Download Toxicological Findingsin Fatal Poisonings

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts

Pharmacokinetics wikipedia , lookup

Transcript
CLINICAL CHEMISTRY, Vol. 19, No. 4, (1973) 361-365
ToxicologicalFindingsin Fatal Poisonings
ArthurJ.
McBay
Anyone who must decide whether the amount of
toxic substance present in a specimen is sufficient to
indicate that the substance may have been the
cause of death is aware of the difficulty of finding information to guide that decision. Opinions are given
concerning therapeutic and toxic concentrations
in
human tissues for most of the common drug and
chemical poisons. These include alcohols, amitriptyline, amphetamine, arsenic, barbiturates, boron, bromides, carbon monoxide, chloral hydrate, chlordiazepoxide,
cyanide,
diazepam,
diphenylhydantoin,
ethchlorvynol,
fluoride, glutethimide,
heroin (morphine), imipramine, lead, LSD, marihuana, meperidine, meprobamate, methadone, methamphetamine,
methaqualone, nicotine, nortriptyline, orphenadrine,
paraldehyde, pentazoci ne, phenothiazines, propoxyphene, quinine, salicylates, and strychnine.
Interpretation
of the results of toxicological examinations is not easy. The reference material on which
such decisions must be founded is not always readily
accessible. The opinions and case studies must be
treated as such, because there are many problems
connected with obtaining an adequate and thorough
investigation of even fatal poisonings. Some of these
problems include: insufficient history of the individual; presence of multiple toxic agents; inadequate or
improperly obtained and preserved samples; samples
obtained from an embalmed body; no autopsy; autopsy performed but a “general unknown” determination requested when signs and symptoms could
lead to a more narrowly directed search; the finding
of a small amount of some agent and attributing
death to this because no other cause of death could
be found (cause of death may not be established in
some cases even after exhaustive investigation, e.g.,
“crib deaths”).
With fatalities
it cannot be too
strongly emphasized that an autopsy is not only desired but essential if death by poisoning is to be established. It may be that the amount of alcohol or
the amount of carbon monoxide present is all that is
desired to determine if either of these had affected
the individual.
In the absence of an autopsy or an
enlightening medical history, it is difficult to determine how the amount of a specific drug in a person
might be interpreted.
From the Office of the Chief Medical Examiner, North Carolina State Board of Health; and the School of Pharmacy and the
Department
of Pathology,
School of Medicine,
University
of
North Carolina, Chapel Hill, N. C. 27514.
Received Oct. 25, 1972; accepted Jan. 16, 1973.
With all toxic agents, individual
variances will
have a profound effect on the interpretation
of drug
concentrations. Many drugs cause irreversible damage when their concentration
in the blood is high
but, because the person does not die immediately,
the concentration at the time of death may be much
lower. Death may result when two or more drugs are
each present in sublethal amounts. The types of
analyses that may be performed and the specimens
that are desired for analysis vary from laboratory to
laboratory, depending upon the expertise of the analysts, the availability
of equipment, and the workload of the laboratory. Drugs that may be determined when present in lethal amounts may be infinitely more difficult or impossible to find in therapeutic amounts. Liver tissue and large volumes of blood
may be obtained from the dead whereas in the living
only urine or a small amount of blood may be available. An earlier paper dealt with chemical findings
in poisonings (1). The present paper gives the latest
information
available, which usually has been obtained by virtue of advances in methodology.
The opinions I offer are based on present information. As more information
becomes available, it is
certain that some of the opinions will have to be
changed.
Ethanol
(Ethyl Alcohol)
Impairment from ethanol may be detected by special measurements when the concentration is as low
as 500 mg/liter of blood. Everyone’s judgment is impaired by the time the concentration reaches 1 g/
liter (0.10%). Intoxication
occurs at about 2 g/liter.
Stupor occurs at about 3 g/liter, and coma and
death at concentrations greater than 4 to 5 g/liter.
The blood ethanol concentration
must be about 5
g/liter to be considered the cause of death, but an
individual may not die until the concentration is as
low as 2 g/liter if it takes 10 to 12 hours to succumb.
Although the concentration of alcohol in the blood
will not change materially after death, in the living
it will decrease by about 100 to 200 mg/liter
per
hour. Lower concentrations of alcohol may be very
significant when sublethal amounts of other drugs
are present also. The fatal dose of ethanol is between
500 and 1000 ml of 100-proof liquor (50% ethanol),
ingested in an hour or two. Although the figure
varies with individual tolerance, weight, and experience, it generally takes at least 180 ml of 100-proof
CLINICAL CHEMISTRY, Vol. 19, No. 4, 1973
361
liquor ingested in a short period to produce an ethanol concentration of 1 g/liter. Most people appear to
be drunk at levels of 1.5 to 2.5 g/liter, a level attained by rapidly ingesting about 250 to 450 ml of
100-proof liquor. An excellent reference on alcohol is
available (2).
Methanol
(Methyl
Alcohol)
In cases of fatal poisonings, concentrations
of
methanol in blood generally exceed 1 g/liter (3). The
toxic dose of methanol varies greatly because it depends on the amount of ethanol in the body that
may have to be preferentially metabolized instead of
methyl alcohol. Ethanol serves as an antidote for
methanol. Methanol may be found in the blood for
several days after poisoning. When methanol is detected, a test for formaldehyde should be made. If
formaldehyde is found, contamination with embalming fluid or tissue fixative should be suspected.
Formaldehyde solutions usually contain 10 to 15 ml
of methanol per 100 ml, as a preservative.
Isopropanol
(Isopropyl
Alcohol)
Isopropyl alcohol, which is present in many sampies of rubbing alcohol, may be intentionally or accidentally ingested. When isopropanol is found in
blood, its metabolite,
acetone, should be present
also. Concentrations
of 1 g/liter of blood or more
have been found in fatal poisonings (4). The fatal
dose is about 250 ml. Isopropanol is occasionally
present in embalming fluid.
Paraldehyde
Findings of 500 mg of paraldehyde per liter of
blood indicate fatal poisoning (5). Lower concentrations are hazardous when ethanol is present. Paraldehyde, which decomposes to acetic acid, may produce serious metabolic acidosis. Doses of about 30 ml
or less have been the evident cause of fatalities.
Intramuscular
injection of 10 ml of the drug produced a concentration as high as 77 mg/liter of plasma, and therapeutic doses gave concentrations ranging from 34 to 150 mg/liter of blood (5).
Carbon
Monoxide
Everyone has a small amount of carbon monoxide
his blood. This is usually less than 5% of the saturation concentration.
Heavy smokers and those in
certain occupations may reach about 10% saturation.
The effects of continuous exposure to these low concentrations is not known. Healthy individuals should
survive blood saturations of 40% for a minute or of
20% for a week. Those with circulatory or respiratory
diseases could die from such exposures. Those fatally
exposed to the fumes of an internal combustion engine usually have blood saturations of 60% or more.
It is possible to be found dead as a result of a fire
and not have significantly
increased concentrations
of carbon monoxide in the blood. A person may have
a high level of carbon monoxide and not appear
in
362
CLINICAL CHEMISTRY, Vol. 19, No. 4, 1973
“pink.”
The blood in a dead body neither
absorbs
nor loses carbon monoxide.
Barbiturates
Oral doses of 600 mg of barbiturates produced the
following average maximum
(per liter) concentrations in the blood: pentobarbital,
3.3 mg; secobarbital, 4.8 mg; amobarbital,
9.6 mg; butabarbital,
14
mg; and phenobarbital, 23 mg (6).
To determine the significance of the concentration
of a barbiturate it is necessary to know whether the
barbiturate is slow-acting or rapid-acting and whether the person is tolerant or not.
In a study (7) of deaths attributed to the barbiturates, most samples had the following ranges of barbiturate concentration:
Bar biturates alone
mg/liter
Secobarbital
Pentobarbital
Amobarbital
Butabarbital
Phenobarbital
of blood
15-24
15-44
10-24
10-24
30-54
10-29
15-19
10-54
15-29
30-39
105-134
20-44
Amo- and Secobarbital
Barbiturate plus
ethanol
When the blood contained more than 1 g of ethanol per liter, as little as 5 mg of barbiturates per liter
of blood was considered sufficient to be the cause of
death. About 12 100-mg doses of a rapid-acting barbiturate may be sufficient to cause death. But only
600 mg may cause death when the blood contains
about 1.5 g of alcohol per liter.
Glutethimide
(‘Doriden,”
Ciba)
A single therapeutic oral dose of 1 g of glutethimide has produced a blood concentration of about 7
mg/liter. Serious intoxication will follow the absorption of 10 g or more of the drug. Deaths have been
attributed to concentrations of 30 mg/liter of blood.
If a patient survives for several days after a toxic
dose, the concentration in blood will decline so that
a postmortem concentration of 10 mg/liter, which is
in the therapeutic range, may indicate poisoning (8).
Ethchlorvynol
(“Placidyl
,“
Abbott)
Oral ingestion of 200 mg of ethchlorvynol produces
blood concentrations less than 2 mg/liter and urinary concentrations less than 1 mg/liter (5). Concentrations greater than 20 mg/liter
of blood or 20
mg/kg of liver have been considered sufficient for the
drug to be considered the cause of death.
Meprobamate
Oral doses of 400 and 1200 mg of meprobamate
produced blood concentrations of 5 and 15 mg/liter
(9). Fatal concentrations
in the blood are usually
greater than 50 mg/liter and in the liver greater than
100 mg/kg (5).
Chloral
Hydrate
After oral ingestion of 1 g of chloral hydrate, its
concentration
in blood reached a maximum of 1.5
mg of trichlorethanol
per liter; no chloral hydrate
was detected (10). The amounts of chloral hydrate
usually reported in poisonings are greater than 10 mg
of chloral hydrate per liter of blood.
blood concentration of about 50 to 100 mg per liter.
Arthritic
patients taking 10 to 12 g every 24 hours
have concentrations as high as 400 mg/liter of blood.
Concentrations
greater than 250 mg/liter
indicate
intoxication. Death may occur many hours after concentrations as high as 1 g/liter in the blood have
produced their damage; the level at the time of
death may be much lower (16).
Phenothiazines
Hospitalized patients who survived treatment for
overdosages of phenothiazines had concentrations of
1 to 2 mg of chlorpromazine, trifluoperazine,
promazine, or prochlorperazine,
and 2 to 5 mg of thioridazme per liter of serum (11). Deaths have been attributed to phenothiazines in cases where concentrations
in blood were less than 5 mg/liter when the liver
contained at least 50 mg of the drug per kilogram
wet weight. Sudden deaths after the administration
of therapeutic amounts of phenothiazines,
particularly thioridazine,
have been reported (12). It is expected that the concentrations of drug in the blood
and liver would be lower than those stated above for
poisonings.
Diphenylhydantoin
(“Dilantin,”
Parke, Davis)
Therapeutic doses of 600 mg of diphenylhydantoin
produce maximum concentration in blood of 10 mg/
liter (6). Concentrations
greater than 70 mg/liter
or 100 mg/kg of liver have been found in fatal poisonings.
Orphenadrine
Blood containing at least 4 mg of orphenadrine per
liter and liver containing more than 20 mg/kg were
considered sufficient evidence that the drug caused
death (13).
Chlordiazepoxide
(“Librium,”
Roche)
Chlordiazepoxide
is a rather safe drug. The documented cases in which this drug has been blamed for
deaths appear to be those where it has been present
with another drug that it might potentiate. Cases
have been reported in which up to 1 g was ingested
without producing coma (14). Oral doses of 150 mg/
day produce concentrations in plasma of less than 10
mg/liter; 400 to 600 mg per day produces concentrations up to 40 mg/liter. Concentrations as high as 40
mg/liter do not result in deep coma.
Diazepam
(“Valium,”
Roche)
This benzodiazepine, like chlordiazepoxide,
has a
very low toxicity. The blood concentrations
of diazepam are very low. Oral doses of 10 mg may produce concentrations in blood of about 0.2 mg/liter,
and when 150 to 200 mg is taken the level may reach
2 mg/liter (15).
Salicylates
(Acetylsalicylic
Methyl Salicylate)
A therapeutic
Acid,
dose of 1 g of aspirin will produce a
Morphine-Heroin-Quinine
Heroin is converted to morphine in the body. Most
methods of determining heroin hydrolyze the drug to
morphine. Since much of the material sold as heroin
contains relatively large amounts of quinine, finding
small amounts of quinine in biological specimens
suggests the abuse of heroin. One hour after intravenous injection of a single 10-mg intravenous dose of
morphine by adults, serum morphine concentration
is about 0.1 mg/liter,
decreasing to less than 10 zg/
liter in about four to eight hours (17). The urine of
heroin addicts contains an average of 22 mg of total
morphine per liter (18). In fatal poisonings, morphine concentrations of 20 to 200 zg/liter have been
found (19). Liver should contain 0.1 to 1.0 mg of total
morphine per kilogram. Morphine persists in much
greater concentrations for 24 or more hours in urine
or bile, so these specimens may serve as useful
screening samples. It is thought that morphine
should be demonstrated in blood to certify sudden
death because of “intravenous
narcotism.”
In fatal
quinine intoxication
relatively
large amounts are
found. The blood may contain more than 10 mg of
quinine per liter, the liver more than 50 mg/kg.
Deaths have been related to heroin when no evidence
of quinine was found in the body.
Methadone
Robinson reported a series of 11 deaths related to
methadone, in the significant cases the concentrations were 0.2 to 3 mg per liter of blood and 2 to 50
mg per kg of liver (20).
Propoxyphene
(“Darvon,”
Lilly)
Drug concentrations
reached a maximum of 0.2
mg/liter of plasma in 1 h after a 195-mg oral dose
and 0.3 mg/liter in 30 mm after a 50-mg intravenous
dose (21). The concentration
in plasma reached a
maximum of 0.3 mg/liter after administration
of 13
oral doses of 65 mg of the propoxyphene hydrochloride or 100 mg of the newer propoxyphene napsylate
(22). In fatal poisonings, concentrations of at least 2
mg/liter of blood and 30 mg/kg of liver are attained.
Pentazocine
(“Talwiri,”
Winthrop)
Therapeutic oral, intravenous, and intramuscular
doses produce conc?ntrations of about 150 g of pentazocine per liter of blood (23). In a death attributed
to pentazocine, 5 mg/liter was found in the blood
and 45 mg/kg was found in hydrolyzed liver.
CLINICAL CHEMISTRY, Vol. 19, No. 4, 1973
363
Meperidine
(“Demerol,”
Winthrop)
Intramuscular
injections of 100 mg of meperidine
produced concentrations of 1 mg/liter of serum (24).
Blood containing 10 mg/liter and liver containing 10
mg/kg have been considered sufficient evidence of
cause of death.
Amphetamine
and Methamphetamine
No amphetamine
was found in the plasma of a
subject taking 30 mg of dextroamphetamine
daily
(25). Concentrations
of amphetamine
reported in
cases of fatal poisoning are (per liter or kilogram):
0.5 mg for blood, 4 mg for urine, and 0.3 mg for liver.
For methamphetamine
the corresponding figures are,
respectively: 0.6, 0.1, and 0.7 mg. These concentrations were attained after intravenous administration.
Concentrations
of 40 mg/liter in blood and greater
than that in organs were associated with a fatal oral
ingestion (26).
Methaqualone
In human subjects, this drug attained a concentration of 2 mg per liter of plasma in 30 minutes after a
single 250-mg oral dose (27). In fatal poisonings the
blood concentration usually exceeds 5 mg per liter,
the concentration in liver 40 mg per kilogram.
Amitriptyline
and Nortriptyline
after chronic poisoning. Urine containing more than
1 mg of arsenic per liter is indicative of poisoning.
Concentrations above 5 mg/kg in the liver are significant. Analysis of fingernails is unhelpful in the living-the
distal portions will not contain arsenic unless it had been given many months previously. Hair
rarely constitutes a good sample in the living because such a large quantity of the entire length of
hair is required.
Lead
Urines from normal individuals
contain 0 to 0.1
mg of lead per liter (median, about 0.03). Normal
blood specimens contain 0 to 1 mg of lead per liter
[median, about 0.2 (33)]. Urine containing more than
0.1 mg of lead per liter or more than 10 mg of oaminolevulinic
acid per liter indicates exposure to
lead (34). Concentrations of more than 2 mg of lead
per liter of blood and concentrations over 10 mg of
lead per kg of liver have been found in fatal poisonings. Normal livers have less than 5 mg of lead per
kg.
Cyanide
Detectable amounts of cyanide in blood indicate
poisoning. Concentrations
of about 10 mg/liter
of
blood are found in poisoning (35).
Fluorine
Adults receiving 25 to 75 mg of nortriptyline
orally
three times a day for four to seven days had drug
concentrations of 30 to 160 gig/liter of plasma (28).
In autopsy cases involving these drugs the concentrations in the blood were between 0 and 11 mg of
amitriptyline,
and between 8 and 26 mg of nortriptyline per liter. The liver contained more than 50 mg of
drug per kilogram (29).
Normal blood contains 0.01 to 0.1 mg of fluorine
per liter. Concentrations greater than 3 mg of fluorine per liter of blood have been found in poisonings
(36). The liver appears to have about half as high a
concentration
as the blood. Normal urines have
mean concentrations of the order of 0.3 to 0.4 mg per
liter.
Imipramine
Boron-Boric
(“Tofranil,”
Geigy)
Acid-Borates
Patients receiving 150 to 300 mg per day had drug
concentrations 0.1 to 0.6 mg per liter (30). In fatal
cases the blood contained at least 2 mg/liter,
the
liver 10 mg/kg (31).
Blood boron “normals” are in the range of 0 to 0.8
mg per liter. More than 40 mg of boron per liter of
blood suggests boron poisoning.
Nicotine
Blood concentrations of 1 g of bromide per liter are
significant.
The normal bromide concentration
in
human blood is reportedly 1.5 to 50 mg bromine per
liter (37).
Smoker’s blood should contain less than 0.3 mg of
nicotine per liter. Concentrations
greater than 5
mg/liter are found in blood and 10 mg/kg in liver in
cases of fatal poisoning (32).
Strychnine
Any strychnine found is significant, because it is
now rarely used medicinally. The blood will usually
contain more than 2 mg/liter, the liver more than 4
mg/kg in poisonings (32).
Arsenic
Urine is the best specimen from the living for
quantitating
this poison because abnormally
high
amounts of arsenic persist in the urine for about a
week after acute poisoning and up to about a month
364
CLINICAL CHEMISTRY. Vol. 19, No.4, 1973
Bromides
Marihuana
(Cannabis)
Cannabinoids in plasma averaged 70 ag/liter after
the subjects smoked two marihuana cigarettes containing either 11 or 22 mg of tetrahydrocannabinol
(38). Cannabinols may be detected in the saliva and
urine of smokers, and on their hands. Methods for
measuring marihuana (and LSD) are very new and
are not routinely available.
LSD (Lysergic
acid diethylamide)
A radioimmunoassay
tion of LSD in urine
method for the determinahas been presented. Human
subjects who received 0.2 mg and 0.3 mg oral doses
had concentrations
between 5 and 50 izg/liter in
urine (39).
The most significant findings in drowning deaths
are the discovery of sand, mud, plants and other material in the airways and lungs. Differences between
the blood of the right and left heart, such as in the
amounts of chlorides and in the specific gravities, are
not usually significant in fresh-water drownings, and
only occasionally significant in salt-water drownings.
Many times these findings are the reverse of what is
expected. The finding of diatoms after the wet digestion of tissue may be of significance (40).
References
1. McBay,
A. J., Chemical findings
Med. 274, 1257 (1966).
2. Alcohol and the Impaired Driver,
Association,
1970.
3. Stratton,
F., Determination
in poisonings.
Chicago,
of methanol
New
American
in body
Engl.
J.
Medical
fluids.
Amer.
alcohol
(Rub-
J. Clin. Pat hot. 25, 1071 (1955).
4. Adelson,
L., Fatal
bing alcohol). AmerJ.
intoxication
with
isopropyl
Clin. Pathol. 38, 144 (1962).
5. Maes, R., Hodnett,
N., Landesman,
H., et al., The gas chromatographic determination of selected sedatives (ethchlorvynol,
paraldehyde, meprobamate,
carisoprodol) in biological material.
J. Forensic Sci. 14, 235 (1969).
6. Parker, K. D., Elliott, H. W., Wright, J. A., et al., Blood and
urine concentrations of subjects receiving barbiturates,
meprobamate, glutethimide
or diphenylhydantoin.
Clin Toxicot. 3, 131
(1970).
G., McGarry,
E., and Daigle, J., Toxicological
for fatalities
due to carbon monoxide
J. Forensic Sci. 17, 640 (1972).
and barbiturates
data
in Ontario.
8. Algeri, E. J., and Katsas, G. G., Toxicology of glutethimide. J.
Sci. 5, 217 (1960).
9. Finkle, B., The identification, quantitative determination, and
distribution
of meprobamate, glutethimide in biological material.
J. Forensic Sci. 12, 509(1967).
10. Kaplan, H. L., Forney, R. B., Hughes, F. W., and Jam, N.
C., Chloral hydrate and alcohol metabolism in human subjects.
J. Forensic Sci. 12, 295 (1967).
11. Tompsett, S. L., The spectrofluorimetric
determination
of
phenothiazine
drugs in blood serum. Acta Pharmacol.
Toxicol. 26,
298(1968).
12. Leestma,
J. E., and Koenig, K. L., Sudden deaths and phenothiazines. Arch. Gen. Psychiat.
18, 137 (1968).
13. Clarke, E. G. C., Isolation
and Identification
of Drugs, The
Pharmaceutical
Press, London, 1969, p436.
14. Gjerris, F., Poisoning with chlordiazepoxide.
Dan. Med. Bull.
13, 170(1966).
15. DeSilva, J. A., Koechlin,
B. H., and Boden, G., Blood level
distribution
patterns
of diazepam and its major metabolite in
man.J.
Pharm. Sci. 55, 692(1966).
16. Done, A. K., Salicylate
intoxication.
Pediatrics 26,800(1960).
Forensic
17. Spector,
man. Science
19. McBay, A. J., and Turk, R. F., Heroin Deaths. Bull. mt. Ass.
Toxicol., June 1972, p 12.
20. Robinson, A. E., and Williams, F. M., The distribution
of
methadone in man. J. Pharm. Pharmacol.
23, 353 (1971).
21. Wolen, R. L., Gruber, C. M., Kiplinger, G. F., and Scholz, N.
E., Concentration
of propoxyphene
in human plasma following
oral, intramuscular,
and intravenous
administration.
Toxicol.
Appl. Pharmacol.
19, 480 (1971).
Forensic
Drownings
7. Cimbura,
18. Payte, J. T., Wallace, J. E., and Blum, K., Acid hydrolysis:
A requisite for morphine detection in urine. Reported to the Committee on Problems of Drug Dependence, February 1971.
S., and Vesell,
174, 421 (1971).
E.
S.,
Disposition
of morphine
in
22. Wolen, R. L., Gruber, C. M., Kiplinger, G. F., and Scholz, N.
E., Concentration
of propoxyphene
in human plasma following
repeated oral doses. Toxicol. Appi. Pharrnacol.
19, 493 (1971).
23. Berkowitz, B. A., Asling, J. H., Schnider, S. M., and Leong
Way, E., Relationship of pentazocine plasma levels to pharmacological activity in man. Clin. Pharmacol. Ther. 10, 320(1969).
24. Fochtman,
F. W., and Winek, C. L., Therapeutic
serum concentrations of meperidine. J. Forensic Sci. 14, 213 (1969).
25. Beckett, A. H., and Rowland, M., Urinary excretion kinetics
of amphetamine
in man. J. Pharm. Pharmacol. 17, 628(1965).
26. Cravey, R. H., and Reed, D., Intravenous amphetamine
poisoning report of three cases. ,J. Forensic Sci. Soc. 10, 109 (1970).
27. Berry, D. J., Gas chromatographic
determination
of methaqualone at therapeutic
levels in human plasma. J. Chromatogr.
42,39 (1969).
28. Asberg, It., Cronholm, B., Syoqvist, F. and Tuck, D., Relationship between plasma level and therapeutic
effect of nortriptyline.
Brit. Med. J. 3, 331 (1971).
29. Bonnichsen,
B., Maehly,
A. C.,
autopsy
cases involving
amitriptyline
Med. 67, 190(1970).
30. Curry,
and Skold, G., A report on
and nortriptyline.
J. Legal
A. S., Seven fatal cases involving
16, 265 (1964).
imipramine
in man.
J. Pharm. Pharmacol.
31. Fatteh,
A., Blanke,
32. Registry
Amer. Acad.
R., and Mann,
G. T., Death
from
imipra-
J. Forensic Sci. 13, 124 (1968).
mine poisoning.
of Human
Toxicology
Reports,
Forensic Sci., 1968-70 inclusive.
Toxicology
Section,
33. Goldwater,
L. J., and Hoover, A. W., An international
study
of “normal”
levels of lead in blood and urine.
Arch.
Environ.
Health 15, 60(1967).
34. Blanksma,
L. A., Sachs, H. K., Murray,
E. F., and O’Connell, M. J., Failure
of the urinary
delta-aminolevulinic
acid test
to detect pediatric
lead poisoning.
Amer. J. Clin. Pathol. 53, 956
(1970).
35. Curry, A. S., Poison Detection in Human Organs. 2nd ed.,
Charles C Thomas, Springfield, 111., 1969, p 48.
36. Gettler, A. 0., and Ellerbrook, L., Toxicology of fluorides.
Amer. J. Med. Sci. 197, 625 (1939).
37. Stewart, C. P., and Stolman, A., Toxicology,
H, Academic
Press,
New York,
N. Y., 1961, p 797.
38. Dott, A. B., Effect of marihuana
ulated
passing
task. DHEW Pubi.
10.
on risk acceptance
in a simNo. (HSM)
72-10010,
1972, p
39. Taunton-Rigby,
A., Sher, S. E., and Kelley, P. R., Radioimmunoassay
for L.S.D. and its detection
in human biological
fluids. Presented at 6th. Int. Mtg. of Forensic Sciences, Edinburgh,
1972.
40. Neidhart,
D. A., and Greendyke,
R. M., The significance of
diatom
demonstration
in the diagnosis
of death
by drowning.
Amer. J. Clin. Pat hot. 48, 377 (1967).
CLINICAL CHEMISTRY, Vol. 19, No. 4, 1973
365