Review Article
Detection of poisoning by substances other than drugs:
a neglected art
Neil R Badcock
From the Department of Chemical Pathology, The Women’s and Children’s Hospital, 72 King
William Road, North Adelaide 5006, South Australia, Australia
Emergency toxicology deals with the problems involved
in the rapid presumptive diagnosis and treatment of
suspected poisoning.1±5 In my experience, the most
frequent request by clinicians in poisoning cases is for
identi®cation of the toxin. However, in the current era of
®scal restraint, rationalization in the contemporary
toxicology laboratory dictates that more selec-tive
testing occur. This invariably involves employing simple
analytical techniques to detect drugs, and testing for
poisons other than drugs is largely ignored. 6±13 A
comprehensive drug screen in the hands of
experienced toxicologists will allow identi®cation of
most drug classes, actual drugs and their characteristic
metabolite patterns; recognized exceptions are a
number of quaternary ammonium compounds (water-
soluble, solvent-insoluble), such as the muscle relaxant
pancuronium chloride, the 2-agonist clonidine,
various -adrenergic blockers (e.g. sotalol) and 2-
adrenergic agonists [e.g. salbuta- mol
(albuterol) and
terbutaline]. However, there are serious
limitations when a comprehensive drug
screen is used as the sole means of
diagnosing poisoning,14±17 since these
screens rarely include poisons that are not
drugs.6,9 If evaluation of the poisoned
patient is restricted to a comprehensive
drug screen, carbon monoxide (the principal
single cause of death by poisoning in
England and Wales in 199418) could go
undetected in the absence of informed
discussion between toxicologist and
requesting clinician.
In reality, of course, the toxicologist may be
screening for several poisons without recognizing
this fact. The drug screen exclusivity occurs in a
climate in which there is a decrease in the number
of drug-relatedpoisoningsand an increasein those
19,20
causedbyhouseholdproducts. This occurs,for
example, in children because of tamper-proof
containers. In this group, many poison exposure
cases involve non-pharmaceuticals, such as
petroleum distillates, bleaches, detergents,
Correspondence: Dr Neil R Badcock.
E-mail: badcockn@wch.sa.gov.au
146
Ann Clin Biochem 2000; 37: 146±157
camphor, camphor oil, mothballs, caustic soda,
paints and painting chemicals (turpentine, paint
stripper), rodent killer, ¯uoride/iron tablets, alcohols
(e.g. ethylene glycol and propanol), insecticides
(e.g. from pet care chemicals), swim-ming pool
chemicals, vitamins, heavy metals and many other
21±23
non-drugs. Most of these will not be detected
by a comprehensive drug screen, but the patienthas
ingestedor has been in contactwith a substance that
has produced an injurious or deadly effect. There is
an urgent need for simpler, reliable, low-cost
methods for poison detection.
Rapid access to information that will assist
clinician and toxicologist should be available for
non-pharmaceutical poisonings as well as for
19
medications. A quick differential diagnosis is
desirable to help minimize damage and to ensure
that adequate treatment is initiated quickly. It is
axiomatic that the analyses must be completed in
time to be useful and that the results can be
interpreted. A poison test, even after a lengthy
analysis, can avoid months of fruitless clinical,
biochemical and haematological investigations,
especially in children. It can be an important
consideration in deciding outcome following
organ removal from poisoned donors, with
attention recently being drawn to possible graft
24
damage caused by some poisons. Knowledge
of toxins that have a tendency to cause seizures
25
may also prove invaluable. A broad-based
screen can aid in diagnosis and management,
13
exclude other potential diagnoses and more
expensive tests, or eliminate the need for further
treatment. Moreover, the ®ndings may assist in
de®ning the risk of mutagenicity and genotoxi-
26±29
city for the patient.
Analytical diagnosis is not always simple in
questions of poisoning. Every assistance must
be solicited. A history is useful, including:
What labelled poisons were in the house to
which the patient had access? What is the
case history? Is there a suicide note? What
poisons are common in the area? Does

circumstantial and clinical evidence point to
the ingestion of a speci®c poison?
Do any of the patient’s clinical symptoms
®t the poison, and can appropriate tests be
tailored to these signs and symptoms? Can
the clinical symptoms be reliably linked to
poisons, even multiple ingestions?
What is the smell, colour, pH and general
appearance of the sample? (Indeed, to look
at and smell the urine or stomach contents
should be routine for a good poisons
laboratory.)
What were the speed and intensity of onset?
Has the administration of an antidote had an
effect on the poisoning? In some instances,
use of an antidote may in itself be diagnostic.
Can routine biochemistry, the incorporation of
external biomarkers, radiography, etc., serve
as predictors of poisoning?
Do any non-selective assays have value as
a ®rst step in prompting speci®c tests?
Do the negative ®ndings make a diagnosis
of poisoning unlikely, or do the range and
variety of indicators used permit poisoning
to be excluded de®nitively?
As well as the above, the clinician should
be aware of agents that cause signi®cant
harm if not detected and treated quickly. Iron
and carbon monoxide are two examples of
lethal agents that need a high index of clinical
suspicion for early recognition and require
speci®c tests and speci®c therapy to ensure
a good outcome.
It would be highly desirable if the attending
physician and/or toxicologist had access to
simple, sensitive, rapid and speci®c tests
requir-ing a minimum of equipment and
yielding results in minutes ± i.e. spot tests.
Analogies in drug screening would be the o-
cresol test for paracetamol, the Fujiwara test
for chloral, Trinder’s test for salicylate, colour
reaction using photo-oxidation on thin-layer
chromato-graphy (TLC), or even the
tetrabromophenol-phthalein ethyl ester colour
formation test for certain basic drugs.30±38
Generally, because spot tests lack absolute
speci®city, false positives occur much more
frequently than false negatives.8 Conversely, a
false negative may result from a number of
conditions, including low sensitivity of the
method used, binding of the agent or its
metabolites to protein or other high molecular
weight substances, coupling of the agent or its
metabolites with highly adsorptive or reactive
Poisoning by substances other than drugs 147
compounds, metabolites that react differently
to the parent compound, evaporation of, or
chemical change in, the poison during proces-
sing, masking of colour by other substances
present, outdated or unstable reagents, or
insuf®cient solvent extraction of the com-
pound.39 Some of these pitfalls can be
overcome by including positive and negative
controls in the assay procedure; such controls
should be considered mandatory.
The spot tests described here do not constitute
complete and unambiguous toxicological screen-
ing methods. They are outlined for the purposeof
helping to provide a tentative diagnosis in the
emergency treatment of acute poisoning. The
results of these spot tests must be evaluated with
considerable discretion, which generally comes
after much experienceand insightin toxicological
analysis.
HOUSEHOLD POISONS
Table 1 provides a list of dangerous household
40±42
chemicals. Many of these toxic substances
have come into common use as a result of the
rapid development of new agricultural and
pesticide poisons and because of their ease of
purchase from large hardware supermarkets.
Less than 5% of the poisons in this list will be
detected using a routine drug screen.
ANALYTICAL PREREQUISITES
Proper provision of biological specimens is
necessary for effective poison screening.10,43
Collection of specimens should preferably
occur before any drugs/antidotes are
administered in treatment.
In all cases, collect:
Blood: 5 mL of lithium heparinized blood, 2
mL of blood with sodium ¯uoride pre-servative
and 5 mL of blood without anti-coagulant.
Avoid the use of swabs containing alcohols
and heparin containing phenolic preservative.
Protect from light and freeze at 20 C after
separation of plasma/serum. Urine: send all of
the ®rst sample of urine passed; then collect
a 24-h urine sample. Avoid preservatives,
thymol, sodium azide, etc., and refrigerate at
4 C. Note whether collection involved
catheterization.
Gastric contents: note whether this is vomit,
gastric aspirate or ®rst stomach wash.
Centrifuge or ®lter and carry out tests on
supernatant/®ltrates. Retain solid material
Ann Clin Biochem 2000: 37
148 Badcock

TABLE 1. Examples of household poisons

Medicines Fluoride, antacids, calamine, vitamins, iron, lithium, liniments, antiseptics, haematinics
Plants Foxglove, oleander, poison ivy, mushrooms, seeds/kernels, cherry, thorn apple
Insecticides Ant, cockroach, rodent and moth poisons, animal ¯ea collars and powders
Household products Acids, alkalis, camphor, carbon monoxide, bleach, drain cleaner, rug cleaner, wallpaper
cleaner, laundry ink, disc batteries, moth balls, cosmetics, essential oils, detergents
Garage Kerosene/paraf®n, ®re lighters, ®re starting tablets, ®re extinguishers, paints, painting
supplies, weedkillers, slug pellets, petrol, arsenic, lead, swimming pool chemicals, antifreeze,
fumigants, car cleaning products, hobby chemicals

and do not add preservative. Gastric contents
can be extremely useful if collected shortly
after the poison was ingested.
Others: hair, nails, saliva, sweat and meco-
nium. Submit and retain any materials
found with the patient or that may be
implicated in the poisoning (bottles, labels,
capsules, plant material, suicide note, etc.).
Testing may involve adding reagent to the
sample, or dissolving the material to be
tested in an appropriate solvent prior to the
addition of colour reagent.
A toxicology request form should be carefully
completed and accompany the specimens to the
laboratory. Essential information that can be
obtained through such a request form includes
clinical summary (condition of patient, signs,
symptoms), drugs/poisons suspected, current
treatment and all drugs administered prior to
44
sample collection.
SIGNS AND SYMPTOMS AS PREDICTORS
A careful clinical evaluation using the history,
physical examination and the more readily
available laboratory tests may allow a tentative
45,46
diagnosis and initiation of treatment. Clin-ical
®ndings of importance include altered blood
pressure, pulse, respiration and body tempera-
ture, the presence of coma, agitation, delirium or
psychosis, and muscular weakness. An ophthal-
mological examination is also important in the
47
acutely poisoned patient. Oral burns or
dysphagia may occur following ingestion of any
strongly reactive substance, but the absence of
oral burns does not exclude the possibility of
48
oesophageal injury. Odours and skin colour
49
may also contribute to the diagnosis.
The presence of a particular clinical manifes-
tation may be enough to direct attention toward a
3
particular group or type of poison. Alter-natively,
it may help to rule out other possibilities. For
example, a coma could point to organic solvents,
naphthalene etc., rather
than strychnine or dieldrin,25 as long as the
vehicle in which it is formulated is not itself an
organic solvent (e.g. kerosene or toluene).
40,42,50,51
Poisons have characteristic effects.
Consequently, clinical assessment, accompanied
by knowledge of which symptoms are associated
with which causative agent, can be used to direct
45
poison screening efforts. Toxins mediate re-
cognizable patterns of symptoms by stimulating
an agonistic or antagonistic response at one or
more receptors. There are two toxidromes
associated with cholinergic poisoning: one
caused by muscarinic agonists and the other by
nicotinic agonists. Potential toxins causing these
syndromes are outlined in Table 2, together with
toxins that have anticholinergic properties and
other symptoms.
SPOT TESTS
Routine drug screening requires many analytical
tools, such as colour tests, immunoassays, Toxi-
Lab (Ansys Diagnostics, Lake Forest CA, USA),
TLC, gas±liquid chromatography, high-
performance liquid chromatography and/or gas
2,15,52±55
chromatography±mass spectrometry. In
non-drug poisoning, however, information ob-
tained from very simple, rapid, invariably
colourimetric, and inexpensive screening tests is
often invaluable, especially when combined with
conventional biochemical screening and routine
haematological analysis.
40,42,56
A variety of spot tests are summarized in Table
57±89
3. They constitute a group of simple chemical
reactions requiring limited or no sample preparation
which, through their relative non-speci®city, can be
used to indicate potential poisons quickly or rule out
the presence of select compounds. Prominent are
those that would be performed as part of a drug
screening protocol and can also be used for the
screening of certain poisons. Although tests such as
atomic absorp-tion spectroscopy are more
de®nitive, a positive result from a relatively non-
speci®c test may direct the analyst to more speci®c
tests or suggest

Ann Clin Biochem 2000: 37

 Poisoning by substances other than drugs 149
TABLE 2. Physiological responses to various poisons

Signs/symptoms Likely poison(s)

General
Diarrhoea, urination, miosis, bradycardia, Organophosphates, betel nut, pilocarpine, carbachol,
bronchorrhoea, emesis, lacrimation, salivation acetylcholine, poisonous mushrooms
(DUMB-BELS)
Tachycardia, hypertension, weakness or paralysis, Insecticides, nicotine, spider venom
muscle fasciculations
Delusions, hallucinations, convulsions, coma Volatile substance abuse
Salivation, lacrimation, urinary incontinence, Carbamates
diarrhoea, gastrointestinal cramping, emesis
Breath odour
Bitter almonds Cyanide
Garlic Malathion, parathion, arsenic, phosphorus, tellurium
Alcohol Phenols, alcohols
Ethereal (sweet) Ether
Stale tobacco Nicotine
Acetone/penetrating Lacquer
Coal gas Carbon monoxide
Acrid Paraldehyde
Phenolic (disinfectants) Creosotes, phenols
Shoe polish Nitrobenzene
Pears Chloral
Colour of skin and mucous membranes
Hyperaemia Cyanide, alcohol
Jaundice/yellow skin Mushrooms, nitro compounds, phosphorus, picric acid,
carbon tetrachloride, atrabine
Cyanosis Aniline, nitrobenzene, nitrites, nitrates, parathion,
chlorates, marking ink
Cherry red or pink skin Carbon monoxide, cyanides
Pallor Benzene, lead, naphthalene, chlorates, solanine, ¯uoride,
plant poisons, carbon monoxide
Blue-grey skin Silver salts
Blue-black gum line Bismuth, lead, mercury
Skin rash Antimony, arsenic, turpentine, coal-tar derivatives
Etching of the skin Corrosives
Discolouration of mouth or pharynx, distension Any poison
and spasticity of the abdomen
Vomiting, neck stiffness Strychnine
Red (boiled lobster) skin/desquamation Boric acid
Respiration
Increased Dinitrophenol, cyanide, carbon monoxide
Wheezing Cholinesterase inhibitors
Eyes
Miosis Carbamate pesticides, organophosphates
Mydriasis Barium, benzene, thallium, camphor
Temperature
Increased Arsenicals, boric acid, camphor, dinitrophenols
Decreased Aconite (herbal preparations), ether, chloroform, nitrites
Sweating Organophosphate insecticides
Genitourinary system
Anuria Mercurials, bismuth, chloride, carbon tetrachloride,
turpentine

the need for further evaluation. In an environ- completed in minutes. The analytical time
ment in which ef®ciency is paramount, the use of required to carry out all the procedures listed is
established protocols and screening assays is approximately 3 h, but, by modifying the proce-
preferable. Most individual spot tests can be dure to incorporate only those poisons suspected

Ann Clin Biochem 2000: 37

150 Badcock

TABLE 3. Spot tests (many are adaptations/extensions of some commonly used spot tests for drugs)

Test Sample Common analyte(s) Additional poisons detected

Acid hydrolysis, o-cresol/ Urine, gastric Paracetamol Iodine, iodide, radio-opaque material
53,57
ammonia contents (purple fumes), sulphide (yellow
fumes), bromide (reddish-brown
fumes); aniline, nitrobenzene (blue),
ethylenediamine (green)
Aminolaevulinic acid Urine, plasma Lead Gold, vinyl chloride, hexachloroben-
78±80
(ALA) zene, polychlorinated biphenyls, poly-
brominated biphenyls, dioxin, lindane,
silver, 2,4,5-T (2,4,5-trichlorophenox-
yacetic acid), lead (ALA increased)
Basophilic stippling (zinc Blood Lead Mercury, bismuth ( 30 stippled red
42
protoporphyrin) cells per 10 000 cells)
53,77
Blood colour Blood Carbon monoxide Cyanide (cherry-red), nitrates, nitrites,
chlorates, aniline, dyes (chocolate),
solanine, lead, chlorates, naphthalene,
plants, snake bite (anaemia)
Cholinesterase inhibition test Serum, red Organophosphate Carbamates
(pseudocholinesterase ± acute; cells
4
true cholinesterase ± chronic)
Clinitest (Ames ) Urine Acetone Isopropanol, hippuric acid (purple)
53,61,75
Conway/dichromate Blood, urine, Ethanol Methanol, chloroform, aldehydes (e.g.
gastric contents metaldehyde), ethylene glycol (green-
Coproporphyrin
80 blue)
Urine, hair, Lead Heavy metals ± chronic exposure (co-
77 nails proporphyrin increased)
Digoxin immunoassay
Urine Digoxin Aconitine alkaloids, colchicine, cardiac
57,61±63 glycosides (cross-reactivity)
Diphenylamine
Gastric Ethchlorvynol Hypochlorites, chlorates, dichromates,
contents phenazopyridine nitrites, bromates, peroxides, iodates,
vanadates, glyceryl trinitrate, perman-
ganates (blue)
Direct ultraviolet spectrophoto- Diluted gastric Compounds with high Disinfectants, pesticides (paraquat),
59,60
metry (standard scan contents, absorbances herbicides (ametryne), rodenticides
350±220nm; standard zero ingested (warfarin)
order, ®rst and second material
derivatives)
53
Dithionite/alkali Urine, gastric Paraquat, diquat Benzalkonium, cetylpyridinium chlor-
§ 83 contents ides (blue-black)
Ethyl alcohol assay (EMIT )
Gastric Ethanol Methanol, isopropyl alcohol (increased
contents absorbance change)
Exposure biomarkers [glucaric Urine Various Various
acid, thioethers, urinary
bacterial assay for mutagenic
activity (as an equivalent to
thiocyanate in de®ning
84±87
smoking status)]
42
Fluorescence Urine, gastric Fluorescein Ethylene glycol (from antifreeze
contents colourant), also calcium oxalates
Fujiwara (pyridine/NaOH)
30,58 (glycolic acid tests as con®rmation)
Urine, gastric Chloral hydrate Chloroform, carbon tetrachloride,
contents 2,4,5-T, toxaphene, dichloral phena-
zone, strobane, methyl bromide, chlor-
amphenicol, trichloroethylene (red-
Gas chromatography
64±66 purple colour in pyridine)
Blood, urine, Volatile compounds Pesticides
1,53 gastric contents
Gastric contents (odour)
Gastric Volatile Lysol, camphor, creosotes, methyl sal-
contents icylate (characteristic odours)

(Continued)

Ann Clin Biochem 2000: 37

 Poisoning by substances other than drugs 151
TABLE 3. (Continued)

Test Sample Common analyte(s) Additional poisons detected

53 Gastric Blue ferrous Dye from rat poison, tablet, capsules,
Gastric contents (colour)
contents phosphate etc. (various)
Gastric contents (pH; normal Gastric Acid Alkali
53
pH 3±4) contents
76
LaBrosse spot test Urine Vanillylmandelic acid Styrene (violet)
81,82
Malondialdehyde Urine, blood Lipid peroxidation Heavy metals, carbon tetrachloride,
paraquat
Merckoquant test strips (Merck Gastric Arsenic, nitrate, nitrite Manganese, chloride lead, iron, chro-
KGaA*) contents mate, bromide, iodide, zinc, copper,
cyanide (colours indicated on analytical
kits)
Paracetamol/ammonia (positive Urine, gastric Naphthalene, para- Chlorothion, creosote, benzene, resor-
paracetamol control minus contents thion, phenols cinol, EPN, dicapthion, methylpar-
o-cresol) athion (blue)
57,63,67
Platinum wire ± ¯ame Gastric Barium salts Lithium (crimson-red), thallium, cop-
77,88,89 contents per (green), sodium (orange-yellow)
Radiology Abdominal Radio-opaque Chlorinated pesticides, hydrocarbons,
radiograph or material arsenic, enteric coated material, iron
ultrasound tablets, mercury, lead, lithium (radio-
Reinsch
57 opaque)
Urine, gastric Arsenic Antimony, bismuth (black), mercury
contents (silver), sulphur, tellurium (dull black)
[NB: heavy metal poisonings have
resulted following exposure to herbal
medicines, especially tonics, aphrodi-
Rothera’s
68,69 siacs and treatment for eczema]
Urine, gastric Ketones -Butyrolactone (blue)
contents
Silver nitrate (nitric acid, barium Gastric Anions Bromide, iodide (yellow), cyanide
3,4
chloride) contents (grey), chloride, hypochlorite, various
acids, thiocyanate (white)
Toxi-Lab A (standard protocol) Urine, gastric Basic drugs Thymol, phenol, cresol, naphthol, ma-
contents lathion, strychnine, nicotine, turpentine
(Rf and colours)
Toxi-Lab A (Badcock: xanthine, Urine, gastric Theophylline Alkaloids, xanthines, nitrogenous bases
70,71
pre-extraction modi®cation) contents (enhanced stain)
Toxi-Lab A (residue, alkaline Urine Thioethers Hydrocarbons, arylamines/halides/es-
hydrolysis, Ellman’s reagent, ters, nitro/cycloalka(e)nes, sulphur,
72,73
412nm) mustards (enhanced absorbance)
Toxi-Lab (alcohol) Plasma Ethanol Methanol, ethylene glycol (blue spot)
Toxi-Lab B (aliquot in separate Urine Hippuric acid Benzene, toluene, xylene, benzoate,
well, benzenesulphonyl chloride styrene (red-orange), nitrobenzoyl
74
in pyridine) chloride (yellow)
Toxi-Lab B (standard protocol: Urine, gastric Acidic drugs Warfarin (yellow spot)
acidi®ed KMnO4 solution contents
following HgCl2/diphenyl-
carbazone)
35
Trinder’s Urine Salicylates Methyl salicylate, benzene, phenol,
ketones, oxalates, thiocyanates, azides
(violet), acetic acid (orange-red), tur-
Turmeric paper
1 pentine (violet-blue)
Gastric Borates Iodates, nitrites, bleach, chlorates,
42 contents bromates (bleached turmeric paper)
Urine colour Urine Metabolic Lead, aloe (rose colour), turpentine,
phenols (blue) cascara, phenolphtha-
lein, senna, ¯uorescein (orange) nitro-
Urine odour
42 benzene (brown)
Urine Metabolic disorder Turpentine (violets), chloroform
(sweet), disinfectants (phenolic)
*E Merck, Darmstadt, Germany. Ansys Diagnostics Inc., Lake Forest CA, USA. Bayer Diagnostics,
§
Mulgrave, Australia. Enzyme Multiplied Immunoassay Technique, Behring Diagnostics, Cupertino CA, USA.
EPN=phenyl-phosphonothioic acid O-ethyl O-(4-nitrophenyl) ester.

Ann Clin Biochem 2000: 37

152 Badcock
clinically, this time can be reduced considerably.
On mostoccasions,thepoisoningestedwill re¯ect
the clinical condition of the patient.
Biological specimens that are highly pigmen-
ted, visually contaminated (e.g. with food
particles) or proteinaceous may require isolation
procedures. Spot tests are then applied to the
4
extracted and concentrated residues. These
tests may involve direct colour formation of the
sample with added reagent or dissolving the
material to be tested in an appropriate solvent.
All reagents are stable for at least 3 months
when stored at room temperature and protected
from direct sunlight.
The most useful methods for initial
screening are those that combine two or more
major groups of poisons. As with all screening
tests, a positive result is presumptive and
points towards more speci®c assays. Intuition
also plays a role in a general screen.
Essential spot tests
Several toxins require rapid identi®cation.
59,90,91
Those discussed here (Table 4) should be offered
on an emergency basis. Although symptoms from
ingestion of cyanide and iron may appear very
rapidly, they may also not manifest for several
hours. Further, following carbon mon-oxide
poisoning, the victim may appear normal upon the
regression of symptoms, but perma-nent cerebral
damage cannot be excluded. Delay in the
appearance of symptoms or the apparent absence
of after-effects can give rise to a false sense of
security. Treatment with the appro-priate antidote is
urgent, and can save lives.
HAIR AND NAILS
In theory, hair and nails would appear to be
ideal biological indicators since sampling is
non-invasive, the medium is inde®nitely stable
on storage, and a temporal pro®le of
exposure along the hair or nail length is
possible.92±95 Further, trace element
concentrations in hair are approximately 10-
fold greater than in blood or urine.96
TABLE 4. Spot tests that are essential if there is any suspicion that the listed poisons have been ingested
Test
Lee±Jones test (NaOH/FeSO4/HCl)
K3FeCN6 (potassium ferricyanide)
K4FeCN6 (potassium ferrocyanide)
NH4OH
Ann Clin Biochem 2000: 37
In practice, however, there are severe limita-
tions on the use of hair and nails as systemic or
internal indicators of exposure. It is virtually
impossible to avoid external contamination by
ubiquitous heavy metals (e.g. lead), and there
are no accurate validation techniques for
assessing hair cleaning, although this in itself
may prove a valid external exposure indicator if
not an internal indicator. Hair analysis is useless
for thallium because thallium is not incorpo-rated
93
into hair.
In addition to methodological hazards, the
biokinetics of heavy metals in hair and nails
are not understood suf®ciently well to allow
their reliable use as biological indicators.
ANTIDOTES
Antidotes, administered after presumptive iden-
ti®cation of the poison, can also be diagnos-
40,42,97±102
tic. For example, the cholinesterase
inhibitor physostigmine, when used as an
antidote, can reverse toxic anti-muscarinic
effects. Table 5 lists some antidotes and
protective agents used to treat acute poisoning.
NATURAL TOXINS
Most naturally occurring toxins are very com-
plex and cannot be easily identi®ed by normal
laboratory methods. Therefore, the identi®ca-
tion of natural toxins and the diagnosis of
toxicity may be dif®cult. However, the labora-
tory has a very important role in the manage-
ment of these patients.41,42,103
Plants containing cardiac glycosides
Patients poisoned by plants containing cardiac
glycosides (e.g. foxglove) will have elevated
glycoside levels (digoxin, digitoxin); plants
containing warfarin will cause an elevation in
the prothrombin time.
Plants containing hepatotoxins
Elevations in liver enzymes may be the ®rst
manifestation of toxicity caused by plants and
mushrooms that contain hepatotoxins.
Sample Poison
Gastric contents Cyanide
Gastric contents Fe2+
3+
Gastric contents Fe
Blood Carbon monoxide
 Poisoning by substances other than drugs 153
TABLE 5. Antidotes and their application

Antidote Use

Activated charcoal Many types of overdose

Atropine Organophosphate poisoning
2,3-Dimercaptosuccinic acid Oral chelating agent for lead, mercury, arsenic poisoning
(DMSA)
Desferrioxamine Given intravenously or intramuscularly for chelating iron
Dimercaprol (British anti- Chelates mercury, arsenic, lead
Lewisite, BAL)
Calcium disodium edetate Primarily used to chelate lead
Amyl nitrite Cyanide
Ethanol Competes for alcohol dehydrogenase, thereby preventing the production of the
toxic metabolites of methanol and ethylene glycol
Folic acid, leucovorin In conjunction with ethanol in the treatment of methanol (folinic acid) poisoning
Haemodialysis Lithium
Hyperbaric oxygen Carbon monoxide, hydrogen sulphide and carbon tetrachloride toxicity
Methylene blue Methaemoglobinaemia
4-Methylpyrazole (investiga- Methanol and ethylene glycol poisoning
tional)
Physostigmine To reverse effects from poisoning with an anticholinergic agent
Pralidoxime Organophosphate poisoning
Pyridoxine Poisoning with isoniazid, monomethyl hydrazine (Gyromitra esculenta mushroom)
and, in combination with ethanol, in the treatment of ethylene glycol poisoning
Thiamine hydrochloride In conjunction with ethanol in the treatment of ethylene glycol poisoning

Snakes attempting suicide by self-poisoning is

The snake-bite victim usually dies from a diffuse
coagulopathy or renal failure secondary to
myoglobinuria.
104
There have been some recent
advances in the diagnosis of snake bite in
Australia using an enzyme-linked immunosor-
105,106
bent assay to determine the species of
snake responsible for the bite. This test has been
used in the ®eld and has been fairly reliable.
There are no tests currently available for
determining pit viper envenomation. Laboratory
assessment of coagulation is helpful.
OTHER PREDICTORS
As well as spot tests, clinical information and
biomarkers, there are other predictors of
poisonings. These include demographic vari-
ables (gender, age, race, educational level),
calendar season, location (metropolitan or non-
metropolitan), exposure to chemicals at work, by
students in science or technology classes and so
107±111
on. For example, children aged less than 3
years and boys were most often the victims of
accidental poisoning,
112
and the incidence of
poisonings was 80% higher during the working
hours of the day than during the late afternoon,
evening hours or the weekends, the times when
both parents are usually at home.
113
With adults,
however, the risk of
greatest in the early evening (20:00±21:00h),
whereas the risk of successful suicide by self-
poisoning is greatest during the late morning
(10:00± 13:00h).114±116
LABORATORY BIOCHEMISTRY
Many routine biochemical tests can provide
markers for the presence of poisons and can
be helpful in the diagnosis of both acute and
chronic poisoning and in assessing prognosis.
Laboratory tests should include serum osmol-
ality, electrolytes, glucose and urea and
estima-tion of the anion and osmolar
gaps.45,117,118 The electrocardiogram can also
provide useful in-formation.119
As examples, hypokalaemia occurs in barium
poisoning, hyponatraemia can result from many
causes, including water intoxication, hypocal-
caemia can occur in ethylene glycol poisoning
and hyperkalaemia or hypernatraemia occurs in
iatrogenic, accidental or deliberate overdose with
potassium or sodium salts. Metabolic acidosis
with a raised anion gap may result from severe
poisoning with boric acid, carbon monoxide,
cyanide, iron, ethylene glycol, metha-nol,
41,42
¯uoroacetates and paraldehyde. Table 6
summarizes abnormal laboratory biochemistry in
non-drug poisonings.

Ann Clin Biochem 2000: 37

154 Badcock

TABLE 6. Biochemical abnormalities associated with toxins

Abnormality Potential toxins

Hypocalcaemia Oxalates, potassium phosphate, ethylene glycol, ¯uorine, organic tin compounds
Hypercalcaemia Vitamin D
Hyponatraemia Dilution (e.g. water intoxication)
Hypernatraemia Dehydration, sodium, potassium salts
Hypokalaemia Barium salts
Hyperkalaemia Foxglove, scilliroside
Hypoglycaemia Alcohols, lithium, calcium salts, pyridoxine, akee, plant toxins
Hyperglycaemia Nicotine
Increased osmolar gap Methanol, ethanol, glycerol, isopropanol, ethylene glycol
Metabolic acidosis with Iron, lithium, carbon monoxide, cyanide, benzyl alcohol, toluene, methanol,
raised anion gap paraldehyde, ethylene glycol, strychnine
Respiratory acidosis Carbon monoxide, cyanide

When combined with other biochemistry, 3 Kaye S. Handbook of Emergency Toxicology,

these laboratory tests are likely to be even
more useful in clinical toxicology. For
example, calcium oxalate or hippurate crystals
in the urine of a patient with a high anion gap,
metabolic acidosis and increased serum
osmolar gap will provide a rapid result of great
value as an indicator of ethylene glycol
poisoning; similarly, increased osmolar gap
and anion gap, metabolic acidosis and ocular
®ndings strongly suggest methanol
poisoning.120 Blood glucose is increased after
lead or alcohol poisoning and serum uric acid
is also increased after alcohol ingestion.
CONCLUSION
Several simple chemical reactions can be used
to indicate or rule out the presence of potential
poisons. When they form part of, or can be
readily adapted from, a routine drug screening
protocol, the range of the screen is broadened.
These colour or spot tests are direct tests that
involve limited or no sample preparation. They
can provide at least an initial indication of
poisons present or absent, and an uncon®rmed
identi®cation of the poison or family of poisons,
often within minutes of receiving specimens. A
positive result initiates more speci®c con®rma-
tory tests or suggests the need for further
evaluation.
REFERENCES
1 Curry AS. Poison Detection in Human Organs,
3rd ed. Spring®eld IL: Charles C Thomas, 1976
2 Jatlow PI, Bailey DN. Analytical toxicology. In:
Sonnenwirth A, Jarett L, eds. Gradwohl’s Clinical
Laboratory Methods and Diagnosis. St Louis MO:
Mosby, 1980: 387±434
4th ed. Spring®eld IL: Charles C Thomas, 1980
4 Moffat AC, ed. Clarke’s Isolation and
Identi®cation of Drugs, 2nd ed. London:
Pharmaceutical Press, 1986
5 Baselt RC, Cravey RH. Disposition of Toxic
Drugs and Chemicals in Man, 3rd ed. Chicago
IL: Year Book Medical, 1990
6 McCarron MM. The use of toxicology tests in
emergency room diagnosis. J Anal Toxicol 1983;
7: 131±5
7 Skelton H, Dann LM, Ong RTT, Hamilton H, Ilett
KF. Drug screening of patients who deliberately
harm themselves admitted to the emergency
department. Ther Drug Monit 1998; 20: 98±103
8 Bailey DN. Comprehensive toxicology screening:
the frequency of ®nding other drugs in addition
to ethanol. Clin Toxicol 1984; 22: 463±71
9 Bateh, RP. Drug screening in hospital clinical
laboratories. Clin Lab Med 1987; 7: 371±88
10 Hepler BR, Sutheimer CA, Sunshine I. The role
of the toxicology laboratory in emergency
medicine. Study of an integrated approach. Clin
Toxicol 1985; 22: 503±28
11 Done AK. The toxic emergency: using the
toxicology laboratory. Emerg Med 1984; 284: 1650
12 Ingel®nger JA, Isakson G, Shine D, Costello CE,
Goldman P. Reliability of the toxicology screen in drug
overdose. Clin Pharmacol Ther 1981; 29: 570±5
13 Taylor RL, Cohen SL, White JD. Comprehensive
toxicology screening in the emergency
department an aid to clinical diagnosis. Am J
Emerg Med 1985; 3: 507±11
14 Stewart MJ. Drug analysis in poisoned patients.
The need to be speci®c. Ann Clin Biochem
1982; 19: 254±7
15 Bailey DN. Results of limited versus comprehen-
sive screening in a university medical centre. Am
J Clin Pathol 1996; 105: 572±5
16 Wiley JF. Dif®cult diagnoses in toxicology.
Poisons not detected by the comprehensive drug
screen. Pediatr Clin North Am 1991; 38: 725±37
17 Catrou PG, Khazanie P. Limited toxicology
screening. End of a controversy? Am J Clin
Pathol 1996; 105: 527±8

Ann Clin Biochem 2000: 37


18 Watson ID. Laboratory support in poisoning.
Ther Drug Monit 1998; 20: 490±5
19 Hepler BR, Sutheimer CA, Sunshine I. Role of
the toxicology laboratory in the treatment of
acute poisoning. Med Toxicol 1986; 1: 61±75
20 Marchi AG, Messi G, Renier S, Gallone G,
Peisino MG, Vietti-Ramus M, et al. The risk
associated with poisonings in children. Vet Hum
Toxicol 1994; 36: 112±6
21 Braggion F, Ceriotti F, Chiumello G. Pediatric
emergency laboratory. Z Med Lab Diagn 1991;
32: 159±62
22 Chitsike I. Acute poisoning in a paediatric
intensive care unit in Harare. Cent Afr J Med
1994; 40: 315±9
23 Perharic L, Shaw D, Colbridge M, House I, Leon
C, Murray V. Toxicological problems resulting
from exposure to traditional remedies and food
supple-ments. Drug Saf 1994; 11: 284±94
24 Hantson P, Vekemans MC, Squif¯et JP, Mahieu P.
Outcome following organ removal from poisoned
donors: experience with 12 cases and a review of
the literature. Transpl Int 1995; 8: 185±9
25 Kunisaki TA, Augenstein WL. Drug- and toxin-
induced seizures. Emerg Med Clin North Am
1994; 12: 1027±56
26 Barton HA, Das S. Alternatives for a risk
assessment on chronic noncancer effects from
oral exposure to trichloroethylene. Regul Toxicol
Phar-macol 1996; 24: 269±85
27 Bhisey RA, Govekar RB. Biological monitoring of
bidi rollers with respect to genotoxic hazards of
occupational tobacco exposure. Mutat Res 1991;
261: 139±47
28 Marks HS, Anderson JL, Stoewsand GS. Inhibi-
tion of benzo[a]pyrene-induced bone marrow
micronuclei formation by diallyl thioethers in
mice. J Toxicol Environ Health 1992; 37: 1±9
29 Faux SP, Gao M, Aw C, Braithwaite RA.
Molecular epidemiological studies in workers
exposed to chromium-containing compounds.
Clin Chem 1994; 40: 1454±5
30 Fujiwara K. Sitzungsber Abh Naturforsch Ges
Rostock 1914; 33: 6
31 Rio GR, Hodnett CN. Evaluation of a colorimetric
screening test for basic drugs in urine. J Anal
Toxicol 1981; 5: 267±9
32 Volf K, Zloch Z. Color reaction in the detection of
drugs using photooxidation on thin-layer
chroma-tography. Soudni Lek 1995; 40: 6±8
33 Fiegel F, Anger V. Spot Tests in Organic
Analysis, 7th ed. Amsterdam: Elsevier, 1966
34 Sunshine I. Methodology for Analytical Toxicology,
2nd ed. Cleveland OH: CRC Press, 1975
35 Trinder P. Rapid determination of salicylate in
biological ¯uids. Biochem J 1954; 57: 301±3
36 Forrest IS, Forrest FM. Urine color test for the
detection of phenothiazine compounds. Clin
Chem 1960; 6: 11±5
37 Forrest IS, Forrest FM, Mason AS. A rapid urine
color test for imipramine. Am J Psychiatry 1960;
116: 1021±2
38 Decker WJ, Treuting JJ. Spot tests for rapid
diagnosis of poisoning. Clin Toxicol 1971; 4: 89±97
Poisoning by substances other than drugs 155
39 Woolf AD, Shannon MW. Clinical toxicology for
the pediatrician. Pediatr Clin North Am 1995; 42:
317±33
40 Dreisbach RH, Robertson WO. Handbook of
Poisoning: Prevention, Diagnosis and Treatment,
12th ed. Norwalk CT: Appleton & Lange, 1987
41 Goldfrank LR, Flomenbaum NE, Lewin NA,
Weisman RS, Howland MA, Hoffman RS, eds.
Goldfrank’s Toxicologic Emergencies, 5th ed.
Nor-walk CT: Appleton & Lange, 1994
42 Ellenhorn MJ, Schonwald S, Ordog G, Wasserber-
ger J. Ellenhorn’s Medical Toxicology: Diagnosis
and Treatment of Human Poisoning, 2nd ed.
Baltimore MD: Williams & Wilkins, 1997
43 Forrest AR. ACP Broadsheet No. 137: April
1993. Obtaining samples at post mortem
examination for toxicological and biochemical
analyses. J Clin Pathol 1993; 46: 292±6
44 National Committee for Clinical Laboratory
Standards. Development of requisition forms for
therapeutic drug monitoring and/or overdose
toxicology. NCCLS Document T/DM1-A, Vol. 11,
No. 1. Wayne PA: NCCLS, 1991
45 Olson KR, Pentel PR, Kelley MT. Physical
assessment and differential diagnosis of the
poisoned patient. Med Toxicol 1987; 2: 52±81
46 Bond GR. The poisoned child. Evolving conceptsin
care. Emerg Med Clin North Am 1995; 13: 343±55
47 Good WV, Jan JE, DeSa L, Barkovich AJ,
Groenveld M, Hoyt CS. Cortical visual impair-ment
in children. Surv Ophthalmol 1994; 38: 351±64
48 Clausen JO, Nielsen TL, Fogh A. Admission to
Danish hospitals after suspected ingestions of
corrosives. A nationwide survey (1984±1988)
comprising children aged 0±14 years. Dan Med
Bull 1994; 41: 234±7
49 Flanagan RJ, Ives RJ. Volatile substance abuse.
Bull Narc 1994; 46: 49±78
50 Liang HK. Clinical evaluation of the poisoned
patient and toxic syndromes. Clin Chem 1996;
42: 1350±5
51 Lima JS, Reis CA. Poisoning due to illegal use
of carbamates as a rodenticide in Rio de
Janeiro. J Toxicol Clin Toxicol 1995; 33: 687±90
52 Ray JE, Reilly DK, Day RO. Drugs involved in
self-poisoning: veri®cation by toxicological
analy-sis. Med J Aust 1986; 144: 455±7
53 Widdop B. Simple tests to detect poisoning. J
Clin Pathol 1988; 41: 996±1004
54 Dawling S, Ward N, Essex EG, Widdop B. Rapid
measurement of basic drugs in blood applied to
clinical and forensic toxicology. Ann Clin
Biochem 1990; 27: 473±7
55 Pach J, Panas M, Soltycka M, Wilimowska J. The
use of REMEDI HS in toxicological diagnostics of
patients poisoned with drugs at the Department of
Toxicology Collegium Medicum of the Jagiellonian
University in Krakow. Przegl Lek 1996; 53: 377±9
56 Diaz J, Tornel PL, Martinez P. Reference intervals
for blood ammonia in healthy subjects determined
by microdiffusion. Clin Chem 1995; 7: 1048
57 Flanagan RJ, Braithwaite RA, Brown SS, Widdop B,
de Wolff FA. Basic Analytical Toxicology. Geneva:
World Health Organization, 1995
Ann Clin Biochem 2000: 37
156 Badcock
58 Moss MS, Rylance HJ. The Fujiwara reaction:
observations on the mechanism. Nature 1966;
210: 945±6
59 Jinno K, Kuwajima M, Hayashida M, Watanabe T,
Hondo T. Automated identi®cation of toxic
substances in human poisoned ¯uids by a retention
production system in reversed-phase liquid chro-
matography. J Chromatogr 1988; 436: 11±21
60 Kohler P, Hahn W. Spectrophotometric demon-
stration of poison in the routine clinical chemistry
laboratory. Z Gesamte Inn Med Ihre Grenzgeb
1977; 32: 489±91
61 Stair EL, Whaley M. Rapid screening and spot
tests for the presence of common poisons. Vet
Hum Toxicol 1990; 32: 564±6
62 Wong SHY, Sunshine I, eds. Handbook of
Analytical Therapeutic Drug Monitoring and Tox-
icology. Boca Raton FL: CRC Press, 1997
63 Bamford F. Poisons: Their Isolation and Identi®ca-
tion, 3rd ed. London: J&A Churchill, 1951
64 Foerster EH, Garriott JC. Analysis for volatile
compounds in biological samples. J Anal Toxicol
1981; 5: 241±4
65 Flanagan RJ, Ruprah M, Meredith TJ, Ramsey
JD. An introduction to the clinical toxicology of
volatile substances. Drug Saf 1990; 5: 359±83
66 Manno BR, Manno JE. A simple approach to gas
chromatographic analysis of alcohols in blood
and urine by a direct injection technique. J Anal
Toxicol 1978; 2: 257±61
67 Fiegel F, Anger V. Spot Tests in Inorganic
Analysis, 6th edn. Amsterdam: Elsevier, 1972
68 Rothera ACH. Note on the sodium nitro-prusside
reaction for acetone. J Physiol 1908; 37: 491±4
69 Badcock NR, Zotti R. Rapid screening test for
gamma-hydroxybutyric acid (GHB, Fantasy) in
urine. Ther Drug Monit 1999; 21: 376
70 Badcock NR, Zoanetti GD. Modi®cation of Toxi-
Lab procedure for enhanced theophylline detec-
tion. Ann Clin Biochem 1994; 31: 586±8
71 Badcock NR, Zoanetti GD. Modi®cations to Toxi-
Lab for the routine screening for drugs in paediatric
toxicology. Ann Clin Biochem 1996; 33: 75±7
72 Ellman GL. Tissue sulfhydryl groups. Arch
Biochem Biophys 1959; 82: 70±7
73 Burgaz S, Borm PJ, Jongeneelen FJ. Evaluation
of urinary excretion of 1-hydroxypyrene and
thioethers in workers exposed to bitumen fumes.
Int Arch Occup Environ Health 1992; 63:
397±401
74 Tomokuni K, Ogata M. Direct colorimetric
determination of hippuric acid in urine. Clin
Chem 1972; 18: 349±51
75 Stevens HM. The detection of some non-drug
poisons in simulated stomach contents by
diffusion into various colour reagents. J Forensic
Sci Soc 1986; 26: 137±45
76 LaBrosse EH. Biochemical diagnosis of
neuroblas-toma: use of a urine spot test. Proc
Am Assoc Cancer Res 1968; 9: 39±42
77 Weisman RS, Howland MA, Verebey K. The
toxicology laboratory. In: Goldfrank LR, et al., eds.
Goldfrank’s Toxicologic Emergencies, 5th ed.
Norwalk CT: Appleton & Lange, 1994: 99±108
Ann Clin Biochem 2000: 37
78 Goujon R, Philibert E, Bernard P, Normand J,
Boucherat M. Determination of plasma delta-
aminolaevulinic acid levels. Applications. Ann
Biol Clin 1992; 50: 675±7
79 Graziano JH. Validity of lead exposure markers
in diagnosis and surveillance. Clin Chem 1994;
40: 1387±90
80 Simmonds PL, Luckurst CL, Woods JS. Quanti-
tative evaluation of heme biosynthetic pathway
parameters as biomarkers of low-level lead ex-
posure in rats. J Toxicol Environ Health 1995;
44: 351±67
81 Badcock NR, Zoanetti GD, Martin ES. A non-
chromatographic assay for the
malondialdehyde± thiobarbituric acid adduct with
HPLC equivalence. Clin Chem 1997; 43: 1655±7
82 Mihara M, Uchiyama M, Fukuzawa K. Thiobar-
bituric acid value on fresh homogenate of rat as
a parameter of lipid peroxidation in aging, CCl 4
intoxication, and vitamin E de®ciency. Biochem
Med 1980; 23: 302±11
83 Jarvie DR, Simpson D. Simple screening tests
for the emergency identi®cation of methanol and
ethylene glycol in poisoned patients. Clin Chem
1990; 36: 1957±61
84 Van Doorn R, Leijdekkers CH-M, Bos RP,
Brouns RME, Henderson PTH. Enhanced
excretion of thioethers in urine of operators of
chemical waste incinerators. Br J Ind Med 1981;
38: 187±90
85 Brewster MA. Biomarkers of xenobiotic
exposures. Ann Clin Lab Sci 1988; 18: 306±17
86 Newman MA, Valanis BG, Schoeny RS, Hee
SQ. Urinary biological monitoring markers of
anti-cancer drug exposure in oncology nurses.
Am J Public Health 1994; 84: 852±5
87 Grandjean P, Brown SS, Reavey P, Young DS.
Biomarkers of chemical exposure: state of the
art. Clin Chem 1994; 40: 1360±2
88 Savitt DL, Hawkins HH, Roberts JR. The radio-
pacity of ingested medications. Ann Emerg Med
1987; 16: 331±9
89 Kulshrestha MK. Lead poisoning diagnosed by
abdominal X rays. Clin Toxicol 1996; 34: 107±8
90 Banner W, Tong TG. Iron poisoning. Pediatr
Toxicol 1986; 33: 393±409
91 Sohn D, Byers J III. Cost effective drug
screening in the laboratory. Clin Toxicol 1981;
18: 459±69
92 Chattopadhyay A, Roberts TM, Jervis RE. Scalp
hair as a monitor of community exposure to lead.
Arch Environ Health 1997; 31: 226±36
93 Taylor A. Usefulness of measurements of trace
elements in hair. Ann Clin Biochem 1986; 23:
364±78
94 Moeller MR, Fey P, Sachs H. Hair analysis as
evidence in forensic cases. Forensic Sci Int
1993; 63: 43±53
95 Badcock NR, Davies A. Assay for itraconazole in
nail clippings by reversed-phase high-
performance liquid chromatography. Ann Clin
Biochem 1990; 27: 506±8
96 Bermejo-Barrera P, Moreda-Pineiro A, Romero-
Barbieto T, Moreda-Pineiro J, Bermejo-Barrero A.

Traces of cadmium in human scalp hair
measured by electrothermal atomic absorption
spectrometry with the slurry sampling
technique. Clin Chem 1996; 42: 1287±8
97 Kruse JA. Methanol poisoning. Intensive Care
Med 1992; 18: 391±7
98 Meredith TJ, Jacobsen D, Haines JA, Berger J-
C, van Heijst APVP, eds. Antidotes for
Poisoning by Cyanide. IPCS/CEC Evaluation of
Antidotes Series, Vol. 2. Cambridge:
Cambridge University Press, 1993
99 Meredith TJ, Jacobsen D, Haines JA, Berger J-C,
eds. Antidotes for Poisoning by Paracetamol.
IPCS/CEC Evaluation of Antidotes Series, Vol. 3.
Cambridge: Cambridge University Press, 1994
100 Proudfoot AT. Acute Poisoning Diagnosis and
Management, 2nd edn. Oxford: Butterworth-
Heinemann, 1993
101 Garza-Ocanas L, Torres-Alanis O, Pineyro-Lopez
A. Urinary mercury in twelve cases of cutaneous
mercurous chloride (Calomel) exposure: effect of
sodium 2,3-dimercaptopropane-1-sulfonate
(DMPS) therapy. Clin Toxicol 1997; 35: 653±5
102 Bayer MJ, McKay C. Advances in poison
management. Clin Chem 1996; 42: 1361±6
103 Sutherland SK. Australian Animal Toxins: The
Creatures, Their Toxins and Care of the
Poisoned Patient. Melbourne: Oxford University
Press, 1983
104 Otten EJ. Venomous animal injuries. In: Rosen et
al., eds. Emergency Medicine: Concepts
and
Clinical Practice. St Louis MO: Mosby, 1992
105 Hurrell JGR, Chandler HM. Capillary enzyme
immunoassay ®eld kits for the detection of
snake venom in clinical specimens. Med J Aust
1982; 2: 236±7
106 Cox JC, Moisidis AV, Sheperd JM, Drane DP,
Jones SL. A novel format for a rapid sandwich
EIA and its application to the identi®cation of
snake venoms and enteric viral pathogens. J
Immunol Methods 1992; 146: 293±4
107 Nielsen CT, Hansen AJ, Kruse T, Mogensen A,
Provstegard E. Risk factors in home accidents
among preschool children. Ugeskr Laeger
1990; 152: 3447±9
108 Schwartz JG, Stuckey JH, Prihoda TJ, Kazen CM,
Carnahan JJ. Hospital-based toxicology: patterns
of use and abuse. Tex Med 1990; 86: 44±51
Poisoning by substances other than drugs 157
109 Ferguson JA, Sellar C, McGuigan MA. Predic-
tors of pesticide poisoning. Can J Public Health
1991; 82: 157±61
110 Kumar V. Accidental poisoning in south west
Maharashtra. Indian Pediatr 1991; 28: 731±5
111 Mueser KT, Yarnold PR, Bellack, AS. Diagnostic
and demographic correlates of substance abuse in
schizophrenia and major affective disorder. Acta
Psychiatr Scand 1992; 85: 48±55
112 Azizi BH, Zulki¯i HI, Kasim MS. Risk factors for
accidental poisoning in urban Malaysian
children. Ann Trop Paediatr 1993; 13: 183±8
113 Petridou E, Polychronopoulo A, Kouri N,
Karpathios T, Koussouri M, Messaritakis Y, et
al. Unintentional childhood poisoning in Athens:
a mirror of consumerism? Clin Toxicol 1997;
35: 669±75
114 Buchet JP, Staessen J, Roels H, Lauwerys R,
Fagard R. Geographical and temporal
differences in the urinary excretion of inorganic
arsenic: a Belgian population study. Occup
Environ Med 1996: 53: 320±7
115 Price JR. Circadian variation in deliberate self
poisoning. BMJ 1994; 309: 1583±4
116 ManfrediniR, GalleraniM, CaraccioloS,
TomelliA, Calo G, Fersini C. Circadian variation
in attempted suicide by deliberate self
poisoning. BMJ 1994; 309: 774±5
117 Osypiw JC, Watson ID, Gill G. What is the best
formula for predicting osmolar gap? Ann Clin
Biochem 1997; 34: 692±3
118 Jacobsen D, McMartin KE. Methanol and
ethylene glycol poisonings: mechanism of
toxicity, clinical course, diagnosis and
treatment. Med Toxicol 1986; 1: 309±34
119 Benowitz NL, Goldschlager N. Cardiac distur-
bances in the toxicologic patient. In: Haddad
LM, Winchester JF, eds. Clinical Management
of Poisoning and Drug Overdose. Philadelphia:
WB Saunders, 1983: 65±98
120 Litovitz T. The alcohols: ethanol, methanol,
isopropanol, ethylene glycol. Pediatr Clin North
Am 1986; 33: 311±23
Accepted for publication 25 August 1999
Ann Clin Biochem 2000: 37