The primary means of exposure in the industrial setting is either by the inhalational or dermal route.  Exposure may be acute or chronic in either instance.  In acute toxicity, inhalational exposure often results in bronchoconstriction, shortness of breath, and possibly pulmonary œdema.  Additionally, if large amounts of a CNS depressant are inhaled, acute exposure may result in narcosis (loss of consciousness).  Chronic exposure by the inhalational route often results in fibrosis and/or tumour formation.  Acute dermal exposure may result in contact dermatitis, degreasing of the skin (solvents), denaturation of skin proteins and corrosion of the epidermal layer (acids, bases).  Chronic dermal exposure most often results in sensitisation and future allergic dermatitis.  Numerous types of chemicals may be encountered in industrial settings.  The following are examples of some of the more commonly encountered chemicals and classes of industrial toxicants.

Vinyl Chloride
Vinyl chloride is used as the precursor in the synthesis of polyvinyl chloride (PVC), which in turn is used in the manufacture of many plastics.  It is a gas and may be either inhaled or absorbed through the skin.  If large amounts of vinyl chloride are inhaled, the initial response is narcosis, due to its ability to depress the CNS.  Chronic exposure results in vasoconstrictive disorders that present as Raynaud's phenomenon (intense vasoconstriction, often in response to cold or stress, that produces cold digits and local cyanosis -- if un-treated it may progress to local areas of necrosis and gangrene), degeneration of bone and skin (again due to local vasoconstriction, ischaemia, necrosis, and loss of function), and hepatic fibrosis which may lead to a rare form of liver tumour, hæmangiosarcoma (so rare that it really only occurs in response to vinyl chloride exposure).  It is thought that the toxic effects of vinyl chloride are mediated by cytochrome P₄₅₀ metabolites, either chloroethylene oxide or chloroacetaldehyde.

Aromatic Amines
Aromatic amines are used in the rubber and dye industries.  The classic example of a toxic aromatic amine is beta-naphthalene.  It is no longer used in industry, but several similar compounds including naphthalene, 2-naphthalene, and benzidine are still employed.  Aromatic amine toxicity is especially prominent in those individuals who are slow acetylators.  The proposed mechanism of beta-naphthalene toxicity is the formation of a toxic metabolite by an alternate pathway (since in slow acetylators, the compound is not acetylated to the non-toxic metabolite).  The classic response to beta-naphthalene exposure in bladder cancer (which is relatively rare in those individuals who have not been exposed to the compound).  Aromatic amines may also cause liver damage of the cholestatic type.  The classic example of this toxic response is the "Epping Jaundice" outbreak, which represents an unintentional food contamination type of exposure.  The aromatic amine diaminodiphenylmethane was being transported in a lorry (truck) when the barrels tipped over and the compound was spilled.  Inadequate cleanup left traces of the amine in the bed of the lorry which was then used to transport flour.  The compound got into the flour which was then delivered to the town of Epping and used to make bread.  Consequently, the individuals eating the contaminated bread developed cholestatic jaundice.  Aniline, a simple aromatic amine, may also cause methæmoglobinæmia and cyanosis.

Bromine
Bromine is used in gold extraction, as a military gas, a bleaching agent for flour and fabrics,  as ethylene bromide as an anti-knock compound in petrol (gasoline), and was once used as the sodium or potassium salt as a sedative/hypnotic and anti-convulsant.  The exposure limit of bromine is 0.1 ppm.  Upon acute exposure, bromine is a strong corrosive, causing complete destruction of skin and mucous membranes.  Acute exposure to the salts will cause nausea and vomiting, abdominal pain, paralysis, coma, and death.  Chronic exposure to the salts results in confusion, irritability, tremor, memory loss, anorexia, headache, slurred speech, psychosis, and ataxia. Mechanistically, bromide displaces chloride from plasma and cells, causing CNS depression and hypochloræmia.  Treatment for bromide toxicity is intravenous NaCl (normal saline) with or without diuretics until plasma bromide levels fall below 50 mg/dL.  At that point, administration may be oral NaCl tablets, until the bromide is cleared from the body.

Solvents/Vapours

General Effects Upon Acute Exposure
Central Nervous System -- disorientation, euphoria, giddiness, memory loss & confusion,  narcosis, paralysis, convulsion, death (cardiopulmonary arrest by CNS depression -- necropsy indicates extensive petechial hæmorrhaging).

Peripheral Nervous System -- paræasthesias, visual and auditory disturbances

Motor Nerves -- weakness, incoordination, fatigue, and tremor

Treatment for acute inhalational toxicity (for any CNS depressant) -- remove the victim from the source of the exposure and supply oxygen.

Specific Effects

Benzene, Toluene, and Xylene -- chronic headache and drowsiness, anorexia, nervousness, pallor, bleeding, and petechia.  Benzene and toluene may produce aplastic anæmia and benzene may produce leukæmia.  Toluene is a common ingredient in glues and the early CNS effects are the reason for their abuse.

Chlorinated Aliphatic Hydrocarbons -- Chloroform and Carbon tetrachloride.  These agents have been discussed in previous sections.  Briefly, in addition to the CNS depression described above, exposure to these compounds may result in fatty infiltration in the liver and/or kidney, causing fibrosis and hepatic cirrhosis.

Aliphatic Hydrocarbons

Hexane -- used in cracking and distillation of crude oil and as a solvent in glues, paints, and varnishes.  Acute exposure results in mild CNS depression.  Chronic exposure results in sensorimotor polyneuropathies that manifest as bilateral paræsthesias and motor weakness.  The response to exposure includes axonal swelling, demyelination, and retrograde nerve fibre degeneration.

Gasoline/Kerosene -- Massive, acute exposure (>2000 ppm) results in dizziness, coma, cardiopulmonary collapse, and death.
 

Non-specific solvents have recently been implicated in a risk for reproductive toxicity and teratogenicity, with miscarriage, spontaneous abortion, major and minor birth defects, and low birth weights all being correlated to solvent exposure in the workplace during pregnancy.

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