICALBIO-MONITORING OHS ACT GUIDELINES INDUSTRIAL TESTING AGRICULTURAL TESTING FOOD HANDLERS DRUG TESTING ARTICLES

Fate of a chemical from the environment to the target molecules in the organism. From Lauwerys, R.R., Casarett and Doull’s Toxicology.

The Basic Science of Poisons, Amdur, M., Doull, J., and Klaassen, C., Eds., Pergamon, New York, 1991

Distribution (blood, tissues)

Biotransformation

Substance at the workplace

Absorption

Active metabolites Inactive metabolites

Distribution (blood, tissues)Excretion

Binding to critical sites Repair

Binding to non-critical sites

Degradation productsNon-toxic effects

Early (reversible) adverse effects

Preclinical lesions Clinical lesions

Ambient monitoring

Biological monitoring of exposure

Health surveillance

Diagnosis of occupational diseases

43




TABLE 3 SUBSTANCES: BIO EXPOSURE INDICES

44BIO-MONITORING OHS ACT TABLE 3 TARGET ORGANS GUIDELINES INDUSTRIAL AGRICULTURAL FOODHANDLERS DRUGS ARTICLES



SUBSTANCE & DETERMINANT SAMPLING TIME SPECIMEN BEI

TABLE 3 SUBSTANCES: BIOLOGICAL EXPOSURE INDICES

ANILINE

Total p-aminophenol in urine End of shift Urine on ice 50 mg/g creatinine

Methaemoglobin in blood During shift / end of shift Heparin tube (green top) on ice 1.5 % of haemoglobin

ARSENIC

Inorganic arsenic metabolites in urine End of workweek Urine 50 ug/g creatinine

BENZENE

Total phenol in urine End of shift Urine on ice 50 mg/g creatinine

CADMIUM

Cadmium in urine Not critical Urine 10 ug/g creatinine

Cadmium in blood Not critical Heparin tube (green top) 10 ug/l

CARBON-DISULFIDE

2-Thiothiazolidine-4-carboxylic acid in urine End of shift Urine on ice 5 mg/g creatinine






CARBON MONOXIDE

Carboxyhaemaglobin in blood End of shift Heparin tube (green top) on ice less than 8% of haemoglobin

CHROMIUM (VI)

Total chromium in urine End of shiftEnd of workweek Urine 30 ug/g creatinine

N,N-DIMETHYL-FORMAMIDE (DMF)

N-Methylformamide in urine End of shift Urine on ice 40 mg/g creatinine

ETHYL BENZENE

Mandelic acid in urine End of shift End of workweek Urine on ice 1.5 g/g creatinine

FLUORIDES

Fluorides in urine Prior to shiftEnd of shift Urine on ice 3 mg/g creatinine

10 mg/g creatinine






n-HEXANE

2,5-Hexanedione in urine End of shift Urine on ice 5 mg/g creatinine

MERCURY

Total inorganic mercury in urine Prior to shift Urine 35 ug/g creatinine

Total inorganic mercury in blood End of shift End of workweek Trace Element K2 Edta tube 15 ug/l

MEHAEMOGLOBIN INDUCERS

Methaemoglobin in blood During or end of shift Heparin tube (green top) on ice 1.5 % of haemoglobin

METHANOL

Formic acid in urine Pre shift at end of workweek Urine on ice 80 mg/g creatinine

METHYL CHLOROFORM

Trichloroacetic acid in urine End of workweek Urine on ice 10 mg/l






Total trichloroethanol in urine End of shift End of workweek 30 mg/l

Total trichloroethanol in blood End of shift End of workweek Purple top tube x 2 1 mg/l

METHYL- ETHYL-KETONE

MEK in urine End of shift Urine on ice 2 mg/l

METHYL- ISOBUTYL-KETONE

MIBK in urine End of shift Urine on ice 2 mg/l

NITROBENZENE

Total p-nitrophenol in urine End of shift End of workweek NO TEST 5 mg/g creatinine

Methaemoglobin in blood End of shift Heparin tube (green top) on ice 1.5 % of haemoglobin






ORGANOPHOSPHATES

Cholinesterase activity in red blood cells Discretionary Purple top tube 70% of individual’s baseline

PARATHION

Total p-nitrophenol in urine End of shift NO TEST 0.5 mg/g creatinine

Cholinesterase activity in red blood cells Discretionary Purple top tube 70% of individual’s baseline

PENTACHLOROPHENOL

Total PCP in urine Prior to last shift of workweek Urine on ice 2 mg/g creatinine

Free PCP in plasma End of shift Purple top tube x 2 5 mg/l

PERCHLOROETHYLENE

Perchloroethylene in blood Prior to last shift of workweek Purple top tube x 2 1 mg/l

Trichloroacetic acid in urine End of workweek Urine on ice 7 mg/l

PHENOL






Total phenol in urine End of shift Urine on ice 250 mg/g creatinine

STYRENE

Mandelic acid in urine & End of shift Prior to next shift Urine on ice 800 mg/g creatinine

300 mg/g creatinine

Phenylglyoxylic acid in urine End of shift Prior to next shift

240 mg/g creatinine 100 mg/g creatinine

Styrene in venous blood End of shift Prior to next shift Purple top tube x 2 0.55 mg/l

0.02 mg/l

TOLUENE

Hippuric acid in urine & End of shift Urine on ice 2.5 g/g creatinine

o-Cresol in urine End of shift 1 mg/g creatinine

Toluene in venous blood End of shift Purple top tube x 2 1 mg/l






TRICHLOROETHYLENE

Tricholoroacetic acid in urine & End of workweek Urine on ice 100 mg/g creatinine

Trichloro. compounds & trichloroethanol in urine

End of shift End of workweek 300 mg/g creatinine

Trichloroethanol in blood End of shift End of workweek Purple top tube x 2 4 mg/l

XYLENE

Methylhippuric acid in urine End of shift Urine on ice 1.5 g/g creatinine

PRIOR TO SHIFT: 16 hours after exposure ceases. DURING SHIFT: after 2 hours exposure. END OF SHIFT: as soon as possible after exposure (a minimum of 6 hours). END OF SHIFT END OF WORKWEEK: 4/5 consecutive days exposure.

51



TARGET ORGANSBIO-MONITORING OHS ACT TABLE 3 TARGET ORGANS GUIDELINES INDUSTRIAL AGRICULTURAL FOODHANDLERS DRUGS ARTICLES

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52



SCREEN GUIDELINES

Includes:

• Executive Medicals• Food Handlers• Vehicle Operators• Radiation Workers• Other


53



EXECUTIVE MEDICALS Aimed at Management Staff to guage corporate wellness

FULL BLOOD COUNT & ESREffective screening test to determine underlying disease & anaemia

FASTING GLUCOSETo detect Diabetes Mellitus

FASTING LIPOGRAMEarly detection of coronary risk

LIPOPROTEIN (a)To detect familial hypercholesterolaemia

ALT/AST/GAMMA-GTTo detect liver disease and alcohol abuse

For male employees over 40:

PSATo detect prostate hypertrophy

FOOD HANDLERSTo minimise food poisoning during the food manufacturing process

NASAL SWABTo determine staphylococcus aureus carrier status

STOOL SPECIMENTo detect salmonella and / or shigella carrier status

VEHICLE OPERATORSThis profile is intended to minimise alcohol and / or drug related driving accidents

GAMMA-GT

GLUCOSE

CHOLESTEROL

CANNABIS

COCAINE

MANDRAX

CDT

RADIATION WORKERSTo detect over-exposure to radiation

FULL BLOOD COUNT (FBC)

OTHER

METAL EXPOSURE

HAZARDOUS CHEMICALS EXPOSURE

INFECTIOUS DISEASES (E.G. TB, HEPATITIS)

PESTICIDE EXPOSURE

DRUGS OF ABUSE TESTING

PATHOLOGY SCREEN GUIDELINES


54



INDUSTRIAL TESTING

Includes:

• Plastics Industry• Paint Industry• Printing & Signage Industry• Packaging Industry• Electroplating / Galvanising• Heavy Industry• Industrial Solvents


55




PLASTICS INDUSTRYAcetone, Benzene, Methanol, MEK, Styrene, Cadmium, TDI, Toluene, Xylene

PAINT INDUSTRYBenzene, Lead, Methanol, Toluene, Xylene, Mercury, Chromium, Cadmium, Solvents, Aromatic Hydrocarbons

PRINTING & SIGNAGE INDUSTRYToluene, MEK, MIBK, n-Hexane, TDI

PACKAGING INDUSTRYStyrene, Ethyl Benzene, n-Hexane

ELECROPLATING & GALVANISINGCadmium, Chromium, Lead, Mercury, Nickel, Zinc, TDI, Aluminium

HEAVY INDUSTRYLead, Cadmium, Carboxyhaemoglobin, Chromium, Mercury, Cobalt, PAH, Manganese

INDUSTRIAL SOLVENTSHexane, Benzene, Toluene, Xylene, Carbon Tetrachloride, Acetone, MEK

INDUSTRIAL TESTING




TABLE 3 SUBS. CHEMICAL SAMPLING TIME SPECIMEN BEI

AGRICULTURAL TESTING

Includes:

• Testing for Crop Sprayers





Who should be tested?• All who work with organophosphates / carbamates (mixing and/or spraying) or

suffer chronic exposure.

What to test for:• Baseline whole blood cholinesterase (ChE) (before crop spraying

starts).• Serum cholinesterase (S-ChE / pseudo-ChE) for acute symptoms.• Repeat whole blood ChE during spray season (after 30 days).• Do both tests should worker develop symptoms during crop

spraying.

Which specimens are required?• Purple top tube (EDTA) for whole blood ChE.• Gel tube for serum ChE.

What is serum / whole blood ChE?• ChE is an enzyme found in the red blood cell, serum and nervous system.• Serum ChE / pseudo-ChE reflects acute poisoning.

• Whole blood ChE reflects chronic exposure.

LABORATORY TESTING FOR CROP SPRAYERS





When and how often have workers to be tested?• Before the crop spraying season starts.• After about a month of exposure.• When the worker experiences acute symptoms.

How does exposure occur?• Inhalation.• By the oral route (eating / drinking).• Absorption through the skin.

Prevention:• Wear protective clothing, shoes, masks and limit exposure to a

minimum.• After exposure, access to proper washing facilities.

What happens if the worker has too much exposure?

Acute:• May die.• Severe sweating, pinpoint pupils, severe tear formation, salivation, wheezy

breathing, cramps, vomiting and diarrhoea.• Urine retention, vision disturbance, cyanosis (oxygen deficiency), anxiousness,

restlessness and convulsions.






Chronic:• Headache, muscle weakness, thickheaded feeling, anorexia and disorientation.• Worker tires easily, disturbed sleeping pattern.• Shakiness and abnormal sensation.

How are results interpreted?• It is PARAMOUNT that all results of the worker be discussed with a

doctor and that records be kept of all the worker’s results.• Laboratory reference values are of LIMITED value in

organophosphate exposure.• The same laboratory should be used for all the testing to exclude the

influence of methodological variation on the result.• The patient’s own whole blood ChE is used as the baseline level and

should be determined once the worker has been exposure free for 30 days.

• A follow-up determination is done after 30 days of organophosphate / carbamate exposure.

• A serum ChE (pseudo-ChE) level is indicated if the worker has symptoms of acute poisoning.






Whole blood ChE:15-25% below baseline: Retest.25-30% below baseline: Retest and re-evaluate safety precautions.> 30% below baseline : Remove worker from exposure and investigate safety conditions.

Serum-ChE:15-25% below baseline: Retest.25-40% below baseline: Retest and re-evaluate safety precautions.> 40% below baseline: Remove worker from exposure and investigate safety conditions.

Causes of a reduced / increased pseudo-ChE?Reduced levels:

Poisons:Organophosphates, carbamates.Medications:Cortisone, contraceptive pill, lithium, phenothiazines.Diseases:Genetic variants of ChE, hepatitis / liver cirrhosis, metastases, cardiac failure, chronic renal disease, myocardial infarction, muscle dystrophy, dermatomyositis, pulmonary embolism, late pregnancy, malnutrition.






Increased levels:Hyperthyroidism, diabetes, hypertriglyceridaemia, pernicious anaemia, alcoholism, nephrotic syndrome. Haemolysis may result in falsely elevated levels.

Causes of a reduced / increased whole blood ChE?Reduced levels:

Poisons:Organophosphates, carbamates.Diseases:Paroxysmal nocturnal haemoglobinuria, megaloblastic anaemia, myasthenia gravis on treatment.

Increased levels:Sickle cell anaemia.


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FOOD HANDLER TESTING

Definition:A food handler is a staff member that handles food that they are not going to consume. This includes preparation, manufacturing and the serving of food.


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HEALTH SCREENS FOR FOOD HANDLERS:

NASAL OR THROAT SWAB:Cultured for Staphylococcus Aureus and Streptococcusbacteria. Food contaminated by these organisms cancause food poisoning to the consumer. Although StaphAureus is present in the majority of human beings, it is themost common cause of abscesses, boils and foodpoisoning in the food industry. EXCLUDE FROM WORKUNTIL SUCCESSFULLY TREATED.

RECTAL SWAB OR STOOL SPECIMEN:Culture for Salmonella and Shigella. Parasites andCholera can be cultured in a stool specimen. Theseorganisms can also cause food poisoning and may bepresent in the bowel. EXCLUDE FROM WORK UNTIL 3CONSECUTIVE NEGATIVE CULTURES, DONE 48HOURS APART.

SPUTUM TB:This test is done to detect the presence of TB. TB is nottransmitted via food but is highly contagious from person to

person. EXCLUDE FROM WORK UNTIL UNDERGONE 7DAYS OF EFFECTIVE TREATMENT.

HEPATITIS A IgG & IgM:IgG to test for Hepatitis A immunity.IgM to test for Hepatitis A infection.Hepatitis A can be transmitted via contaminated food, milk and water. EXCLUDE FROM WORK FOR 6 WEEKSFROM ONSET OF JAUNDICE.

HEPATITIS B ABS (for Immunity):This test is to check for Hepatitis B antibodies to determine immunity against infection. Hepatitis B is not transmitted via foodstuffs.

WIDAL H/O TITRES:This is a blood test which can be done to determine thepresence of Salmonella Typhi infection (Typhoid Fever),which can be transmitted via contaminated milk , water and foodstuffs.

FOOD HANDLER INFORMATION & GUIDELINES

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FAI protects the health and safety of consumers by administering compulsory speci-fications for fish and fishery products and canned meat products. FAI administers these compulsory food specifications on behalf of the Minister of Trade and Industry in terms of the Standards Act 29 of 1993. FAI is also appointed as the competent authority for the export certification of fishery products to the European Union. In order to demonstrate credibility of inspection results and to verify the competence of the inspection system, the Department is accredited to ISO 17020 standards. This inspection system is based on monitoring and surveillance of factories, processes and products.

The objectives of the Department are to:1. Protect the health and safety of the consumer.2. Ensure compliance to food and associated regulations.3. Assist role players to comply with local and international requirements.4. Promote fair trade and to protect national and international markets.

At national level, the Department works in close co-operation with several other legislators in the food arena and FAI inspectors are also appointed by the Department of Health as inspectors in terms of the Foodstuffs, Cosmetics and Disinfectants Act. Internationally FAI participates in various

SABS REGULATORY AFFAIRS & ASSOCIATED INDUSTRIES (FAI)

65




activities of Codex Alimentarius and has also entered into international technical agreements with regulatory counterparts in other countries. South Africa is a member of the World Trade Organization (WTO) and South African food regulatory authorities are obliged to ensure compliance with the WTO Sanitary & Phytosanitary (SPS) and Technical Barriers of Trade (TBT) agreements.

Compulsory Specifications Administered:• Canned meat & canned meat products.• Canned fish, marine molluscs & crustaceans.• Frozen fish & marine molluscs.• Frozen rock lobster.• Frozen shrimps, langoustines & crabs.• Smoked snoek.

These specifications are aligned with international guidelines and practices and harmonized with the Standards and Codes of Practice of Codex Alimentarius. They apply to all products sold in South Africa (whether locally produced or imported) and exports to other countries.

The minimum requirements of the compulsory specifications are based on Good Manufacturing Practices (GMP) and Good Hygiene Practices (GHP) as set by Codex Alimentarius.


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The Compulsory Specifications Address:

1. Requirements for the factory:• Construction, layout & conditions.• Equipment for production.• Quality of the water used during handling & processing.• Requirements for employees engaged in the handling, preparation,

processing, packaging & storage of the product.• Hygiene of factory, equipment and processes.• The handling, preparation, processing, packaging & transportation of

the product.

2. Ingredients and Product:• Product specific composition & quality.• Microbiological requirements.• Chemical requirements.• Packing & packaging material.• Labelling.• Methods of physical, chemical & microbiological evaluation.


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Specific Regulatory Services provided:• Inspection services.• Food technology assistance.• Assistance with food standards.• Issuing of health certificates.

People have the right to expect the food they eat to be safe and suitable for consumption. Food borne illness and food borne injury are at best unpleasant; at worst, they can be fatal. But there are also other consequences. Outbreaks of foodborne illness can damage trade and tourism, and lead to loss of earnings, unemployment and litigation. Food spoilage is wasteful, costly and can adversely affect trade and consumer confidence. International food trade and foreign travel areincreasing, bringing important social and economic benefits. But this also makes the spread of illness around the world easier.

Eating habits too, have undergone major changes in many countries and new food production, preparation and distribution techniques have developed to reflect this. Effective hygiene control is vital to avoid the adverse human health and economic consequences of food borne illness, food borne injury and food spoilage. Everyone, including farmers and growers, manufacturers and processors, food handlers and consumers, has a responsibility to ensure that food is safe and suitable for consumption. These General Principles lay a firm foundation for ensuring food hygiene and should be used in

RECOMMENDED INTERNATIONAL CODE OF PRACTICE GENERAL PRINCIPLES OF FOOD HYGIENE CAC/RCP 1-1969, Rev. 3-1997, Amd. (1999)

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conjunction with each specific code of hygienic practice, where appropriate, and the guidelines on microbiological criteria. This follows the food chain from primary production to final consumption, highlighting the key hygiene controls at each stage. It recommends a HACCP-based approach wherever possible to enhance food safety as described in Hazard Analy-sis and Critical Control Point (HACCP) System and Guidelines for its Application (Annex). These controls are internationally recognized as essential to ensure the safety and suitability of food for consumption and are recommended to Govern-ments, industry (including individual primary producers, manufacturers, processors, food service operators and retailers)and consumers alike.

THE CODEX GENERAL PRINCIPLES OF FOOD HYGIENE• identify the essential principles of food hygiene applicable throughout the food chain (including primary production

through to the final consumer) to ensure that food is safe and suitable for human consumption.• recommend a HACCP-based approach as a means to enhance food safety.• indicate how to implement those principles.• provide a guidance for specific codes which may be needed for sectors of the food chain; processes or commodities;

to amplify the hygiene requirements specific to those areas.

DEFINITIONSFor the purpose of this Code, the following expressions have the meaning stated:

Cleaning – the removal of soil, food residue, dirt, grease or other objectionable matter.


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Contaminant – any biological or chemical agent, foreign matter or other substances not intentionally added to food which may compromise food safety or suitability.

Contamination – the introduction or occurrence of a contaminant in food or food environment.

Disinfection – the reduction by means of chemical agents and/or physical methods of the number of micro-organisms in the environment, to a level that does not compromise food safety or suitability.

Establishment – any building or area in which food is handled and the surroundings under the control of the same management.

Food hygiene – all conditions and measures necessary to ensure the safety and suitability of food at all stages of the food chain.

Hazard – a biological, chemical or physical agent in, or condition of, food with the potential to cause an adverse health effect.

HACCP – a system which identifies, evaluates, and controls hazards which are significant for food safety.


70




Food handler – any person who directly handles packaged or unpackaged food, food equipment and utensils, or food contact surfaces and is therefore expected to comply with food hygiene requirements.

Food safety – assurance that food will not cause harm to the consumer when it is prepared and/or eaten according to its intended use.

Food suitability – assurance that food is acceptable for human consumption according to its intended use.

Primary production – those steps in the food chain up to and including, for example, harvesting, slaughter, milking, fishing.

PRIMARY PRODUCTION

OBJECTIVESPrimary production should be managed in a way that ensures that food is safe and suitable for its intended use. Where necessary, this will include:

• avoiding the use of areas where the environment poses a threat to the safety of food.

• controlling contaminants, pests and diseases of animals and plants in such a way as not to pose a threat to food safety.

• adopting practices and measures to ensure food is produced under appropriately hygienic conditions.


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RATIONALETo reduce the likelihood of introducing a hazard which may adversely affect the safety of food or its suitability for consump-tion at later stages of the food chain.

ENVIRONMENTAL HYGIENEPotential sources of contamination from the environment should be considered. In particular, primary food production should not be carried on in areas where the presence of potentially harmful substances would lead to an unacceptable level of such substances in food.

HYGIENIC PRODUCTION OF FOOD SOURCESThe potential effects of primary production activities on the safety and suitability of food should be considered at all times. This includes identifying any specific points in such activities where a high probability of contamination may exist and taking specific measures to minimize that probability.

Producers should as far as practicable implement measures to:• control contamination from air, soil, water, feedstuffs, fertilizers (including natural fertilizers), pesticides, veterinary drugs

or any other agent used in primary production.• control plant and animal health so that it does not pose a threat to human health through food consumption or

adversely affect the suitability of the product.


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• protect food sources from faecal and other contamination. In particular, care should be taken to manage wastes and store harmful substances appropriately.

HANDLING, STORAGE & TRANSPORTProcedures should be in place to:• sort food & food ingredients to segregate material which is evidently unfit for human consumption.• dispose of any rejected material in a hygienic manner.• protect food & food ingredients from contamination by pests or by chemical, physical or microbiological contaminants

or other objectionable substances during handling, storage and transport.

Care should be taken to prevent, so far as reasonably practicable, deterioration and spoilage through appropriate measures which may include controlling temperature, humidity, and/or other controls.

CLEANING, MAINTENANCE AND PERSONNEL HYGIENEAppropriate facilities and procedures should be in place to ensure that: • any necessary cleaning and maintenance is carried out effectively. • an appropriate degree of personal hygiene is maintained.

CONTROL OF OPERATION

OBJECTIVESTo produce food which is safe and suitable for human consumption by :


73




• formulating design requirements with respect to raw materials, composition, processing, distribution and consumer use to be met in the manufacture and handling of specific food items.

• designing, implementing, monitoring and reviewing effective control systems.

RATIONALETo reduce the risk of unsafe food by taking preventative measures to ensure the safety and suitability of food at an appropriate stage in the operation by controlling food hazards.

MICROBIOLOGICAL CROSS-CONTAMINATIONPathogens can be transferred from one food to another, either by direct contact or by food handlers, contact surfaces or the air. Raw, unprocessed food should be separated physically or by time, from ready-to-eat foods with effective intermediate cleaning and where appropriate, disinfection.

Access to processing areas may need to be restricted or controlled. Where risks are particularly high, access to processing areas should be only via a changing facility.


74




Personnel may need to put on clean protective clothing including footwear and wash their hands before entering. Surfaces, utensils, equipment, fixtures and fittings should be thoroughly cleaned and where necessary disinfected after raw food, particularly meat and poultry, has been handled or processed.

PHYSICAL & CHEMICAL CONTAMINATIONSystems should be in place to prevent contamination of foods by foreign bodies such as glass or metal shards from ma-chinery, dust, harmful fumes and unwanted chemicals. In manufacturing and processing, suitable detection or screening devices should be used where necessary.

INCOMING MATERIAL REQUIREMENTSNo raw material or ingredient should be accepted by an establishment if it is known to contain parasites, undesirable micro-organisms, pesticides, veterinary drugs or toxic, decomposed or extraneous substances which would not be reduced to an acceptable level by normal sorting and/or processing.Where appropriate, specifications for raw materials should be identified and applied. Raw materials or ingredients should, where appropriate, be inspected and sorted before processing. Where necessary, laboratory tests should be made to establish fitness for use. Only sound, suitable raw materials or ingredients should be used. Stocks of raw materials and ingredients should be subject to effective stock rotation.


75




PERSONAL HYGIENE

OBJECTIVESTo ensure that those who come directly or indirectly into contact with food are not likely to contaminate food by:• maintaining an appropriate degree of personal cleanliness.• behaving and operating in an appropriate manner.

RATIONALEPeople who do not maintain an appropriate degree of personal cleanliness, who have certain illnesses or conditions or who behave inappropriately, can contaminate food and transmit illness to consumers.HEALTH STATUSPeople known, or suspected, to be suffering from, or to be a carrier of a disease or illness likely to be transmitted through food, should not be allowed to enter any food handling area if there is a likelihood of their contaminating food. Any person so affected should immediately report illness or symptoms of illness to the management. Medical examination of a food handler should be carried out if clinically or epidemiologically indicated.


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ILLNESS AND INJURIESConditions which should be reported to management so that a medical examination and/or possible exclusion from food handling can be considered include:• jaundice.• diarrhoea.• vomiting.• fever.• sore throat with fever.• visibly infected skin lesions (boils, cuts, etc.)• discharges from the ear, eye or nose.

PERSONAL CLEANLINESSFood handlers should maintain a high degree of personal cleanliness and, where appropriate, wear suitable protective clothing, head covering, and footwear. Cuts and wounds, where personnel are permitted to contin-ue working, should be covered by suitable waterproof dressings.

Personnel should always wash their hands when personal cleanliness may affect food safety eg:• at the start of food handling activities.• immediately after using the toilet.


77




• after handling raw food or any contaminated material, where this could result in contamination of other food items; they should avoid handling ready-to-eat food, where appropriate.

PERSONAL BEHAVIOURPeople engaged in food handling activities should refrain from behaviour which could result in contamination of food eg:• smoking.• spitting.• chewing or eating.• sneezing or coughing over unprotected food.

Personal effects such as jewellery, watches, pins or other items should not be worn or brought into food handling areas if they pose a threat to the safety and suitability of food.

TRANSPORTATION

OBJECTIVESMeasures should be taken where necessary to:• protect food from potential sources of contamination.


78




• protect food from damage likely to render the food unsuitable for consumption.• provide an environment which effectively controls the growth of pathogenic or spoilage micro-organisms and the

production of toxins in food.

TRAINING

OBJECTIVESThose engaged in food operations who come directly or indirectly into contact with food should be trained and/or instructed in food hygiene to a level appropriate to the operations they are to perform.

RATIONALEInadequate hygiene training and/or instruction and supervision of all people involved in food related activities pose a potential threat to the safety of food and its suitability for consumption.

TRAINING PROGRAMMESFactors to take into account in assessing the level of training required include:• the nature of the food, in particular its ability to sustain growth of pathogenic or spoilage micro-organisms.• the manner in which the food is handled and packed, including the probability of contamination.• the extent and nature of processing or further preparation before final consumption.• the conditions under which the food will be stored.• the expected length of time before consumption.


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INSTRUCTION AND SUPERVISIONPeriodic assessments of the effectiveness of training and instruction programmes should be made as well as routine super-vision and checks to ensure that procedures are being carried out effectively. Managers and supervisors of food processes should have the necessary knowledge of food hygiene principles and practices to be able to judge potential risks and take the necessary action to remedy deficiencies.The first section of this document sets out the principles of the Hazard Analysis & Critical Control Point (HACCP) system adopted by the Codex Alimentarius Commission. The second section provides general guidance for the application ofthe system while recognizing that the details of application may vary depending on the circumstances of the food opera-tion.

The HACCP system, which is science based and systematic, identifies specific hazards and measures for their control to ensure the safety of food. HACCP is a tool to assess hazards and establish control systems that focus on prevention rather than relying mainly on end-product testing. Any HACCP system is capable of accommodating change, such as advances in equipment design, processing procedures or technological developments.HACCP can be applied throughout the food chain from primary production to final consumption and its implementation should be guided by scientific evidence of risks to human health. As well as enhancing food safety, implementation of HAC-CP can provide other significant benefits. In addition, the application of HACCP systems can aid inspection by regulatory authorities and promote international trade by increasing confidence in food safety.

HAZARD ANALYSIS & CRITICAL CONTROL POINT (HACCP) SYSTEM & GUIDELINES FOR ITS APPLICATION Annex to CAC/RCP 1-1969 (Rev. 3 - 1997)

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The successful application of HACCP requires the full commitment and involvement of management and the work force. It also requires a multidisciplinary approach; which should include, when appropriate, expertise in agronomy, veterinary health, production, microbiology, medicine, public health, food technology, environmental health, chemistry and engineer-ing. The application of HACCP is compatible with the implementation of quality management systems, such as the ISO 9000 series, and is the system of choice in the management of food safety within such systems.

DEFINITIONS

Control (verb) – To take all necessary actions to ensure & maintain compliance with criteria established in the HACCP plan.

Control (noun) – The state wherein correct procedures are being followed and criteria are being met.

Control measure – Any action & activity that can be used to prevent or eliminate a food safety hazard or reduce it to an acceptable level.

Corrective action – Any action to be taken when the results of monitoring at the CCP indicate a loss of control.

Critical Control Point (CCP) – A step at which control can be applied & is essential to prevent or eliminate a food safety hazard or reduce it to an acceptable level.

Critical limit – A criterion which separates acceptability from unacceptability.

Deviation – Failure to meet a critical limit.


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Flow diagram – A systematic representation of the sequence of steps or operations used in the production or manufacture of a particular food item.

HACCP – A system which identifies, evaluates & controls hazards which are significant for food safety.

HACCP plan – A document prepared in accordance with the principles of HACCP to ensure control of hazards which are significant for food safety in the segment of the food chain under consideration.

Hazard – A biological, chemical or physical agent in, or condition of, food with the potential to cause an adverse health effect.

Hazard analysis – The process of collecting & evaluating information on hazards & conditions leading to their presence to decide which are significant for food safety and therefore should be addressed in the HACCP plan.

Monitor – The act of conducting a planned sequence of observations or measurements of control parameters to assess whether a CCP is under control.


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Step – A point, procedure, operation or stage in the food chain including raw materials, from primary production to final consumption.Validation – Obtaining evidence that the elements of the HACCP plan are effective.

Verification – The application of methods, procedures, tests & other evaluations, in addition to monitoring to determine compliance with the HACCP plan.

PRINCIPLES OF THE HACCP SYSTEMThe HACCP system consists of the following seven principles:

PRINCIPLE 1 – Conduct a hazard analysis.PRINCIPLE 2 – Determine the Critical Control Points (CCPs).PRINCIPLE 3 – Establish critical limit(s).PRINCIPLE 4 – Establish a system to monitor control of the CCP.PRINCIPLE 5 – Establish the corrective action to be taken when monitoring indicates that a CCP is not under control.PRINCIPLE 6 – Establish procedures for verification to confirm that the HACCP system is working effectively.PRINCIPLE 7 – Establish documentation about all procedures & records appropriate to these principles & their application.

GUIDELINES FOR THE APPLICATION OF THE HACCP SYSTEMPrior to application of HACCP to any sector of the food chain, that sector should be operating according to the Codex General Principles of Food Hygiene, the appropriate Codex Codes of Practice, and appropriate food safety legislation.


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Management commitment is necessary for implementation of an effective HACCP system. During hazard identification, evaluation, and subsequent operations in designing and applying HACCP systems, consideration must be given to the impact of raw materials, ingredients, food manufacturing practices, role of manufacturing processes to control hazards, likely end-use of the product, categories of consumers of concern, and epidemiological evidence relative to food safety.

The intent of the HACCP system is to focus control at CCPs. Redesign of the operation should be considered if a hazard which must be controlled is identified but no CCPs are found. HACCP should be applied to each specific operation separately. CCPs identified in any given example in any Codex Code of Hygienic Practice might not be the only ones identified for a specific application or might be of a different nature.

The HACCP application should be reviewed and necessary changes made when any modification is made in the product, process, or any step. It is important when applying HACCP to be flexible where appropriate, given the context of the application taking into account the nature and the size of the operation.


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DRUG TESTINGBIO-MONITORING OHS ACT TABLE 3 TARGET ORGANS GUIDELINES INDUSTRIAL AGRICULTURAL FOODHANDLERS DRUGS ARTICLES

Includes:

• Toxicology Screen• Drug Information• Specimen Collection• Extract from OHS Act• Signs of drug use• Useful websites• Detection Guidelines• Screening vs Confirmatory

Tests

85




• AMPHETAMINES / METAMPHETAMINES (including Tik)• BARBITURATES • BENZODIAZEPINES• CANNABINOIDS • COCAINE • MANDRAX (METHAQUALONE)• METHADONE• OPIATES• PHENCYCLIDINE

Specimen required for complete screen = 1 x urine.

* SEE INDIVIDUALLY LISTED DRUGS FOR MORE INFORMATION.

The drug testing information categorizes drugs by name, street name, mode of use, health effects, detection time, interferences and specimens required.

TOXICOLOGY SCREEN

86

DRUG STREET NAMES MODE OF USE DETECTION TIME & INTERFERENCES

SPECIMEN REQUIREDHEALTH EFFECTS


ALCOHOLBeerWineSpirits

Juice, dop, booze.

Oral. Loss of inhibitions, poor judgment, reduced coordination, sedation, respiratory suppression, slurred speech, clumsiness, euphoria, convulsions, hypothermia, hypoglycaemia.

7 – 12 hours. BLOOD:Fluoride (grey top) tube.

Can use SST (gel) tube but must be tested within 8 hrs.

(Do not clean the arm with alcohol).

AMPHETAMINESAmphetamineMethamphetamineEcstasyRitalinNobeseThinz

Speed, ice, uppers, meth, rock, glass, Obex, crystal, candy, crank, tik.

Ecstasy – Adam, eve, E, XTC, love drug.

Snorting, oral, smoking,injected.

CNS stimulant, euphoria, increased energy, appetite suppression, dilated pupils, restlessness, tachycardia, hypertension, dry mouth, headache, loss of coordination, sweating, insomnia, raised temperature, dehydration, nausea, muscle tension.

Use caution when driving / operating machinery as it causes dizziness, blurred vision.

Depends on urine pH: 2 - 4 days. In alkaline urine: up to 9 days.

Metamphetamine: 60hrs – 6 days.

Interferences:Decongestants (pseudoephidrine),diet pills, Zantac, blood vessel dilators, theophylline.

Urine.

BARBITURATESPhenobarbitalSecobarbitalPentobarbitalSeconalAmytalNembutal

Barbs, Bellatard, Mysoline, yellows, reds, downers, tranqs.

Oral, injected. Narcotic/suppressant. CNS depression, sedation, hypnosis, narcosis, coma, respiratory suppression, decreased heart rate & BP, euphoria.

Up to 2 weeks, but may be up to 21 days depending on the drug used. 18 days for chronic users.

Urine.

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BENZODIAZEPINESAnxiolyticsSedatives: eg RohypnolAnti-epileptics:eg ClonazepamMuscle relaxants

Downers, Panix, Valium, roofies, Librium, Ativan, Serepax.

Oral, injected. Narcotic, agitation, sedation, hypnosis, amnesia, muscle relaxation, disorientation, narcosis, nausea, dry mouth, euphoria, clumsiness, impaired memory, coma.

WITHDRAWAL: Tremors, insomnia, rebound anxiety, palpitations, panic attacks, metallic taste, auditory hallucinations, convulsions.CONTRA-INDICATIONS:Depression.

Depends on original substance half-life and metabolites & dosage taken.3 days – 30 days.

NSAID’s can give a false positive.

Urine.

CANNABIS Dagga, weed, hashish, marijuana, joint, zol, arms, bankies, boom, pyp, bong, skyf, THC, pot.

Smoking, oral (cooked and eaten in baked goods).

CNS stimulant, hallucinogen, euphoria, altered perception, memory loss, irritability, agitation, aggression, paranoia, hallucinations, learning problems, increased appetite, disorientation, photophobia, bloodshot eyes, increased pulse rate, irrational behaviour. Has high lipid solubility resulting in extensive storage in lipid compartments and slow excretion.

Casual/single use: 3 days.Moderate use (4xweek):5-7 days.Daily use:10-15 days.Chronic user: 3 to 6 weeks.

Efavirenz cross reacts with cannabis assays.

Urine.

COCAINE Coke, crack, rocks, blow, snort, powder, columbia(n), snow, bernies, flake.

Snorting, oral, injected, smoking.

CNS stimulant, euphoria, hyperactivity, increased libido, agitation, anxiety, hyperthermia, hypertension, tachycardia, convulsions, insomnia, decreased appetite & sleeptime, increased BP, paranoid delusions, impaired performance, sedation, depressed respiration, seizures.

24 – 36 hrs.

Chronic user:Up to 22 days.

Half-life:0.7 – 1.5 hrs.

Urine.

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LSDLysergic acid diethylamide

LSD, caps, squares, acid, microdots, candy.

Oral. Altered perception, hallucinations, flashbacks, vomiting, diarhoea, hyperthermia, inattention, dilated pupils, tachycardia, raised blood sugar, increased temperature, salivation, tearing.

48 hours, but may be up to 120 hours.

Urine.

METHAQUALONEMandrax

Mandrax, buttons, soapies, omo, surf, Mx.

Oral, smoked as ‘White pipe’ with dagga,Injected.

Sedation, hypotension, vertigo, respiratory suppression, slurred speech, disorientation, tingling sensation, dry mouth, loss of appetite, nausea, vomiting, headache.

Up to 14 days. Urine.

OPIATESHeroin (semi-synthetic derivative of morphine)Morphine (from poppy seed)Codeine (from poppy seed)Methadone (long acting opioid)Pethidine

MOP, smack, H, horse, mud, china white, mexican brown, tar, thai white, black pills, dreamer, hard candy, brown sugar and hard ball.

Snorting, smoking, injected.

Narcotic, analgesic, anti-tussive, anti-diarrhoeal. Euphoria, drowsiness, sedation, loss of appetite, emotional detachment, impaired vision, contracted pupils, moodiness, loss of weight, hypotension, nausea, vomiting, CNS depression, dizziness.

2 – 4 days.

Half-life:2 – 11 hrs.

Interferences: any substance that contains morphine eg OTC medicines with codeine – grandpa; food with poppy seeds; Rifampicin gives false positive.

Urine.

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PHENCYCLIDINE PCP, angel dust, crystal, magic dust, cyclone.

Oral, injected. CNS stimulant, anaesthetic used for hallucinogenic properties, depression, sensory deprivation, loss of inhibitions, raised BP & temperature, vomiting, agitation, loss of appetite, rapid involuntary eyeball movements, psychosis, stupor, coma, seizures.

1 – 4 days.

Chronic users: up to 21 days.

Urine.

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SPECIMEN COLLECTION

This procedure applies to all staff required to collect specimens for the testing of drugs of abuse (recreationaldrugs) including alcohol (if required) from employees brought in or sent by their employers.

PROCEDURE:

• Identify the employee.• Complete the requisition form.• Indicate for which drug/s the specimen must be

tested. (The drugs of abuse / recreational drug screen includes the following drugs: Urine Amphetamines; Barbiturates; Benzodiazepines; Cannabinoids; Cocaine; Mandrax (methaqualone); Methadone; Opiates; Phencyclidine).

• Obtain consent. Ask the employee to sign the con-sent form, informing them that they are also signing

agreement that all persons documented both on the requisition form and the consent form may be given a copy of the results. Make sure that all persons who may receive the results are documented on both forms.

• Explain the procedure for the collection of an unadul-terated urine specimen to the employee in a way they can understand.

SAMPLE COLLECTION PROCEDURE:

• Explain to the employee that we need to make sure that no specimen substitution or adulteration takes place. The employee must be treated gently as he/she may be nervous and resentful of the whole procedure.

• If possible call a male lab member to assist a male employee and a female member to assist a female employee.

• Ask the employee to remove his/her jacket and shoes and any other loose clothing. It is not necessary to strip

ADDITIONAL DRUG TESTING INFO

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the employee as far as underclothing. The lab member must briefly hand-search the employee, looking for any concealed container that might be used to substitute / adulterate / dilute the specimen. If the shoes contain no hidden containers, they may be put back on again.

• The sister/lab member must be present in the room during the passing of the specimen. Specimens must not be passed in the toilets as the toilet pan water may be used for dilution.

• The employee must pass urine into a clean container. ± 50 ml of urine is required. The staff member must trans-fer the urine into a specimen jar and label the container in front of the employee.

• If the employee has difficulty passing a specimen in front of the staff member, the staff member may stand immediately outside the door of the room – BUT THE DOOR SHOULD BE LEFT SLIGHTLY AJAR.

• If the employee has to be left alone during the passing of the specimen, the room in which the urine specimen is to be passed should not contain any bottles or tubes filled with liquid that could be used for dilution/adul-

teration. This method of passing urine should be used as a last resort only. In these cases, make a note on the request form whether the filled specimen jar was WARM or COLD. Cold specimens may indicate substitu-tion. See notes.

• Specimens brought in to the depot. Bring the possibility of specimen substitution or adulteration to the attention of the employer. The employer must take the responsi-bility for the quality of the sample.

• Unaccompanied employees delivering a urine sample must be asked to pass another sample as per above. If they refuse or are unable, document under clinical data that you cannot verify that the correct sample collection procedure has been followed.

NOTES:

• Shake the specimen to determine if soap has been added. Excessive bubble formation that is long-lasting can indicate an attempt to adulterate the specimen.

• Liquid drain cleaner, bleach, liquid soap, ammonia,


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hydrogen peroxide, lemon juice and eye-drops can be used to manipulate the urine.• Colour – normally ranges from pale yellow to clear depending on the

concentration. Urine specimens collected in the early morning are the most concentrated and usually provide the most reliable information. Unusual colours are due to medication, foods or diseases and should be recorded on the request form.

• Temperature – should initially be 32-38’C and can remain warmer than 33’C for up to 15 minutes. Temperatures outside this could indicate substitution.

• PH – normally 4.5 to 8.0. Suspect contamination if PH < 3 or > 11 or SG < 1.002 or > 1.020.

• Creatinine: The urine concentration may influence the result. A false negative result may be obtained with very dilute specimens.

• < 4mmol/L is an indication of a diluted specimen. < 1.8 mmol/L is too dilute for analysis and a negative result should be regarded as invalid.

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2A. INTOXICATION1. Subject to the provisions of sub-regulation (3), an employer or a user, as the case may be, shall not permit any person

who is or who appears to be under the influence of intoxicating liquor or drugs, to enter or remain at a workplace.2. Subject to the provisions of sub-regulation (3), no person at a workplace shall be under the influence of or have in his

or her possession or partake of or offer any other person intoxicating liquor or drugs.3. An employer or a user, as the case may be, shall, in the case where a person is taking medicines, only allow such

person to perform duties at the workplace if the side effects of such medicine do not constitute a threat to the health or safety of the person concerned or other persons at such workplace.

WORKPLACE SUBSTANCE ABUSE:The use of a potentially impairing substance to the point that it adversely affects performance or safety at work, directly through intoxication or hangover or indirectly through social or health problems.

Substance abuse policy:• Decide purpose and objectives.• Define substance abuse.• Decide who is covered.• Employee’s right to confidentiality.• Employee education.• Assisting chronic users (EAP).• How to deal with impaired workers.

EXTRACT FROM THE OHS ACT

• Circumstances of testing.• Disciplinary actions.

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•

HOW WOULD I KNOW IF SOMEONE ABUSES DRUGS?

USEFUL WEBSITESPRIVATE CLINICSCrescent Clinic: http://www.crescentclinic.co.zaStepping Stones: http://www.steppingstones.co.za

GOVERNMENT CLINICSTeen Challenge: Email: [email protected]

INTERVENTION & INFORMATIONSANCA (National Council on Alcohol/Drug Abuse)http://www.sancanational.org.za/treatment.htm orwww.sancawc.co.za

SUPPORT GROUPSNarcotics Anonymous: http://www.na.org.zaNar-anon: http://www.naranon.org.za(Support for family and friends of addicts)Alcoholics Anonymous: http://www.alcoholics.org.zaAlanon and Alateen: http://www.alanon.org.za(Support for family and friends of alcoholics)

• Change of behaviour / character.• Change of friends.• Restlessness and Insomnia.• Tiredness; irritability; drowsiness.• Loss of eye contact.• Away from home a lot.• Deterioration of hygiene / untidiness.• Secretive telephone calls. • Blood-shot eyes.• Loss of weight.• Unnaturally talkative.• Wearing of sunglasses indoors; using eye drops.• Giggle attacks.• Deterioration of academic achievements.• Adaptation of symbols, tattoos.• Loss of coordination / slow reactions.• Paranoia.• Amnesia.• Smell of smoke / dagga.• Yellow / brown stains on hands.• Criminal activities.

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DRUGS OF ABUSE - DETECTION LIMIT GUIDELINES

How long do drugs stay in your system?The length of time that the presence of drugs of abuse in the body can be detected is an important factor in drug screen-ing. The chart below outlines approximate duration times in human urine. When interpreting the duration for the presence of drugs of abuse in the body, you must take into consideration variables including the body’s metabolism, the subject’s physical condition, overall body fluid balance, state of hydration and frequency of usage. The amount of time that a drug/metabolite remains detectable in urine can vary, depending on the following factors:

• Amount and Frequency of Use: Single, isolated, small doses are generally detectable at the lower boundary. Chronic and long- term use typically result in detection periods near or at the upper boundary.

• Metabolic Rate: Individuals with slower body metabolism are prone to longer drug detection periods.• Body Mass: In general, human metabolism slows with increased body mass, resulting in longer drug detection periods.

In addition, THC (marijuana’s active ingredient) and PCP are known to accumulate in fatty lipid tissue. Chronic users, physically inactive users, and individuals with a high percentage of body fat in relation to total body mass are prone to longer drug detection periods for THC and PCP.

• Age: In general, human metabolism slows with age, resulting in longer drug detection periods.• Overall Health: In general, human metabolism slows during periods of deteriorating health, resulting in longer drug

detection periods.• Drug Tolerance: Users typically metabolize a drug faster once a tolerance to the drug is established.• Urine pH: Urine pH can impact drug detection periods. Typically, highly acidic urine results in shorter drug detection

periods.

Note: In a small percentage of cases, users may test positive longer than times shown - mostly because of above-mentioned variables.

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DRUG COMMERCIAL NAMES DRUG CLASS / USE DETECTION TIMESTREET NAMES


Amphetamine Dexedrine, Benzedrine, Biphetamine

Speed, Black Beauties, Crosses, Hearts, Bennies, Truck driver, Uppers, LA turnaround, Hi, Hiballs,Beans

ADHD, Obesity, Narcolepsy

1 to 3 days (Highly pHdependent)

Methamphetamine Desoxyn, Methedrine Crank, Crystal, Ice, Speed, Chalk, Fire, Glass, Go fast, Meth

ADHD, Obesity, Narcolepsy

1 to 3 days

Ecstasy DOB, DOM, MDA, MDMS (3.4-Methylne- dioxymetamphetamine)

Ecstasy, XTC, ADAM, Lover’s speed, STP, Disco biscuits

None. 1 to 3 days

Cocaine Cocaine hydrochloride

Coke, Crack, Rock cocaine, Snow, Flake, Rocks, Blow, Charlie, Toot, Sugar, Nose candy, Base

Local anesthetic,Vasoconstrictor

1 to 4 days

Cannabinoids (THC)

(Cut-off - 50)

Marijuana, Marinol Dope, Weed, Hash, Hemp, Colombian, Pot, Blunt, Grass, Reefer, Sinsemilla, Mary Jane, Skunk, MJ, Roach, Blunts

Antiemetic, insomnia, weight loss, Glaucoma, Spasticity in multiple sclerosis, Alzheimer’s disease, Mental disorders, Pain, etc.

Single use:

2 to 4 daysModerate use: (4x per week) Up to 5 days

Heavy use (Daily): Up to 14 days

Chronic use/very high body fat:Up to 30 days

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Phencyclidine PCP, Sernylan Angel dust, Boat, Hog, Love Boat, Peace pill, Silver/gold glitters, Star dust

Anesthetics (veterinary) Single use:Up to 14 days

Chronic use: Up to 30 days

Codeine Tylenol, Empirin, RobitussinA-C

Captain Cody, Cody, Schoolboys, Doors & fours, Pancakes & syrup

Analgesic, Antitussive 3 days

Barbiturates (not Phenobarbital)

Amobarbital (Amytal), Seconal, Donnatal, Nembutal

Downers, Barbs, Goof balls, Reds, Yellow jackets, Phennies, Tooies, Red birds, Yellows, M&M’s, Sleepers

Anesthetic, Anticonvulsant, Hypnotic, Sedative

Short acting:2 days

Long acting:1 - 3 weeks

Phenobarbital Barbita, Comizial, Gardenale, Fenilcal, Luminal, Solfoton

Purple hearts Epilepsy, Short-term treatment of anxiety, sleeplessness, tension and fear.

7 - 14 days

Benzodiazepines Diazepam (Valium), Oxazepam (Serax), Chlordiazepoxide, Chlorazepate, Librium, Xanax, Serax, Restoril, Tranxene

Bennies, Roofies, Tranks, Xanax Antianxiety, Anticonvulsant, Hypnotic, Sedative

Therapeutic use:+/- 3 days

Chronic use (1 or more years):4 to 6 weeks

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Rohypnol (Rape drug) Falls in the class ofBenzodiazepine drugs.

Roofies, Roche, R-2, Rip and rope, Rophies, Circles

Hypnotic, Sedative, Muscle relaxer, Tranquilizer

Single use:8 hours (may be up to24 hours)

Long term use:2 to 4 days

Gamma-Hydroxybutyerate (Rape drug)Cannot perform test

GHB G, Liquid X, Liquid E, Scoop, Soap, Gook, Easy Lay, Gamma 10, Grievous Bodily Harm, Georgia Home Boy, Natural sleep-500, Cherry, Salty water

Analgesic, Hypnotic, Sedative, Fat burner

8 hours (may be up to24 hours)

Morphine Duramorph, Roxanol Chasing the Tiger, M, Miss Emma, Monkey, White stuff

Analgesic 1 to 3 days

Heroin Diacetylmophine Smack, Tar, Brown sugar, Junk, White horse, Skunk, H, Dope, Horse, Scag, Black Tar, Jones

None 1 to 4 days

LSD Lysergic acid diethylamide

Acid, Microdot, Sugar, L, Blotter

None 2 to 24 hours (May be up to 3 days

Methadone Amidone, Dolophine, Methadose

Fuzzies, Done, Junk, Jungle juice

Analgesic, Treatment for opiate dependence

3 days (may be up to 7 days)

Propoxyphene Darvon, Darvocet, Novopropoxyn

Yellow footballs Analgesic 6 hours to 2 days

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Methylphenidate Ritalin, Concerta (A time-release capsule), Metadate, Methylin, Rubifen

Kibbles and bits, Kiddy cocaine, Diet Coke, Kiddy Coke, Skittles, R Pop, Coke Junior, Study buddies, Poor Man’s Cocaine, Pineapple, Skippy, Jif, Uppers, Rids, Smarties, Smart Drug, Vitamin R, R-Ball, West Coast

ADHD, narcolepsy 1 to 2 days

Nicotine (Cotinine - breakdownproduct of nicotine)

Habitrol patch, Nicorette gum, Nicotrol spray, Prostep patch

Cigars, Cigarettes, Smokeless tobacco, Snuff, Spit tobacco

Treatment for nicotine dependence

BLOOD Infrequent user:1 - 2 days

Chronic user:up to 14 days (May be up to 30 days)

Mescaline (Obtained from a small, spineless cactus Peyote - Lophophora Williamsi) Cannot perform test

Mescalito Buttons, Cactus, Mesc, Peyote None 1 to 3 days

Ketamine Ketamine, Ketalar, Vetalar, Vetaket

K, Kit Kat, Vit K, Special K, Super acid, Jet

Anesthetic, Hallucinogen(Veterinary)

1 to 3 days

Psilocybin (Mushroomscontaining psilocybin and psilocin)Cannot perform test

Indole of the tryptamine family

Magic, Mushroom, PurplePassion, Shrooms

None 1 to 3 days

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Hashish Same group as THC Hash, Boom, Hash oil, Hemp, Chronic gangster, Nup

Weight loss, insomnia 1 to 30 days (See specific times with Cannabis)

Anabolic Steroids Testosterone (T/E ratio), Stanazolol, Nandrolene, Oxandrin, Anadrol, Durabolin, Equipoise

Roids, Juice Hormone replacement therapy

Oral:+/- 3 weeks

Injected:+/- 3 months

Opium Laudanum, Paregoric Dober’s powder, Big O, Black stuff, Block, Gum, Hop

Analgesic, antidiarrheal 6 hours to 2 days

Methaqualone Quaalude, Sopor, Cateudil, Isonox, Motolon, Normi- Nox, Optimil, Parest, Revonal, Somnafac, Sovinal

Quaalude, Ludes, Mandrax, buttons, disco biscuits, love drug, ludes, mandies, mandrakes, quads, quay

Depressant, treatment for insomnia

6 days (May be up to2 weeks)

Fentanyl (Synthetic opiate)

Actiq, Duragesic, Sublimaze Apache, China girl, China white, Dance fever, Friend, Goodfella, Jackpot, Murder 8, TNT, Tango and Cash

Chronic pain, Analgesic

8 to 24 hours (May be up to 3 days)

Oxycodone Oxycontin, Percodan, Percocet, Roxicodone

Oxy, O.C., Killer, Oxycotton, Hillbilly Heroin

Analgesic 8 to 24 hours (May be up to 3 days)

Dextromethorphan Robitussin, Vicks, Dimetapp, NyQuil, Coricidin, Tussin, Delsym

DXM, CCC, Triple C, Skittles, Robo, Poor Man’s PCP

Cough suppressant, Antihistamine, Decongestants

1 to 3 days (Not proven)

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Tri-CyclicAntidepressants

Adapin, Amitriptyline, Amoxapine, Asendin, Desipramine, Doxepin, Elavil, Imipramine, Ludiomil, etc.

TCA, Downers, Blue Angels, Blue Birds, Janimine

Antidepressants Therapeutic: Up to 3 days

Extended use:7 to 10 days

Alcohol Ethanol Alcohol Beer , Wine, Liquor Antidote to methanol poisoning

BLOOD1 to 12 hours

References available: Please contact Special Operations.

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SCREENING VS. CONFIRMATORY TESTS

There are two main categories of urine drug testing - screening and confirmatory. Screening tests are initial qualitative drug tests conducted to identify classes of drugs present in the urine and typically are done using immunoassay. They rely on a set threshold above which a positive result is produced and therefore do not detect lower concentrations of a drug. Can also cause false positive results. Can also cross-react.

Confirmatory tests are used for further analysis of a sample - to confirm whether a positive or sometimes negative, result and typically are done using gas chromatography / mass spectometry (CG/MS), liquid chromatography / mass spectrometry (LC/MS) or high performance liquid chromatography (HPLC). Confirmatory testing can identify a specific drug. It has a higher level of sensitivity and selectivity: maintains stability of the compounds; extensive libraries of compounds also used for non-volatile and thermally fragile molecules. If the goal is to detect a synthetic or semisynthetic opioid, this test should be used as immunoassays do not typically detect these opioids. Below is a comparison of the general characteristics of these two types of testing:

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Screening Confirmatory

Analysis Technique Immunoassay Gas Chromatography - Mass Spectometry (GC-MS) or Liquid Chromatography - Mass Spectrometry (LC-MS) or High Performance Liquid Chromatography (HPLC)

Sensitivity (power to detect a class of drugs)

Low or none when testing for semisynthetic or synthetic drugs

High

Specificity (power to detect an individual drug)

Varies based on assay used - can result in false positives and false negatives

High

Use Qualitative analysis: detects classes of drugs (Heit and Gourley, 2004)

Quantitative analysis: identifies a specific drug

Cost Inexpensive More expensive

Turnaround On-site rapid Slow

Other Intended for use in drug-free population; may not be useful in pain medicine context

Legally defensible results at some laboratories

SCREENING VS. CONFIRMATORY TESTS

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ARTICLES & RESOURCES

Article Index:

• Aluminium• Arsenic• Chromium• Halogenated Hydrocarbons• Lead• Manganese• Mercury• Testing Drugs of abuse 1• Testing Drugs of abuse 2


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John C Stanfliet, Chemical Pathologist, PathCare; email: [email protected] Schillack, Analytical Toxicologist, V&M ATLS Director; e-mail: [email protected] Essack, Chemical Pathologist, PathCare; email: [email protected]

Keywords: aluminium, occupational health, dementia, contamination, biomonitoring

ABSTRACTAluminium (Al) is a commonly encountered metal that has proven deleterious health outcomes, including neurological, respiratory and other systemic effects. There is growing awareness of the need to identify workers who have an increased burden of Al in order to avoid further exposure and to institute remedial action as appropriate. This need requires accurate identification of such workers. This paper examines the metabolism of Al with the aim of suggesting effective biomonitoring methods.

INTRODUCTIONAluminium (Al), although considered harmless for many years, is one of a number of toxic metals shown to be associated with adverse health effects. It is an abundant metal, comprising about 8% of the earth’s crust. The daily intake of Al from food, cooking utensils, food additives and packaging has been estimated at 4-80 mg. However, in patients taking antacids containing Al, it can be considerably higher. Al can also be found in water, air, personal grooming products, parenteral nutrition, breast milk and as an adjuvant in vaccines. Occupational exposure takes place in Al smelters and Al welding operations, and in the general Al industry. Al has multiple uses in a number of industries and occupational health practitioners are encountering instances of Al exposure more frequently.

ALUMINIUM MONITORING IN OCCUPATIONAL HEALTH - A MINI REVIEW

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Al toxicity depends on its solubility and on delivery to the tissues of trivalent Al (+3) which generates oxygen radicals and damages target organs; by contrast, insoluble forms cause damage by their particulate nature. Al can be absorbed from the gut or the lungs into the systemic circulation. Al is distributed widely to organs such as the liver, bone, muscle and brain, with highest levels found in lung tissue. It can accumulate with long-term exposure and the body’s burden of Al may remain elevated for many years following cessation of occupational exposure. Urine is the main route of elimination; hence, the development of Al toxicity in patients with uraemia. The elimination half-life of Al is complicated and it appears that, following acute exposure, it is in the order of days, whereas it may be as long as three years in those who are exposed chronically.

ALUMINIUM TOXICITYThe clinical picture of systemic Al toxicity includes dementia, repeated infections, microcytic anaemia, osteodystrophy and joint pains. Occupational exposure has been associated with potroom asthma, adverse neurological outcomes, and contact and irritant dermatitis. Some longitudinal studies have failed to demonstrate conclusive evidence of neurotoxicity in Al welders, although the levels of Al accumulation demonstrated were much lower than those seen in patients with dialysis- associated encephalopathy. While It is clear that Al toxicity causes neurological damage as exemplified by dialysis dementia, most researchers no longer believe that Al is causally associated with Alzheimer’s disease. However, respiratory function may be adversely affected. For example, San et al. found that serum Al was significantly higher in exposed workers compared with controls and was inversely correlated with respiratory function.


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ALUMINIUM BIOMONITORINGAl can be measured in plasma, serum or urine. There is wide variation, as much as eight-fold, in reference intervals amongst laboratories, samples, and also between methods. Normal blood and plasma Al levels may vary from 2-40 µg/L and normal urine concentration in people who are not exposed via their occupation is usually < 3 µg/L. The reasons for these wide variations are that often the reference intervals have been derived from sample populations that included patients with uraemia or who were receiving dialysis. Patients with an increased plasma Al > 200 µg/L have a high risk of developing an occupational disease. However, a serum Al level within the reference interval does not exclude Al toxicity. In subjects with normal renal function, urine is preferred to serum as the sample of choice. In occupationally-exposed pa-tients, urine Al may be elevated, whereas serum Al may be little changed compared with controls.

There is debate as to the correlation between Al concentration in the air to which workers are exposed and levels of Al found in either their urine or serum, emphasising the need for individual monitoring. Elinder et al. showed a strong correla-tion between urinary Al concentration and the number of years of exposure in Al welders; this correlation was absent in controls. Urine Al pre-shift reflects the body’s burden of Al, whereas urinary Al at the end of a shift reflects recent exposure. Urinary Al levels were unchanged in 12 workers one year after cessation of Al welding activity, whereas serum Al halved in the same time period.

Graphite furnace atomic absorption spectrophotometry has been the analytical method of choice for many decades but the new technology of inductively coupled plasma mass spectrometry offers very low limits of detection with the added benefits of speed, accuracy and the ability to measure multiple toxic metals in the same sample. Al is ubiquitous and unexpected contamination of the sample during the collection, storage, sample preparation and analysis are important


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causes of false positive results, and should be avoided. Close liaison with the clinical laboratory is an important resource in this regard. Table 1. Practical Aspects of biological monitoring for workers exposed to Aluminium

Parameter Urine

Confounding factors; sources of error

• High risk of contamination – close collabora-tion with the laboratory is needed

• Al-containing food, water or medications

Half-life Appears to be complicated; at least one short (hours-days) and one long (years)

Reference interval (non-occupationally exposed)

< 30 µg/L

Guidelines for occupationally exposed subjects

• DFG: BAT 200 µg/L (ES)• FIOH 160 µg/L (ES)

DFG: Deutsche Forschungsgemeinschaft; BAT: Biological tolerance level; FIOH: Finnish Institute of Occupational Health; ES: end of shift


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TREATMENT OF AL TOXICITYUrine is the preferred sample matrix and industry guidelines have been established (Table 1); repeated serum or plasma Al levels of 50-100 µg/L warrant intervention probably. The management of patients with established Al toxicity is based upon avoidance of further exposure and reduction of the body’s Al burden via treatment with chelating agents. Deferrioxamine is used as one such agent to treat documented Al toxicity, although newer agents are being investigated. There is a paucity of data on the outcomes with chelation therapy, although there are anecdotal reports and trials involving small numbers of patients.

CONCLUSIONAl is a common metal and there is increasing interest in its potential role in human disease. All workers who are exposed to Al should be monitored at some stage as there is great individual variation. Urine is the preferred sample except in those with compromised renal function. Results should always be interpreted in line with the clinical setting. The potential for false positive results, because of the possibility of Al contamination during the testing process, needs to be borne in mind and discussed with the clinical laboratory, as appropriate.

REFERENCESRefer to OH Journal of SA, Vol 21 No 1 Jan / Feb 2015 or contact Special Operations.


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Volker Schillack – V&M Analytical Toxicology Laboratory Services, Director, e-mail: [email protected] John Stanfliet – PathCare Chemical Pathologist, e-mail: [email protected] Younus Essack – PathCare Chemical Pathologist, e-mail: [email protected]

INTRODUCTIONArsenic (As) and other heavy metals [mercury (Hg), lead (Pb), cadmium (Cd), antimony (Sb), chromium (Cr) and manganese (Mn)] are regarded as toxic to living organisms. Their tendency to accumulate, metabolize and target selective tissue is very often a result of their different oxidation states, such as As(V) or As(III). These highly toxic heavy metals have the potential to cross tissue membranes, which may lead to neuro-, nephro-, onco, terato- and immunological disorders.

The toxicity and mobility of arsenic in the environment is dependent on the chemical form in which it exists. Numerous arsenic species are present in the environment and biological systems. Like many other heavy metals, it exists in the environment in a number of oxidative states. It is only recently that scientists realized the impact that certain arsenic states have on the general health of workers. The Agency of Toxic Substances and Disease Registry and the United States Environmental Protection Agency have categorised arsenic as a human carcinogen.

Occupational exposure to arsenic is a major concern for workers involved in the processing of copper, gold, lead, and antimony ores; producing and using arsenicals and arsenic- containing pesticides; burning of arsenic-containing coal in

ARSENIC PERSISTENT HAZARD

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power plants and treating wood with arsenic preservatives or working with such treated wood. Chronic low dose exposure to arsenic compounds is now officially a greater concern than acute exposure, mainly because of the carcinogenic effects of chronic exposure.

METABOLISMAbout 70-90% of ingested inorganic arsenic is readily absorbed from the gastrointestinal tract and then distributed to different organs. Organic arsenic, such as arsenobetaine (AsB), is absorbed completely. Soluble arsenic compounds, e.g. arsenic trioxide, is absorbed rapidly from the lungs, while lead arsenate and calcium arsenate dissolve slowly and are generally retained longer. Inorganic arsenic exposure times are the longest on the skin, gastrointestinal tract, epididymis, thyroid, and skeleton, with the highest concentrations observed in the hair, nails, skin and lungs. Under ideal conditions, the inorganic arsenic is methylated in the body, mainly in the liver, and excreted into the urine as free inorganic arsenic, viz. As (III) and As(V) at 10-20%, monomethylarsonic acid (MMA 10-15%), and dimethyl arsenic acid (DMA 60-80%).

Biomethylation of arsenic is the major metabolic pathway for the metabolism of inorganic arsenic in humans and other mammals. Figure 1 illustrates how (1) inorganic arsenate As(V) is reduced to arsenite As(III) (2) As (III) is oxidatively methylated to monomethylarsonic acid (MMAs(V)), (3) MMAs(V) is reduced to monomethylarsonous acid (MMAs (III)) and then further methylated to dimethylarsinic acid (DMAs(V)), and (4) further steps produce dimethylarsinous acid (DMAs (III)) and trimethylarsine oxide (TMAsO) which, in turn, can be reduced to trimethylarsine (TMAs(III)). The process of methylation is considered complete with the formation of DMAs (V) and probably di-methyl arsinous acid DMAs(III). Recent studies have identified the organic methylated trivalent species as being toxic - even more toxic than the inorganic arsenic species (As2O5 and As2O3).


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Figure 1. Biomethylation of arsenic (Refer to Special Operations).

There are confounders that affect the metabolism of arsenic. Medications, illicit drug use, herbal or traditional medicine, or a diet high in seafood may inhibit the effective metabolism of arsenic by the hepatic cytochrome P450 enzyme system. Confounders that inhibit the natural metabolic process or that deplete the active hepatic enzymes cofactor sites will also result in the accumulation of toxic substances which, in turn, lead to secondary health effects.

Very often, workers exposed to arsenic are subjected to other heavy metals such as Hg, Pb, tin (Sn) and thallium (Th) which compete for the same sites or follow the same detoxifying pathways. Such instances may result in the accumulation of metals. When arsenic exposure exceeds threshold levels or when confounders exceed the methylation capacity, excess arsenic can be retained for longer periods of time resulting in the deposition of arsenic into target tissues with adverse health effects. It has been shown that cigarette smokers have significantly higher urinary total arsenic and MMA(V) levels, and lower secondary methylation index rates, than non-smokers. It is possible that some chemicals in cigarettes compete for some of the enzymes or co-factors involved in the methylation processes, particularly those involved in the second methylation phase.

The capacity of exposed workers to metabolize and detoxify the adsorbed inorganic arsenic is believed to play an important role in disease development. This individual susceptibility may involve genetic and/or acquired factors. The


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proportional ratio of MMA/DMA or levels of urinary species can be used as indicators in the effective metabolism of inorganic arsenic. The concentration of inorganic arsenic in urine represents the unchanged proportion of the exposed dosage, while the MMA and DMA in urine represent the activity of the first and second metabolic phases, respectively.

HEALTH EFFECTSChronic exposure to high levels of arsenic has been correlated with cancers of the skin, bladder and lung, as well as hypertension and cardiovascular effects. Several studies on smelter workers suggest that chronic inhalation exposure to arsenic trioxide increases the risk of death from cardiovascular and cerebrovascular disease. Acute intoxication from inor-ganic arsenic may cause irritation of the gastrointestinal tract and respiratory tract (rhinitis, pharyngitis, and bronchitis). The skin is the critical organ affected, following long-term oral exposure. Skin and mucous membrane lesions include melanosis, hyperpigmentation, depigmentation, hyperkeratosis and skin cancer. Long-term exposure may also affect the peripheral nervous system and cardiovascular system, e.g. Blackfoot disease and Raynaud’s syndrome, as well as the hematopoietic system (anaemia and leukopenia).

THE CARCINOGENICITY OF ARSENICSignificant evidence in the literature is available, suggesting arsenic’s contribution to the incidence of human cancer. Epidemiological studies have demonstrated increased risks of lung cancer among workers exposed to arsenic. Further evidence has demonstrated lung cancer in ore smelters and skin cancer in people exposed to arsenic containing drinking water. Although it has been more than 100 years since the carcinogenic properties of arsenic were suggested, it is still uncertain as to whether inorganic arsenic can cause other cancers apart from lung and skin. Stōhrer (1991) concluded that: (1) more than 400µg arsenic/day is required to cause arsenical disease; (2) skin cancer, internal cancer, and other non-cancerous effect of arsenic all have the same threshold dose and probably result from the same primary


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interaction; (3) hyperpigmentation can therefore serve as a sensitive indicator of arsenic exposure and future cancer risk; (4) synergistic interaction changes the log-normal dose response slope but does not affect the intercept or threshold dose. Possible mechanisms describing the carcinogenicity of arsenic are illustrated in Figure 2. Arsenite (the most likely active carcinogenic species) acts as a non-genotoxic indirect carcinogen, possibly via induction of oncogene expression and inhibition of DNA repair.

Figure 2. Proposed mechanism of Arsenic carcinogenicity (Refer to Special Operations).

BIOLOGICAL MONITORINGThe true toxic status and bio-availability of arsenic compounds can only be determined if all known forms can be identified and quantified. The measurement of total arsenic in biological samples has, for many years, been the preferred method of identifying possible arsenic exposure. Recent studies have demonstrated the importance of arsenic specification in biological and environmental samples, as toxicity is generally dependent on their chemical structure and valency state.

The measurement of total arsenic concentration in urine represents the first step in identifying individuals exposed to arsenic compounds. Arsenic speciation, which includes the analysis of DMAs (V), MMAs (V) and the major inorganic arsenic species in urine, allows for a better understanding of the exposure, metabolic rate and species to which the individual has been exposed. Table 1 lists the different inorganic and organic arsenic species that have thus far been classified as possible carcinogens.


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Table 1. List of arsenic species present in biological samples

Name Abbreviation Chemical formula

Arsenite, Arsenous acid As(III) As(OH)3

Arsenate, Arsenic acid As(V) AsO(OH)3

Monomethylarsonic acid MMAs(V) CH3AsO(OH)2

Monomethylarsonous acid MMAs(III) CH3As(OH)2

Dimethylarsinic acid DMAs(V) (CH3)2AsO(OH)

Dimethylarsinous acid DMAs(III) (CH3)2AsOH

Trimethylarsine oxide TMAsO (CH3)3AsO

Trimethylarsine TMAs(III) (CH3)3As

Arsenobetaine AsB (CH3)3As+CH2COO-

Arsenochline AsC (CH3)3As+CH2CH2OH

Tetramethylarsonium ion Me4As+ (CH3)4As+

Dimethylarsinoyl ethanol DMAsE (CH3)2AsOCH2CH2OH Total arsenic in urine generally reflects inorganic arsenic if the intake of arsenobetaine in seafood is limited. Urinary concentrations of total arsenic in the range 50 to 100 µg/l may be due to seafood, dietary sources and supplements containing arsenic, or inhalation of air containing arsenic. In studies of smelter workers, a significant correlation was found


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between airborne time-weighted average (TWA) exposure to arsenic trioxide and the inorganic arsenic metabolites found in urine collected immediately after the shift, or just before the next shift. Table 2 includes the proposed references for the biological monitoring of arsenic, with the different matrices that can be used for testing purposes.

Table 2. Biological monitoring of arsenic

Measured by HPLC- ICP/MS *

Biological parameter measured

Biologicalmatrix

Normal reference value

Maximum Permissible Concentration

Remarks

Arsenic total arsenic urinebloodhair

<30 µg/g cr.< 10 µg/l< 1 µg/g

55 µg/g cr. In the absence of seafood and arsenic-contam-inated drinking water

sum of As3+& As5+ and MMA & DMA

urine <10 µg/g cr. 55 µg/g cr.If TWA: 50 µg/m3

inorganic arsenicAs3+& As5+

urine <1.5µg/g cr. 13 µg/g cr. If TWA: 50 µg/m3

No interference from seafood

*HPLC-ICP/MS – High Performance Liquid Chromatography – Inductive Couple Plasma / Mass Spectroscopy


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As noted, workers exposed to arsenic are often subjected to other heavy metals, which can interfere with arsenic metabolism. It is therefore important to consider the analysis of these secondary heavy metals. The analytical toxicology data in Table 3, illustrate the importance of measuring the different arsenic species in workers that chronically exceed the urine arsenic biological exposure index (BEI) threshold. Urinary concentrations of arsenic are presented in µg/l and are expressed to creatinine as a ratio (µg/g). Table 3 highlights the importance of arsenic speciation versus the total arsenic concentration. The arsenobetaine concentration due to seafood intake should be noted in respect to the arsenic/creatinine ratio for samples 100/01 and 100/04.

Table 3. Speciation data of urinary arsenic from workers exposed to high concentrations of heavy metals in dust particulate

Sample AsB DMA As(III) MMA As(V) Tot As (µg/L)

Tot As (µg/L)

% Diff g/l µg/g

100/01 37.2 362.3 58.0 177.8 26.9 662.2 717.1 92.3 1.14 580.9

100/02 238.0 17.1 119.4 19.7 392.1 394.1 99.5 0.71 552.2

100/03 120.0 10.2 75.1 13.4 216.6 267.5 81.0 2.31 93.8

100/04 17.4 301.6 22.7 286.5 61.4 689.8 713.9 96.6 0.86 802.0 Under ideal conditions, a ratio of 3:1 for DMA: MMA, is regarded as a good indicator of methylation efficiency. However, this


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is not the case for workers chronically exposed to threshold levels of inorganic arsenic. The methylation efficiency ratio of DMA to MMA tends to be much closer to 3:2 in these individuals. More importantly are the high levels of inorganic As(III) and As(V) which exceed the recommended thresholds indicating a fairly low rate of methylation and possibly resulting in the accumulation of arsenic compounds (body burden effect) over time.

CONCLUSIONThe objective of occupational toxicology is to prevent injury to workers exposed to hazardous chemicals by determining whether certain set thresholds (BEI, BAT, OEL or TWA) have been exceeded. Technological advancements in the field of analytical toxicology has over time played an important role in the work up of individuals chronically exposed to arsenic. Arsenic speciation and the analysis of other heavy metals provide valuable information to the practitioner, which may contribute to the overall effective management of individuals.

REFERENCESRefer to OH Journal of SA, Vol 20 No 4 Jul / Aug 2015 or contact Special Operations.


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CHROMIUM IN OCCUPATIONAL HEALTH - A MINI REVIEW

Younus Essack, Chemical Pathologist, PathCare; email: [email protected] C Stanfliet, Chemical Pathologist, PathCare; email: [email protected] Schillack, Analytical Toxicologist, V&M ATLS Director; email: [email protected]

ABSTRACTChromium (Cr) is a metal that occurs naturally in the environment in the form of metal-ores such as those containing iron. Workers in industry may be exposed to trivalent and hexavalent Cr compounds which have strikingly different metabolic handling and toxicity. The understanding of these properties is important when assessing the risk of potential harm to health.

INTRODUCTIONCr is a metal that is widely distributed in the earth’s crust (soil and rocks), air and water. Naturally occurring Cr occurs mainly in the Cr (III) form as chromite ore, which contains oxygen and other metals, such as iron, whilst Cr (VI), on the other hand, is produced commercially from chromite ore, for a wide variety of uses.

Cr is used in three basic industries: the metallurgical, chemical and refractory (heat resistant applications) industries. These are the most important industrial sources of Cr in the atmosphere. In the metallurgical industry, Cr is an important component of stainless steels and various metal alloys. Cr-based metal alloys are also used as joint prostheses and are widely used in clinical orthopaedics. In the chemical industry, Cr is used primarily in chrome plating, leather tanning, paint pigments and in wood treatment.

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The general population may be exposed to Cr through inhalation, or by ingesting food and drink containing Cr. Cr (III) is an essential element and has been shown to have clinical benefits. It plays an important role in the maintenance of normal carbohydrate, lipid and protein metabolism.

PHARMACOKINETICS AND CLINICAL PRESENTATION The toxicity of Cr is mainly attributed to hexavalent Cr (VI). Exposure to Cr dust or vapour has an effect on the respiratory system, leading to nasal irritation, itching, rhinorrhea, epistaxis, and even asthma in Cr sensitive individuals. Acute ingestion of high doses of Cr has effects on the respiratory, cardiovascular, gastrointestinal, hepatic, renal and neurological systems. Patients may present with circulatory collapse and delayed onset renal failure (12-24 hours after exposure).

Dermal exposure to Cr compounds (VI) leads to contact dermatitis and eczema in sensitized individuals, and to chrome ‘holes‘(sores or dermal ulcers) which can penetrate deep into the skin if left untreated.

One of the major concerns regarding Cr (VI) is the risk of cancer. The International Agency for Research on Cancer (IARC) has classified Cr as a human carcinogen. Breathing air, containing Cr (VI) compounds for prolonged periods may cause lung cancer, e.g. in workers involved in the production of chromates and chromate pigments. Ingestion of Cr (VI) in food or water, however, is not thought to cause cancer.


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Unlike Cr (III), Cr (VI) readily crosses cell membranes. In the cell, Cr (VI) is reduced to Cr (III), a reduction process leading to reactive intermediates such as Cr (V), Cr (IV) and radical species. Cr is excreted primarily via urine where elimination is shown to be rapid. Kinetic studies have suggested the existence of three compartments, demonstrating half-lives of approximately seven hours, 15 - 30 days and three years, respectively. The last few years have seen a lot of interest in blood cobalt (Co) and Cr concentrations in patients with metal hip prostheses. Orthopaedic surgeons have demonstrated a relationship of these metals to clinical events affecting hip replacements. Although the majority of Metal on Metal (MoM) hip replacements has been successful, multiple recent reports have documented markedly increased Co and Cr concen-trations in the joint synovial fluid, periprosthetic tissue, blood, and even peripheral tissues of some patients with MoM hip prostheses. Concerns have been raised regarding the physiological consequences of metal release from MoM hip prostheses into the periprosthetic tissue and systemic circulation. This has led to the Medicines and Healthcare Products Regulatory Agency (MHRA) in the United Kingdom issuing a Medical Device Alert advising that all patients with MoM im-plants be followed annually for at least five years, with blood Cr and Co measurements taken when indicated.

BIOLOGICAL MONITORING OF CHROMIUMThe determination of Cr in urine seems to be the most practical biological method for assessing exposure to water soluble Cr (VI) compounds. It is important to note that urine levels do not exclusively reflect exposure to Cr (VI). They provide information on total Cr exposure, including Cr (III), from occupational and non-occupational sources (dietary and environmental). Studies have demonstrated that urinary Cr is influenced by both recent and past exposure, whereas the difference between Cr values in spot samples collected at the end, and before the work shift reflect current exposure. Cr accumulation is demonstrated by an increasing pre-shift Cr level during the working week, with slowly decreasing urinary Cr levels during periods of discontinued exposure.


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The American Conference of Governmental Industrial Hygienists (ACGIH-2015) has adopted 10 µg/L as the biological exposure index (BEI) increase during a shift, and 25 µg/L BEI at the end of shift (end of work week) corresponding to a time weighted average (TWA) of 0.05 mg/m.

Table 1. Practical aspects of biological monitoring of workers exposed to Chromium

Parameter CR in Urine

Confounding factors Contamination, diet, supplementation MoM prosthesisSmoking status (urinary Cr levels are higher in smokers)

Reference value <1 ug/g creatinine (non-occupationally exposed individuals)

ACGIH BEI (TLV-TWA: 0.05 mg/m3)

Water soluble Cr VI compounds: 10 ug/L creatinine (ES-PS)25 ug/L creatinine (ES-end of work week)

ACGIH - American Conference of Governmental Industrial Hygienists; BEI - biological exposure index; ES - end of shift; PS - pre-shift.


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CONCLUSIONThe carcinogenic nature of Cr (VI) makes it important that the biochemical pathways and valency states be understood during the monitoring process. One of the emerging concerns nowadays is the effect on patients with MoM prosthesis. The occupational practitioner must take into consideration all confounding factors when monitoring exposed individuals.

REFERENCESRefer to OH Journal of SA, Vol 21 No 3 May/Jun 2015 or contact Special Operations.


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HALOGENATED HYDROCARBON PROFILE UPDATE

Halogenated hydrocarbons are a subgroup of aromatic hydrocarbons, in which one of the hydrogen molecules is substituted by a halogen group. The most important halogenated hydrocarbons include carbon tetrachloride, trichloroethylene, tetrachloroethylene, trichloroethane, chloroform, and methylene chloride.

Chlorinated hydrocarbon (CHC) solvents and related compounds cover a variety of chemicals with industrial and research applications. Occupational exposure varies from the production of rubber and plastics, to dry cleaning, paint removal and the laboratory. Trichloromethane (chloroform) and tetrachloromethane (carbon tetrachloride) are applied mainly as laboratory solvents, whilst trichloroethylene, tetrachloroethylene (perchloroethylene), and 1,1,1-trichloroethane have been used mainly in dry cleaning and metal degreasing. Dichloromethane (methylene chloride) is applied in metal degreasing and paint removal whilst ochloroethylene, better known as vinyl chloride is used in the manufacture of plastics.

The toxicity of most halogenated solvents is primarily dependent on their biotransformation to stable, toxic metabolites or reactive, electrophilic ones. Whilst the exposure to these substances can be easily diagnosed, it is the carcinogenic nature of these substances, especially the halogenated ethylenes that cannot be ignored.

Vinyl chloride is considered a group 1 carcinogen (carcinogenic to humans) according to the International Agency for Research on Cancer (IARC), whilst trichloroethylene, tetrachloroethylene, and PCBs are group 2A carcinogens (probably carcinogenic to humans). Dichloromethane, carbon tetrachloride, and chloroform fall under the category of group

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2B carcinogens (possibly carcinogenic to humans). Given the clinical burden of the halogenated hydrocarbons, many professional bodies have laid down guidelines regarding its monitoring. It is well known that the urine metabolite trichloroacetic acid (TCA) is present in individuals exposed to 2-3 different halogenated hydrocarbons. (Trichloroethylene, Tetrachloroethylene and 1,1,1-Trichloroethane). This has created confusion in the monitoring process,with regards to unknown background exposure; different BEI cut off points for the respective hydrocarbons, and has clearly not reflected the true nature of the hydrocarbon. In view of above PathCare laboratories is proud to announce that the following haloge-nated hydrocarbons can now be analyzed directly on BLOOD samples, adding to the available urine metabolite/s testing. This will give the Occupational Practitioner a better idea regarding the kinetics of an individual halogenated hydrocarbon thereby allowing for better monitoring and patient management. The Table below summarizes the newly available blood parameters with their respective BEI values.

Chemical agent Normal range BEI / BAT

1 Dichloromethane < 5µg/100ml 50 µg/100mlEnd of shift, end of workweek

2 Trichloromethane (chloroform) 0.0 µg/100ml Not available

3 Trichloroethanol 0.0 µg/100ml 400 µg/100mlEnd of shift, end of workweek

4 Trichloroethylene < 2 µg/100ml 500 µg/100ml End of shift, end of workweek


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Chemical agent Normal range BEI / BAT

5 Tetrachloroethylene < 2 µg/100ml 50 µg/100ml End of shift, end of workweek

6 Trichloroethane < 2 µg/100ml 400 µg/100mlEnd of shift, end of workweek

BEI are based on the German (BAT values).Sample required: 5ml (EDTA) blood. Analysis technique: Gas Chromatography.Units reported: µg/100ml.TAT: Weekly.

Compiled by:Dr Younus EssackChemical Pathologist- Occupational Division, PathCare Laboratories.

REFERENCESContact Special Operations.


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John C Stanfliet - Chemical Pathologist, PathCare; email: [email protected] Schillack - Analytical Toxicologist - V&M ATLS Director, e-mail: [email protected] Essack - Chemical Pathologist, PathCare; email: [email protected]

ABSTRACTLead is a well-established toxin that continues to pose a health risk. Blood lead levels (BLLs) and urinary chelatable lead are the tests of choice for assessing acute and chronic toxicity. We highlight some of the other tests available. As occupational exposure to lead is often accompanied by other toxic heavy metal exposure, measuring whole blood heavy metal levels should be considered for workers with chronically elevated BLLs.

Keywords: lead, occupational health, toxicity, analysis, blood lead.

INTRODUCTIONLead, a heavy metal, is a major public health risk because of its deleterious effects, and there continues to be significant exposure to it via occupational and non-occupational routes. A blood lead level (BLL) of 10 µg/dl has been identified by the WHO/CDC as a medical action level but research indicates that there is no level below which risk does not exist. Occupational exposure to lead can be significant, with 89 % of occupationally-exposed workers in Nairobi having BLL > 10 µg/dl in one study.

The major routes of lead absorption into the body are the GIT and respiratory systems. Most of the body’s lead burden is stored in bone, and a small fraction circulates in the blood. Lead can diffuse into most organs and penetrate the blood-brain barrier. The principal route of elimination is via urine.

ASSESSING LEAD LEVELS IN OCCUPATIONAL HEALTH - A MINI REVIEW

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BLOOD LEAD LEVELSThe half-life of blood lead is ~ 30 days as lead binds the proteins of circulating erythrocytes. Although blood lead is in equilibrium with bone lead, there is also a contribution from recent intake. Therefore, BLL reflects both recent exposure and lead that has been mobilised from tissue stores.. A study of 803 workers exposed to lead identified BLL as correlating better with neurobehavioural abnormalities than either bone lead or urine chelatable lead. In addition, the presence of other heavy metals should be considered when testing for lead toxicity as exposure to more than one heavy metal may exist. One of the authors (VS) has noted increased levels of antimony, manganese, chromium, nickel, cadmium, aluminium and zinc in a sample of approximately 100 workers with occupational exposure to lead (unpublished data).

PLASMA LEAD LEVELS The utility of measuring plasma lead has been investigated as it represents that part of the body’s pool that is potentially free to cross various membranes, such as the placenta and blood brain barrier. Either serum or plasma is acceptable.

However, plasma lead levels are very low - 1 % of whole blood lead - necessitating new techniques, such as inductively coupled plasma mass spectrometry (ICP-MS). Furthermore, measuring heavy metals in plasma is prone to false increases if the sample is haemolysed. Additional research is needed before the measurement of plasma lead in routine clinical practise can be recommended.

BONE LEADLead accumulates in the body when intake exceeds the body’s potential to excrete it; thus, bone lead is a marker of

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cumulative lead exposure and has a half-life of decades. Bone lead levels are difficult to assess outside of a research setting. Alternatively, measuring BLL repeatedly and plotting the value over time can be used to generate a cumulative blood lead index; this correlates well with bone lead.

URINE LEAD AND LEAD MOBILISATION TESTSRandom urine lead levels are not recommended as the values can fluctuate markedly and independently of BLL. Furthermore, there is little prospective research linking urine lead levels with adverse health outcomes. Conversely, lead levels measured in urine collected for a set period following an IV EDTA or oral dimercaptosuccinic acid (DMSA) challenge may be a measure of the body’s lead burden. Lee et al. found that the urinary chelatable lead level in a 4 h urine collection following oral DMSA challenge correlated with symptoms of potential lead toxicity in a dose-dependent manner in patients who were exposed to lead via their occupation. Hoet et al. proposed an upper reference limit of 22 µg lead in 4 h urine following DMSA 1 g orally.

HAIR TESTINGHair is a sample that is being looked at with increasing interest because of the potential benefits it offers. However, there are a number of confounding factors that have yet to be determined adequately. For example, air pollution may contami-nate the hair and result in spuriously elevated hair lead levels. Hair lead is reported using different units in various studies which makes comparison between studies difficult. Further, there are no established medical action limits. However, this technique is used in forensic medicine to determine long term exposure.

OTHER SAMPLESLead has been measured in other tissues, including teeth, toenails and even human breast milk. Further, lead inhibits a number of enzymes including Δ-amino levulinic acid dehydratase (ALAD). Thus, lead intake results in higher levels of


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urinary amino levulinic acid (ALA) and reduced ALAD enzyme activity; however, these tests have proved unreliable even in the acute setting. None of these samples can be recommended for use in the occupational health setting.

TREATMENT AND MONITORINGChelation therapy must be done under controlled conditions and is recommended if baseline BLL exceeds 40 µg/dl chronically. Chelation therapy, such as DMSA 10 mg/kg body weight orally three times daily, is given for a one to two week period, generally. Repeated lead measurements are recommended before and during treatment. During and immediately after treatment, the BLL may fall dramatically and urinary chelated lead levels may rise; there is a rebound phenomenon following cessation of treatment although BLL and urinary chelated lead levels remain substantially lower than before the initiation of chelation. SUMMARYAlthough there are a number of exciting new developments in the field, BLL and urinary chelatable lead remain the tests of choice with the largest evidence base. The possibilities of other heavy metals should be considered and is a frequent finding. Close collaboration between the clinician and the laboratory allows for the rational use of laboratory tests in this potentially complex setting.

REFERENCESRefer to OH Journal of SA, Vol 20 No 5 Sep / Oct 2014 or contact Special Operations.


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Volker Schillack, Analytical Toxicologist, V&M ATLS Director; e-mail: [email protected] Essack, Chemical Pathologist, PathCare; e-mail: [email protected] C Stanfliet, Chemical Pathologist, PathCare; e-mail: [email protected]

ABSTRACT Although manganese (Mn) is an essential nutrient, toxicity has been demonstrated in workers accidentally exposed to large amounts. Chronic exposure to Mn can damage the nervous system and respiratory tract and result in symptoms similar to Parkinsons disease.

INTRODUCTIONMn is an essential trace element and is provided for, through daily intake, in amounts of 3-7 mg. It acts as a cofactor for a number of important enzymes, namely arginase, cholinesterase, phosphoglucomutase, pyruvate carboxylase, and mitochondrial superoxide dismutase and, together with vitamin K, plays a role in the formation of prothrombin.

Occupational exposure usually occurs through inhalation or ingestion of fumes/dust produced during the mining/refining of Mn ores or the treatment of Mn alloys. Certain organic derivatives of Mn are currently used as octane-improving additives in unleaded gasoline.

Exposure to high levels of Mn may lead to a condition known as manganism/metal fever. An individual involved in the manufacture or processing of steel, welding rods, batteries, ceramics, or pesticides (Mn-containing herbicides) may be at risk, depending on exposure levels.

MANGANISM / MANGANESE POISONING

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MANGANESE TOXICITY Workers absorb Mn mainly through the lungs, with gastrointestinal absorption being low (1-5%). Mn absorption is controlled by homeostatic mechanisms and is shown to be reduced through concomitant ingestion of calcium. There may be sex-specific differences in blood levels of Mn, lead (Pb) and cadmium (Cd), related to underlying iron (Fe) deficiency, oestrogen and variability in the absorption rates of these metals. It is therefore important that these factors be considered by the occupational practitioner during monitoring. Mn is mainly present in the red blood cells and is 25 times higher in these cells than in serum. The liver is the main storage organ, with the kidney and brain acting as secondary reservoirs following chronic exposure. Manganism presents with symptoms and signs similar to Parkinson disease. Patients present with fixed gaze, tremors, body rigidness, and slowed movements (bradykinesia). It has been shown that welders exposed to Mn are more likely to develop Parkinson disease than the rest of the population, especially at an early age. Mn has been shown to interfere with the absorption of Fe, with long-term exposure leading to Fe-deficiency anaemia. Fe-deficiency, on the other hand, can lead to brain Mn accumulation; and research has shown that dietary increases or decreases in Fe might contribute to brain deposition of Mn in populations exposed to Mn. Increased Mn also impairs the activity of the copper metallo-enzymes. Clinical stages of manganese poisoningHistorically, three stages of manganism were described in workers with very high levels of Mn exposure.


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Stage 1 Very subtle symptoms. Individuals present with headaches, exhaustion, weakness and apathy. Symptoms can easily be confused with depression or other illnesses. Some researchers believe that this early stage is reversible.

Stage 2 Individuals may present with short–term memory loss, impaired judgment, slurred speech, and even hallucinations. “Manganese madness” was the term used to describe the compulsive, strange behaviour of workers over-exposed to Mn in the Mn mines.

Stage 3 Symptoms and signs of the last stage include involuntary muscle movements, tremors, poor coordination, a mask–like rigid face, and a staggering strutting gait. This stage is irreversible and may lead to complete disability. Removing a patient from exposure at this point does not seem to be helpful. In one report, the disease progressed over a 10–year period even after the patient was no longer exposed to Mn. It is important to note that the symptoms of manganism may appear any time from months to several years after an individual’s initial exposure to Mn.

METABOLISM AND EXCRETIONMn metabolism is similar to that of Fe. It is absorbed in the small intestine with the absorption process being slow. More than 90% of Mn is excreted in bile. Whole blood Mn, of which the majority is bound to the haemoglobin, averages 9 ug/l (3.9 – 15ug/l) in normal adults, whilst urinary Mn concentrations in unexposed persons have been reported to range from 1-10 ug/l.

BIOLOGICAL AND EFFECT MONITORINGManganism is a clinical diagnosis that requires evidence of overexposure and a clinical syndrome consistent with basal ganglia dysfunction. The role of ancillary tests to support diagnosis, such as MRIs, chest X-rays, lung function tests, full


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blood count and liver function tests, is unknown. Mn has a very short half-life in blood so routine blood monitoring only provides modest information on current exposures. Moreover, no studies have demonstrated a clear relationship between blood Mn and clinical health outcomes. Urine Mn is also not a useful measure of exposure. Hair or nails are currently considered to be more practical for determining chronic exposure to Mn, while bone Mn levels are good indicators of long term exposure. Chelation therapy of Mn intoxication with para-aminosalicylic acid maybe an alternative way to determine accumulation of Mn.

CONCLUSIONManganism is a clinical diagnosis supported by motor, behavioural, and cognitive dysfunction in the setting of overexposure to Mn. Unfortunately, ancillary tests provide, at best, supportive evidence of exposure.

REFERENCESRefer to OH Journal of SA, Vol 21 No 2 Mar / Apr 2015 or contact Special Operations.


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Younus Essack, Chemical Pathologist, PathCare; email: [email protected] C Stanfliet, Chemical Pathologist, PathCare; email: [email protected] Schillack, Analytical Toxicologist, V&M ATLS Director; email: [email protected]

ABSTRACTMercury is ubiquitous in the environment and therefore every human being, irrespective of age or location, is exposed to one form of mercury or another. The major source of environmental mercury is natural degassing of the earth’s crust, whilst industrial activities can raise exposure to toxic levels directly or the through the use of liquid metals or synthesised mercurial compounds. Mercury still gives rise to accidental and occupational exposure. The aim of this mini review is to describe the main factors that influence mercury toxicity and provide a framework for the interpretation of mercury. INTRODUCTIONMercury (Hg2++) is a heavy metal noted for inducing public health disasters - Minamata Bay in Japan, Iraq, and South Africa. Mercury exists in several forms: inorganic mercury which includes metallic mercury (Hg0) and mercury vapor (Hg); mercurous mercury (Hg2++) or mercuric salts; and organic mercury which includes methyl and ethyl mercury. Human toxicity varies with the form of mercury, the dose and the rate of exposure. The target organ for inhaled mercury is primarily the brain, whilst mecurous mercury and mercuric salts chiefly damage the gut lining and kidney.

Human mercury exposure occurs mainly though the inhalational of elemental mercury via occupational or dental amalgam exposure and through the ingestion of mercury bonded to organic moieties (ethyl, methyl, dimethyl mercury), primarily from seafood. Dental amalgams emit mercury vapour which is inhaled and absorbed into the blood stream, while liquid

MERCURY - THE ELUSIVE HEAVY METAL

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metallic mercury still finds its way into homes, causing a risk of poisoning from the vapour and creating major clean-up costs. Amongst humans, the sole source of exposure to methyl mercury (organic mercury) is through the consumption of fish and sea mammals. It has been reported that over 3000 lakes in the US have been closed to fishing due to mercury contamination.

PHARMACOKINETICS OF MERCURYDue to its volatility, metallic mercury (Hg0) is responsible for most cases of inhalational exposure. On entry to the body, mercury vapour is oxidised to mercuric mercury. This conversion process, however, is not rapid enough to prevent Hg0 from crossing the blood brain barrier. Metallic mercury passes easily through the blood brain barrier and the placenta, where it lodges in the foetal brain. The excretory half-lives of metallic mercury and mercuric mercury vary widely, with values ranging from a few days to several months.

Mercurous mercury salt in the form of Hg2

Cl2 (calomel) is poorly soluble in water and is therefore associated with low

toxicity following oral ingestion. Mercuric mercury, typically HgCl2 generally targets the gastro-intestinal tract and the

kidneys. In acute poisoning cases, patients present with abdominal pain, vomiting and bloody diarrhoea, with potential necrosis of the gut mucosa. This may produce death, from peritonitis, septic or hypovolemic shock. Mercuric mercury does not cross the blood brain barrier efficiently but it does accumulate in the placenta, foetal tissue and amniotic fluid. The major burden of mercuric mercury resides in the proximal convoluted renal tubule, while brain dysfunction is less evident than with other forms of mercury.


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Most available data on organic mercury refers to methyl mercury which is a major source of human mercury exposure. Mercury attached to aquatic sediments is subject to microbial conversion to methyl mercury, whereupon it enters the aquatic food chain. It reaches its highest concentration in long lived predatory fish, such as sharks. Once fish and sea mammals are consumed; methyl mercury is deposited throughout the body. Concentration occurs in the brain, liver, kidney, placenta and foetal brain, as well as in the peripheral nerves and bone marrow. The excretory half- life of methyl mercury is 70 days, with approximately 90% being excreted in stools.

Ethyl mercury (thimerosal) is a water soluble compound used as a preservative. It is added to many commercial products, including vaccines. Ethyl mercury appears to be less toxic than methyl mercury, in part as metabolism is more rapid. Low dose ethyl mercury derived from thimerosal in vaccines has been shown to have a blood half-life of 7 days (95% confidence interval: 4-10 days) in 40 full term infants.

CLINICAL PRESENTATION AND TOXICITYThe chief target organ of metallic vapour is the brain. With significant acute exposure, bronchitis and bronchiolitis, potentially leading to respiratory failure, may be accompanied by CNS symptoms such as tremor and erethism.

With low levels of chronic exposure, non-specific symptoms such as weakness, fatigue, anorexia, weight loss and gastro-intestinal tract disturbances have been described. Higher levels of chronic exposure are associated with mercurial tremor, erethism, personality and behaviour changes, insomnia, loss of memory, depression, fatigue and, in severe cases, delirium and hallucinations. Gingivitis and copious salivation have also been described.

The brain is also the primary organ affected by methyl mercury exposure. Adults present with paraesthesia of the


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circumoral area, hands and feet, followed by visual field constriction and ataxia. A major concern of methyl mercury exposure is in the prenatal period, with the foetal brain being more susceptible to mercury induced damage. Massive prenatal poisoning may induce a form of cerebral palsy, while lesser prenatal doses have been associated with neurodevelopmental delays and cognitive deficits. It is for this reason that the FDA has recommended that pregnant women, nursing mothers and young children avoid eating fish with a high mercury content (> 1ppm), such as shark, swordfish, tilefish, whale and king mackerel.

BIOLOGICAL MONITORING OF MERCURY Analysis of mercury in blood and urine requires either atomic absorption spectroscopy hydride system or the more selective inductive coupled plasma mass spectroscopy. Several studies have demonstrated a correlation between the intensity of recent exposure to mercury vapour and the concentration of mercury in blood, urine and saliva. Such a relationship only holds when the exposure has lasted one year. Under chronic exposure conditions, a relationship between blood or urinary Hg concentrations and the occurrence of clinical and biological signs of intoxication by mercury vapour also exists.

In persons non-occupationally exposed to mercury, the concentration of mercury in urine is < 5 µg/g creatinine, and 2 µg/L in blood.


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Urinary HgIn newly exposed workers, urinary excretion does not immediately follow the onset of exposure; there is a latent period during which the body accumulates a certain quantity of mercury, mainly in the kidney. Nephropathological effects of mercury have been known for years and are largely dependent upon the chemical form of mercury exposure. A correla-tion has been demonstrated between the urinary excretion of mercury and the prevalence of neuropsychomotor effects or the prevalence of increased excretion of urinary proteins. Some authors have reported an increased prevalence of slight tremor and biological signs of renal dysfunction in workers excreting > 50 µg/g creatinine of Hg, while other data suggest that exposure to metallic mercury < 50 µg/m3 which leads to urinary excretion values below 35 µg/g creatinine may still increase finger tremors.

The value of 50 µg/g creatinine has been proposed and endorsed by the World Health Organization (1980) as a biological threshold limit value for chronic exposure to mercury vapor. It must be noted that blood, hair and urine mercury levels reflect recent exposure and do not correlate with total body burden.

Blood HgThe concentration of mercury in blood may be influenced by recent exposure, dietary habits, particularly the consumption of fish containing methyl mercury. Studies have demonstrated better correlations between blood mercury and mercury in air, than between urinary mercury and mercury in air.

Hair analysisIn view of the risk of external contamination, hair does not seem to be a suitable biological material for evaluating the uptake of mercury vapour; however, hair analysis seems to be useful for biological monitoring in subjects suspected of


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exposure to methyl mercury. Table 1 indicates threshold values suggested by different bodies with regard to the biological monitoring of mercury.

Table 1. Practical aspects of biological monitoring of workers exposed to mercury.

Parameters Hg in blood Hg in urine

Confounding factors Sample contamination, dental amalgam fillings, drugs, fish consumption, coal stove fires.

Sample contamination, dental amalgam fillings, drugs

Half life Fast phase - 3 daysSlow phase- ± 20 days

About 40 days

Reference: non- occupationally exposed individuals

< 1 µg/dl < 5 µg/g creatinine

ACGIH-BEI Inorganic 15 µg/L (ES, EW) 35 ug/g creatinine (PS)

DFG-BAT Inorganic 25 µg/L (NC)Organic 100 µg/L

100 µg/L (NC)


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ACGIH- American Conference of Governmental Industrial Hygienists; BEI - Biological Exposure Index; BAT - Biological Tolerance Level; ES - End of shift; EW - End of workweek; PS - pre-shift; NC - sampling time not critical; DFG - Deutsche Forschungsgemeinschaft.

TREATMENTDue to difficulties in estimating the total body burden of mercury, provocation with a chelator has been proposed as providing a more reliable estimate of body burden. DMPS (dimercapto-1-propanesulfonate) has been found, by a number of investigators, to provide a reliable estimate of body burden, safer than British Anti-Lewisite (BAL). Since provocation is shown to be safe and inexpensive, indications for its use must be determined on clinical grounds.

CONCLUSIONHeavy metals should be considered as “systemic” toxicants. They have the potential to affect many organs and tissue. Failure in documenting history of exposure can lead to a delay in diagnosis as correlations between symptoms, and mercury concentrations in blood and urine are not well defined. It is important that a clinician collaborate with the laboratory to help understand all factors that influence mercury testing.

REFERENCESRefer to OH Journal of SA, Vol 20 No 6 Nov / Dec 2014 or contact Special Operations.


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TESTING FOR DRUGS OF ABUSE - PART 1

John Stanfliet, Chemical Pathologist, PathCare, [email protected] Essack, Chemical Pathologist, PathCare, [email protected]

ABSTRACTDrugs of abuse are commonly encountered in the workplace and the Occupational Health Specialist is often asked to perform and interpret tests checking for the presence of such substances. A clear understanding regarding the limitations of testing is required for this purpose as this field has many potential pitfalls. This is the first of two articles that provide a broad overview of the commonly encountered drugs of abuse (DOA), the possible samples that can be used, possible interferants and adulterants that may be encountered and the role of the laboratory and pathologist. The second article in this series examines the technology involved, looking briefly at immunoassays and mass spectrometry and issues regarding cut-points and interpretations.

INTRODUCTIONThe possibility that a patient may be using a drug of abuse (DOA) is a frequent clinical scenario that medical practitioners face. Many POCT DOA testing kits are now available to meet this demand. However, the client may be less than willing to co-operate with testing to answer this clinical question due to the possible occupational, legal or forensic consequences. Clinicians nowadays have a number of issues to consider in this regard.

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It is important to note that as a general rule, that the clinical testing for DOA cannot be used for medico-legal purposes as there is no forensic adherence to maintaining a documented and unaltered chain of custody. Secondly, we are occasionally asked by third parties such as concerned parents to perform a DOA surreptitiously. This is unethical and is to be condemned strongly. All testing requires informed consent in keeping with agreed ethical standards. The patient should be informed of the procedures and consequences of the testing process.

Although there are many drugs that can be abused, a dozen or so are encountered commonly and therefore included with most screening programs. Alcohol is the most widely abused drug in South Africa, however the term DOA does not include alcohol usually. Importantly, the prevalence of these DOA may vary by geographical location, and thus knowledge of the DOA common to the area where the clinician practices is important. Certain manufacturers are able to mix and match DOA kits for screening programs with the inclusion of the relevant drugs of interest only. Discussions with local addiction specialists and our experience suggest that the commonly encountered DOA in South Africa are cannabis, opiates, mandrax, methamphetamines, amphetamines, cocaine, benzodiazepines and barbiturates.

SAMPLE REQUIREMENTSUrine is the matrix of choice in almost all circumstances as it offers many advantages. It is easily collected and the parent drugs and their metabolites are concentrated in urine. In addition, they are often present in urine for a prolonged period of hours to weeks and measuring creatinine, temperature, pH and specific gravity in the sample allows one to determine whether the sample has been altered. Ideally, the sample collection should be witnessed, however this is not possible in many cases. This allows for the adulteration of the sample by the patient using a number of agents which include water, bleach and anti-oxidants that can be purchased on the internet. Another possibility includes the substitution of the urine samples.


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Blood sampling is often considered, however the drug is often only present for a very short period of time. For example, in people who abuse cannabis chronically, blood sampling will only detect recent intake within the last few hours, whereas, urine can be positive for up to six weeks after the last ingestion as tetrahydrocannabinol is stored in fatty tissue from which it is slowly released.

Oral fluid (saliva) is a matrix that is being used increasingly. It is relatively easy to collect under supervision and therefore can be used when the risk of sample adulteration is high. Experience has been gained in the last two decades with respect to the metabolism of drugs including their pitfalls. The saliva flow rate is vital and alterations due to physiological stress or medication can have a major impact on the concentration of drugs in the sample. In individuals with slow collection times, the use of agents such as chewing gum to increase salivary flow rate has been shown to reduce the concentration of codeine by at least 50 %. Some drugs, classically cannabis, may be concentrated in the mouth following recent use. There are a number of collection devices available with none being perfect for all drugs. Importantly, oral fluid only addresses recent intake similarly to blood sampling and therefore does not replace urine testing. The presence of a drug in oral fluid is dependent on protein binding and its pKa. Benzodiazepine as an example is present in oral fluid at only a low fraction when compared to the concentration in blood.


Points to remember

• Clinical testing for DOA does

not meet forensic standards

• Informed consent is required

for testing

• A handful of drugs are

encountered commonly

• Urine is the sample of choice

except in rare cases

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Hair sampling offers an intriguing option with many issues that also still need to be resolved. Some of the concerns include the possibility of environmental contamination of the hair, the question of whether hair colour has an impact on how much of a drug is deposited, the role of shampoos, conditioners and hair dyes and very importantly the exact part of the head necessary for sampling. In addition, samples then need to be prepared with no consensus on how best to extract the putative drug from the hair. Cut-points are not universal and interpretation can vary between experts. Thus, although used in certain forensic cases, hair cannot currently be recommended for the clinical settings commonly encounteredBreath as a sample is only used in alcohol testing, particularly road-side testing by the police services. Other samples such as nails and tissue biopsy samples are not discussed further in this article. Discussion with the local pathologist is advised in these circumstances as special precautions and methods may be required when obtaining and preparing the sample in order to achieve the best results.

CONCLUSIONThe testing for DOA is a problem that faces the occupational specialists regularly. Adherence to a number of simple prin-ciples should ensure the minimum likelihood of discrepant or discordant results. Consultation with the laboratory is para-mount before a sample is collected if one remains in doubt.

REFERENCESRefer to OH Journal of SA, Vol 21 No 6 Nov / Dec 2015 or contact Special Operations.


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John Stanfliet, Chemical Pathologist, PathCare, [email protected] Essack, Chemical Pathologist, PathCare, [email protected]

ABSTRACTThis is the second article in this series. The first article looked at some of the commonly encountered drugs of abuse, discussed the range of samples on offer and established why urine is the preferred matrix, and methods of sample adulteration. This part briefly discusses immunoassay technology, the means to comment on the integrity of a sample and issues regarding cut-points and interpretations. The necessity for confirmatory testing of positive test results is discussed and the use of a mass spectrometric method is recommended for this purpose.

CASE VIGNETTEDr. S, an experienced family practitioner of many years, has a mother and her teenaged son in her examination rooms. The mother says that she is worried about the son possibly using drugs, especially cannabis, as his eyes seem strange and his concentration is poor. The son agrees to a random urine drug screen for cannabis. Dr. S gets the result from the laboratory later that day stating “cannabis < 30 ng/mL”. She phones the lab as she is unsure from the laboratory report whether the patient has taken cannabis or not.

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INTRODUCTIONMost urine drugs of abuse (DOA) screening methods employ urine dipstix using an immunoassay technology. These strips are impregnated with an antibody derived from an animal, usually a mouse, which has been exposed to the antigen of interest. The antibody is directed towards an epitope that forms part of the chemical structure common to a family of compounds e.g. opiates. Thus, a single immunoassay can detect different types of opiates such as heroin, morphine and codeine. Therefore, a positive result on an opiate screen can result from the patient having ingested any of these com-pounds as well as other members of the family such as methadone.

There are proven concerns that immunoassays used in screening programs may not be very specific as there are numer-ous commonly encountered drugs and other compounds that may cross-react in the assay because of a similar structure. This cross-reactivity may occur if the antibody binds a molecule that has a similar epitope of interest even if the compound is unrelated to the molecule being examined for, i.e. a false positive result. There are published lists available of cross-reactants that have been described, with most laboratories able to provide this information. An additional issue with regards to immunoassays is the lack of standardisation. Each monoclonal antibody kit is unique to a manufacturer or to those to whom it has licensed the technology. This may result in discordant results occasionally, with one manufacturer’s kit not agreeing with another as the antibodies recognise different parts of the antigen of interest. In addition, certain kits may be more sensitive to a specific DOA in a class than others.

Importantly, as the immunoassay tests for a structure common to a family of compounds, other related substances may also be detected, as in the case of poppy seed cake ingestion resulting in a positive opiate DOA testing, or hemp oil ingestion resulting in a positive cannabis test. These compounds belong to the appropriate family, hence they represent a true positive result but there may well be occupational or legal consequences for the patient if they are


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detected. Ideally, screening strips or cups should also have a means whereby the putative integrity of the sample is confirmed. Several options are utilised and available which include urine creatinine concentration, specific gravity, temperature and pH. The importance of this step is highlighted by an Italian study that found that 3.8% of workplace samples were diluted; however, most of these samples tested positive for a DOA when using very sensitive gas chromatography mass spectrometry.

CUT-POINTS AND LIMITS OF DETECTIONAn underappreciated fact is that urine screening tests use arbitrary cut-points. A cut-point for each DOA is chosen by the manufacturer. Thus, manufacturers may employ different cut-points, resulting in a positive test on one strip and a negative strip when another manufacturer’s device is used. When asked, manufacturers can provide the cut-point of the kit. In addition, manufacturers are able to change the cut-points. Although cut-points are not standardised, certain conventions are emerging in line with legislation in the United States of America (Table 1). These cut-points were developed to help reduce false positive results such as poppy seed ingestion causing positive opiate results.


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Substance level (immunoassay)

Initial urine drug screen(ng/mL)

Confirmatory drug level (MS) (ng/mL)

Marijuana1 50 15

Cocaine2 300 150

Opiates 2000 2000

Amphetamines 1000 500

Metamphetamine3 1000 500 Table 1. Cut-points used for common drugs in US Federal workplace testing

Urine can be a problematic matrix because of the wide and unpredictable range of analytes, concentrations and ionic strengths encountered. The repeatability of some devices around the cut-point may also be sub-optimal with the same sample testing both positive and negative for a DOA at a concentration level close to the cut-point . Clinical laboratories accredited by the South African National Accreditation Service spend a lot of time, effort and resources establishing whether DOA test devices are fit for purpose. Relying solely on the published literature of a manufacturer has proven to be unreliable at times. When a quantitative result is provided, extremely low or undetectable levels of the DOA are often reported as “less than (<)”. This number below which a quantitative result is not reported is the lowest number that the laboratory has shown can be reliably reported given the imprecision and bias of that particular assay.


1Delta-9-tetrahydrocannabinol is looked for2Benzoylecgonine is the cocaine specific metabolite3Specimen must also contain amphetamine ≥ 200 ng/mL

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CONFIRMATORY TESTINGGiven both the poor specificity of screening immunoassays, with a false positive rate of 25% for some analytes, and the consequences of a positive result for the patient, most positive urine DOA tests should be sent for confirmatory testing. Mass spectrometry coupled either to gas or liquid chromatography, is used for this purpose as it is considered the gold standard investigative method. This methodology is highly accurate and precise but requires technical knowledge and expertise to run and interpret and is therefore not suitable as a screening test. A mass spectrometer allows for the exact quantification of analytes at very low concentrations, much lower than that seen in immunoassays, with improved specificity and accuracy.

CONCLUSIONUrine drug screens are widely employed tests but do suffer from several shortcomings. In general, negative tests require no further testing unless at odds with the clinical setting. Positive screening tests should be sent for confirmatory testing using mass spectrometry due to the poor specificity of urine drug screens as well as the likely consequences for the patient.

REFERENCESRefer to OH Journal of SA, Vol 22 No 1 Jan / Feb 2015 or contact Special Operations.


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REFERENCES & HANDY WEBSITES

• Occupational Health & Safety Act.• Hazardous Chemical Substance Regulations.• Industrial Chemical Exposure: Guidelines for Biological

Monitoring (Robert R. Lauwreys & P. Hoet).• Niosh: National Institute of Occupational Safety &

Health• Biological Monitoring Methods for Industrial Chemicals

(Randall C. Baselt).• Handbook of Biological Monitoring for Health

(Canterbury Health Laboratory)• International Labour Organisation (ILO) Encyclopaedia

of Occupational Health & Safety (Dr. Luigi Parmeggiani).

• Agency for toxic substances & disease registry (ATSDR).

• NPTN fact sheets (National Pesticide Telecommunications Network).

• CDC (Centre for disease control & prevention) Department of Health & Human Services.

• Codex Alimentarius.

• www.gov.za - SA Government• www.ilo.org - International Labour Organisation• www.cdc.gov.niosh - NIOSH (National Institute of

Occupational Health & Safety• www.cdhb.govt.nza - Canterbury Health Laboratory• www.atsdr.cdc.gov - ATSDR (Agency for Toxic

Substances & Disease Registry).• www.npic.orst.edu - National Pesticide Network.• www.cdc.gov - CDC (Centre for Disease Control).• www.codexalimentarius.net - Codex Alimentarius.• www.osha.gov - Occupational Safety & Health Admin

USA.• www.fda.gov - USA Food & Drug Administration.• www.regulatory.co.za - SA Bureau of Standards.• www.sasohn.org.za - SA Society of Occupational Health

Nursing Practitioners.• www.sasom.org.za - SA Society of Occupational

Medicine.• www.irca.co.za - Risk Management Solutions.

REFERENCES HANDY WEBSITES

Documents

OCCUPATIONAL HEALTH REFERENCE GUIDE · chemicals including PAH’s, and cigarette smoke is a highly plausible cause of skin irritation and cancers appearing in workers for many industrial