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Occupational Toxicology – Part 1

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Occupational Toxicology – Part 1 Occupational toxicology – Part 1 DR MELISSA YSSEL, MBCHB (PRET), FC PATH (SA) CHEM, DOHM (PRET), INDUSTRIAL TOXICOLOGY CENTRE – LANCET LABORATORIES, P.O. BOX 7001, PRETORIA, 0001 TEL: 012 483 0272, FAX: 012 483 0187, e-mail: [email protected] www.lancet.co.za Occupational toxicology will be presented as a five-part series. CLINICAL TOXICOLOGY e. Neurotoxicity. All substances are potentially toxic. Distinction between ‘toxicity’ f. Dermatotoxicity. and ‘hazard’ – an extremely toxic chemical that is in a sealed con- g. Pulmonotoxicity. tainer on a shelf has inherent toxicity, but presents little or no haz- h. Cardiotoxicity. ard. When the chemical is removed from the shelf and used by i. Reproductive toxicity. someone without appropriate protection, the hazard becomes greater. Thus, the manner of use affects how hazardous the sub- 5. Mechanism of action of the agent stance will be in the workplace. a. Irritants: Corrosive in action. b. Asphyxiants e.g. carbon monoxide: Interferes with oxygen trans- OBJECTIVES OF CLINICAL TOXICOLOGY port or reduced oxygen content of atmosphere (usually in confined 1. To define the capacity of substances to produce toxic/harmful spaces). effects (toxicity). c. Anaesthetics e.g. solvents: Cause drowsiness or unconscious- 2. To measure and analyse the dose at which toxicity occurs (dose- ness. response relationship). d. Mutagens: Alter the genetic material of cells. 3. To assess the probability that injury/illness will occur = hazard e. Teratogens: Interfere with the normal embryonic development and risk assessment. resulting in malformation. f. Carcinogens: Induce cancer. TOXIC AGENTS AND THEIR EFFECTS g. Systemic: Affect different organs in the body. Classification of toxic agents h. Sensitisers: Produce an allergic type reaction. 1. Physical state of the agent. a. Particulates (dusts) e.g. silica, coal dust, asbestos. 6. Clinical effects of the agent b. Fumes e.g. metal/polymer decomposition products. a. Onset of effects. c. Gases e.g. butane, methyl bromide, ethylene oxide. i. Immediate: irritants – due to direct damage to tissues at point of d. Vapours e.g. hexane, trichloroethylene, benzene. initial contact, usually resulting in inflammation. e. Liquids e.g. elemental mercury. ii. Delayed: chemical carcinogens. f. Solids e.g. plastics. b. Reversibility of effects: Depends on the capacity of damaged cells E.g. lead: solid form (harmless) – dust (moderately toxic) – fume to regenerate or recover e.g. brain/nervous system cells – little ca- (highly toxic). pacity to regenerate compared with liver/muscle cells which are very likely to recover after injury. 2. Chemical structure of the agent Chemical structure can determine toxicity. Factors affecting clinical response to a toxic agent a. Different isomers e.g. aromatic amines are carcinogenic when 1. Duration. substituted in other than the para-positions. 2. Frequency. b. Substance stability. 3. Route of exposure: e.g. ethylene glycol is toxic when ingested c. Presence of impurities, contaminants or additives. but poses little threat in the workplace except when sprayed or heated. 3. Medium of the agent 4. Environmental factors The medium in which a toxic substance is found in part determines a. Atmospheric pressure. the population exposed and thus to some extent the hazard, e.g. b. Temperature. oxides of nitrogen in air (vehicle exhaust), trihalomethanes in water c. Humidity. (from chlorination) and nitrosamines in food (from nitrites). 5. Individual factors (‘susceptibility’) a. Race. 4. Site of injury by the agent b. Genetics (controversial) e.g. G6PD deficiency (haemolysis), sickle Effect on target organs cell anaemia (hypoxia) and alpha-1 antitrypsin deficiency (emphy- a. Immunotoxicity. sema). b. Haematotoxicity. c. Age. c. Hepatotoxicity. d. Sex. d. Nephrotoxicity. e. Body weight. 30 JANUARY/FEBRUARY 2006 OCCUPATIONAL HEALTH SOUTHERN AFRICA f. Nutrition. dust particles and fumes from reaching the lungs. g. Immunological status. • Solubility of gases affects absorption. h. Hormonal status. • Highly water soluble gases (ammonia) and sulphuric acid) ab- i. Presence of disease. sorbed in upper airways with marked irritation – serves as a warn- j. Stress etc. ing and limits injury to the lungs. • Noxious gases of low water solubility (nitrogen dioxide and Note: These factors are not independent of one another. phosgene) reach the lungs without any warning and cause delayed injury. TOXICOKINETICS AND TOXICODYNAMICS 3. Percutaneous absorption Toxicokinetics is the movement of toxic substances within the body • Skin – intact/broken. i.e. absorption, distribution, metabolism and excretion, and the re- • Amount of skin absorption proportionate to the surface area of lationship between the dose that enters the body and the level of contact and to the lipid solubility of the toxic agent. toxic substance found in the blood or other biological sample. • Epidermis – acts as a lipid barrier. • Stratum corneum – acts as a protective barrier against noxious Toxicodynamics is the relationship between the dose that enters agents. the body and the measured response (the magnitude of the toxic • Dermis – freely permeable to many toxic substances. response is usually related to the concentration of the toxic sub- • Blood flow to the skin. stance at its site of action). • Use of occlusive skin coverings e.g. permeable clothes and industrial gloves. Bioavailability: Indicates the extent to which the agent reaches its • Topical application of fat-solubilizing agents. site of action. • Skin hydration. If not in a ‘bioavailable form’, it will be promptly removed or inac- • Skin type – soles of hands/feet versus face/neck. tivated before it reaches the site of action. • Skin injury (burns, abrasions, dermatitis). E.g. orally ingested cyanide: absorbed and passes to the liver – 4. Ocular absorption enzyme rhodanese metabolizes a portion of the ingested cyanide • Entrance through the conjunctiva. (inactive). However, inhaled gaseous hydrocyanic acid (HCN): ab- • Bypass hepatic elimination. sorbed through lungs – goes directly to the brain (damage due to • May cause severe systemic toxicity. hypoxia). • E.g. organophosphate pesticides splashed into eyes. Cell membrane permeability and cellular barriers Distribution Absorption, distribution, metabolism and excretion all involve pas- Toxic substances are transported via the blood to various portions sage of toxic agents across cell membranes. of the body. Some are removed by the lymph, and some insoluble compounds are transported through tissues such as the lung via Permeability is dependent upon a toxic substance/s cells such as macrophages. Most toxic substances enter the blood- a. molecular size and shape. stream and are distributed into interstitial and cellular fluids. The b. solubility at the site of absorption. pattern of distribution depends on the physiological and physico- c. degree of ionization. chemical properties of the material. d. relative lipid solubility e.g. obesity with 30–40% body fat = stable The initial phase of distribution usually reflects the cardiac out- reservoir – slow release of the toxin. put and regional blood flow. Lipid-soluble agents that penetrate Distribution is altered by unique cellular barriers e.g. blood-brain membranes poorly are restricted in their distribution, and their po- barrier, blood-testis barrier and the placenta, which may exclude tential sites of action are therefore limited. Exceptions are the blood- toxic substances. brain and blood-testis barriers, which limit the distribution of water- soluble but not lipid-soluble chemicals to these organs. Distribution Absorption may also be limited by the binding of toxic substances to plasma Rate of absorption is dependent on the concentration and solubility proteins. Toxic agents can accumulate in higher concentrations in of the toxic agent. some tissues because of pH gradients, binding to special cellular 1. GIT absorption proteins or partitioning into lipids. Some agents accumulate in tis- • Amount of absorption proportionate to the GIT surface area and sue reservoirs, and this may serve to prolong the toxic action e.g. blood flow and physical state of the toxin. lead may be stored for years in bone and may only be released • Most toxins absorbed in the small intestine. later. • Agents that accelerate gastric emptying will increase absorption. • Agents that delay gastric emptying will decrease absorption. Metabolism • Some toxic substances may be affected by the gastric juice e.g. Lipid-soluble toxic substances may go through a series of meta- the stomach acidity may release cyanide products and form hydro- bolic conversions (biotransformation) to produce more polar (wa- gen cyanide gas, which is even more toxic than the cyanide salt. ter-soluble) products, thereby enhancing removal by urinary excre- 2. Pulmonary absorption tion. Most common site for biotransformation is the liver, but it can • Most common route. also occur in plasma, lung or other tissue. Biotransformation may • Gaseous and volatile toxic substances. result in either a decrease (detoxification or inactivation) or an in- • Access to the circulation is rapid because the surface area of the crease (activation) in the toxicity of a compound. Differences in the lung is large and the blood flow is great. metabolism of toxic substances account for much of the observed • Nasal hair, cough reflex and the mucociliary barrier help prevent differences between individuals and between animal species. OCCUPATIONAL HEALTH SOUTHERN AFRICA JANUARY/FEBRUARY 2006 31
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