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Dead Men Tell No Tales: Drug levels in a drowned, a decayed, and a dumpster corpse
Chapter 19
Dead Men Tell No Tales: Drug levels in a drowned, a decayed, and a dumpster corpse Insurance Claims and Drug Use Drug Detection in Fluid From the Eyeballs and Other Places Postmortem Detection of Alcohol and Methamphetamine Fetal Remains and Maternal Drug Use The Toxicologist and the Pharmacologist Drug Expert
[Narrative] John Plano was a 23-year old college grad from a well-to-do family in South Tulsa. One weekend at Grand Lake, he rented a speedboat and met his friends on the lake. After tying up to a flotilla of moored vessels, he stepped across to the next boat to meetup with his friends. He soon returned to his boat and took a dive into the waters from the bow. His friends became worried, then very agitated when they didn’t see him surface. They called the Grand Lake Water Patrol who responded within 10 min and began searching the waters. After 4 h of searching and darkness approaching, the search crews stopped for the night. Three days later, a fisherman reported a dead body floating in a cove near the scene of the accident. The decedent, Mr. Plano, was identified as the corpse from dental records and autopsy. The toxicological results showed that alcohol and THC was present in fluid samples from the eyeball (vitreous humor) but none from samples of heart or liver. On the basis of this finding, the insurance company refused payment of the decedent’s life insurance policy, on the grounds that the insured party was impaired by drugs at the time of the accident. The parents of the insured sued the insurance company with the assistance of a private law firm. The law firm consulted with a local drug expert regarding the detection of alcohol in vitreous fluid, and the insurance company’s denial due to drug impairment based on these results. In a separate case, the decayed body of a woman was discovered in an apartment by the manager after a neighbor complained of a foul odor. A full autopsy was done with no signs of trauma or obvious pathology. Toxicology was done on putrefied liver samples and the amounts of two prescription drugs and one OTC drug were quantified. On the basis of this toxicology report, the deceased life insurance company refused to pay the death benefit to her mother due to alleged suicide of the insured. The mother sought legal assistance and her attorney contacted a local drug expert to interpret the findings of the toxicology report. In a third case, a shoebox containing fetal remains was discovered in a dumpster by a homeless person. Toxicology of the fetal remains was limited to a decayed liver sample which gave methamphetamine and amphetamine levels in the fetal liver samples. The mother was tracked down and arrested for murder. A national organization for legal rights of pregnant women contacted a local drug expert to opine on the interpretation of the methamphetamine and amphetamine levels found in the fetal remains.
Insurance Claims and Drug Use Private life insurance and accidental death insurance arose as a response to the Industrial Revolution, and primarily the new transportation network of railroads.1 One of the first accident death insurance companies was formed in response to accidents and injuries that occurred with railroad travel in England. In 1863 the Travelers Insurance Company was the 1
Scales AF (2000) Man, God and the Serbonian bog: the evolution of accidental death insurance. 86 Iowa L. Rev. 173.
The Drug Expert. https://doi.org/10.1016/B978-0-12-800048-9.00019-5 © 2020 Elsevier Inc. All rights reserved.
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first company to issue accident policies in the United States.2 The name “Travelers Insurance” is apt and points out to the moorings of the present life insurance and accidental death and dismemberment (AD&D) policy stemming from the special case of persons using the modern conveyances of the time. Nowadays, life insurance is packaged with AD&D policies and coverage is continuous and independent of traveling or not.3 While any death results in the same outcome to the deceased and surviving loved ones (i.e., the insured is dead) all manner of death does not automatically trigger the death benefit. For example, life insurance companies cannot pay out claims from a husband who takes out a large policy on himself with his wife as beneficiary, then kills himself so his wife can live comfortably the rest of her life. Like all insurance companies, life insurance companies do not want to pay any death benefits if they don’t have to; such is the case in every for-profit industry.4 For that reason, there are a number of circumstances when death benefits are excluded. For example, the group Life Insurance and AD&D plan5 offered to employees of the OSU Medical School in Tulsa lists the following death benefit exclusions (bold added):
Accidental Death and Dismemberment Exclusions ReliaStar Life does not pay benefits for loss directly or indirectly caused by any of the following: ● Suicide or intentionally self-inflicted injury, while sane or insane. ● Physical or mental illness. ● Bacterial infection or bacterial poisoning. Exception: Infection from a cut or wound caused by an accident. ● Riding in or descending from an aircraft as a pilot or crew member. ● Any armed conflict, whether declared as war or not, involving any country or government. ● Injury suffered while in the military service for any country or government. ● Injury which occurs when you commit or attempt to commit a felony. ● Use of any drug, narcotic or hallucinogenic agent – – unless prescribed by a doctor. – which is illegal. – not taken as directed by a doctor or the manufacturer. ● Your intoxication. Intoxication means your blood alcohol content meets or exceeds the legal presumption of intoxication under the laws of the state where the accident occurred.
Because the use of alcohol, prescription drugs, OTC drugs, and/or illegal drugs is so common among insured individuals (as it is in all people, see Chapter 1), life insurance companies will often deny death benefits if there is any sign of drug use in the deceased. It is often the job of the drug expert to assist the insurance companies (rarely) and the plaintiffs filing suit against them (commonly), when issues of drug use in the deceased arise.
Drug Detection in Fluid From the Eyeballs and Other Places The ideal postmortem sample for detection of drug use is a vial of femoral blood. Blood is the easiest to use, as the methodology for blood sampling in the living can be applied to blood sampling in the dead. Peripheral bold samples, such as from the femoral vein, also give the best comparison of drug levels between the living and the dead. Nearly every drug, if taken by humans, has a research paper or two on the pharmacokinetics of that drug and corresponding blood levels and time course of those levels. Most drugs approved by the FDA in the last few decades also include peak blood concentration of a drug in the full prescribing information.
Vitreous humor fluid samples for postmortem detection of drugs When femoral blood cannot be obtained from a corpse due to decapitation, dismemberment, or fractionation, there is one place in the body that contains fluid encapsulated in a sealed container: the eyeball. The eyeball holds its shape due to the vitreous humor. Humor is an old word for fluid, as in the four humors of the body.6 Vitreous humor is a clear, colorless fluid 2
Travelers Insurance Company, with its iconic red umbrella logo, is still going strong today. For instance it is said that most home accidents occur in the bathroom. The insured in that case is would not be considered in a state of conveyance from one place to another, i.e., travelling. 4 Like health care, perhaps insurance companies should be embedded in a nonprofit structure. 5 Your Group Life Insurance Plan, for OSU employees, from ReliaStar Insurance Company, subsidiary of the Dutch ING financial group. 6 Early Greek medicine identified the four humors of the body as blood, yellow bile, black bile, and phlegm. 3
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filling the main chamber of the eye. Vitreous humor can be sampled by using a syringe and needle and inserting about 1 cm into the eyeball and slowly withdrawing the vitreous fluid.7 Because of its blood supply, the vitreous humor also reflects a drug’s concentration in the peripheral blood, although the relationship between vitreous fluid and blood levels of a drug is not clear (see later). For this reason, vitreous humor samples are often used for forensic analysis, especially in decayed or decomposing human bodies.8 Studies comparing the use of vitreous fluid or femoral blood samples for use in routine drug screening showed that drug screens in femoral blood resulted in twice as many positive drug tests in blood than vitreous fluid.9 This suggests that vitreous fluid, either by its restricted blood flow and lower drug concentrations or other biological processes, is not as good as blood for routine drug detection in postmortem samples. The vitreous fluid sample taken from the drowned man in the first narrative case of this chapter yielded a vitreous alcohol concentration of 0.10%, which was the basis of the insurance company denial of death benefits to the parents of the dead man. There were no other samples obtained in that case.
Liver samples for postmortem detection of drugs The liver could easily qualify as the number one internal organ in the abdomen. It is the only internal organ that can regenerate itself, and among its many roles, acts as the gatekeeper of all foreign substances that enter the body. Food and drugs taken orally are absorbed in the stomach and small intestine and immediately enter a special blood vessel pathway called the hepatic portal system. Drugs that are given by the IV route, directly in the bloodstream, quickly end up in the liver due to its large blood flow. The liver is also the number one site for drug metabolism. Putrefied liver tissue taken from the decedent described in the second chapter case was analyzed by GC-MS and three drug substances were detected and quantified.10 The toxicology report from the Medical Examiner’s Office reported zolpidem (Ambien®) at 4.5 μg/g (micrograms per gram of liver tissue), carisoprodol (Soma®) at 200 μg/g, and diphenhydramine (Benadryl®) at 30 μg/g in the putrefied liver samples of the decedent. On the basis of these findings, the insurance company denied benefits to the dead woman’s spouse, asserting that the presence of these drugs showed that the decedent purposely overdosed on these medications and committed suicide. Decomposed liver samples from the fetal remains found in third chapter case were also sampled and tested for drugs. The fetal liver tissue had a methamphetamine concentration of 3.0 μg/g and amphetamine was detected but not quantified. On the basis of this finding, the state’s toxicologist opined that the mother’s use of methamphetamine caused intrauterine fetal demise.
Other tissue sources for postmortem drug detection The kidney, brain, and muscle are also used for postmortem drug detection.11 These samples are often used when blood cannot be obtained. Samples can be used from these tissues but they also contain large amounts of lipids (fats) which interfere with the analytic methods used in toxicology. However, there is limited data to compare postmortem and premortem drug concentrations to aid in interpretation of results from these samples. More rarely, bone, hair, and fingernail samples are used for the postmortem detection of drugs, especially in decomposed corpses. Bone tissues are especially useful if the body has undergone severe decomposition, exsanguination, or skeletonization.12 Examination of bone tissue in a completely skeletonized corpse revealed significant levels of the opioid fentanyl. The amount of fentanyl was found to be dependent on the type of bone tissue examined (legbone vs. vertebrae) and area of the bone (outer tissue vs. bone marrow).13 Hair sampling for drug detection is noninvasive and can be obtained in the living and the dead. As discussed in Chapter 6 Hairs of the Innocent, drug detection in hair has a long window of detection as drugs in hair are interwoven into the hair matrix as the hair grows. In postmortem hair samples, depending on the length of the hair, 7
Yee L et al. (2000) Chiral high-performance liquid chromatographic analysis of fluoxetine and norfluoxetine in rabbit plasma, urine, and vitreous humor using an acetylated beta-cyclodextrin column. J Anal Toxicol. 24:651–655. 8 Metushi IG et al. (2016) Assessment and comparison of vitreous humor as an alternative matrix for forensic toxicology screening by GC-MS. J Anal Toxicol. 40:243–247. 9 Metushi IG et al. (2016) Ibid. 10 Gas chromatography-mass spectrometry, the standard method for identifying and quantifying forensic drug samples. See Chapter 5. 11 Margalho C et al. (2011) Illicit drugs in alternative biological specimens: A case report. J Forensic Legal Med. 18:132e135. 12 Orfanidis A et al. (2018) Alprazolam and zolpidem in skeletal tissue of decomposed body confirms exposure. J Forensic Sci. http://dx.doi.org/ 10.1111/1556-4029.13890. 13 Lafrenière NM, Watterson JH (2009) Detection of acute fentanyl exposure in fresh and decomposed skeletal tissues. Forensic Sci Internat. 185:100–106.
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exposure to drugs in the deceased may be determined for the past 6 months or longer. However, this precludes use of hair samples to ascertain immediate or acute drug effects in the deceased. Hair is also an ideal matrix for drug detection in ancient humans, like cocaine metabolites found in Northern Chilean mummies dating back to 2000 BCE.14 In a more recent case, antipsychotic drugs were detected in the fingernails and toenails of an unidentified and bloated corpse.15 Drug testing helped investigators determine the identity of the corpse as it narrowed their search to a long-term user of antipsychotic medicines. As mentioned, liver, kidney, brain, and most of the other tissues samples noted before, as well as vitreous fluid samples from the eye, cannot be obtained in living patients. Therefore the data from toxicological tests using these postmortem samples cannot be directly compared to reference data of drug and alcohol levels measured in living subjects. The drug expert is often the person to make this key point in the trial to avoid the overinterpretation by other experts. Existing data correlating any drug levels obtained postmortem from drug levels in living beings is extremely limited.
Postmortem Detection of Alcohol and Methamphetamine Postmortem blood samples are ideally taken from a peripheral site, with the femoral vein in the leg considered the “gold standard” in medicolegal and forensic research.16 In analytical toxicology guidelines, it is stated that drug levels from postmortem blood samples are most reliable when the interval between death and postmortem sampling is short, and blood samples are collected from a peripheral site, preferably the femoral vein.17 Under ideal conditions, because postmortem blood samples can be compared to peripheral blood samples obtained in living patients, an attempt at correlating therapeutic and toxic (or intoxicating) levels of drugs and ethanol can be made.18 As introduced in Chapter 8, postmortem redistribution (PMR) of drugs occurs when a drug’s concentration in the blood is different before and after death. This is important as nearly all of the data on the blood level of a drug and any adverse or toxic effects are based on blood levels in living subjects (antemortem samples). Depending on the drug, PMR can artificially increase blood concentrations when postmortem processes draw drugs from tissues in to the blood. Conversely, the process of PMR can decrease blood levels of a drug after death by the stoppage of blood circulation and drug absorption into fat tissue. For many drugs, PMR processes can be negligible with no change in antemortem and postmortem levels.19 In any event, in many cases the drug expert only has postmortem drug concentration data and is asked to form an opinion. Some opinions can be made when the drug levels are in extremis, for example, super-high levels of a drug might easily relate to drug concentrations found in forensic studies of documented suicides using the drug at issue.20 Many cases yield astonishing low levels of drug in postmortem samples, supporting a nonexistent role of acute drug use in the decedent.
Vitreous fluid sample for alcohol determination With all the instances of alcohol mentioned in this book, the reader might be tempted to leave the coffee shop and head to a nearby bar.21 However, the postmortem redistribution of alcohol is an important topic to bring up because so many people drink alcohol and drive, or jump off a boat, and end up dead that reports of postmortem alcohol levels often find their way to the drug expert’s desk. Because a femoral blood sample is considered the most reliable site of sampling for forensic interpretation (see earlier), much forensic research compares the ethanol concentration from vitreous fluid to ethanol concentration from femoral blood 14
Cocaine metabolites were found in these hair specimens. Baez H et al. (2000) Drugs in prehistory: chemical analysis of ancient human hair. Forensic Sci Internat. 108:173–179. 15 Chen H et al. (2014) Determination of clozapine in hair and nail: the role of keratinous biological materials in the identification of a bloated cadaver case. J Forensic Leg Med. 22:62–67. 16 Launiainen T, Ojanperä I (2014) Drug concentrations in post-mortem femoral blood compared with therapeutic concentrations in plasma. Drug Test Anal. 6:308–316. 17 Flanagan RJ, Connally G, Evans JM (2005) Analytical toxicology: guidelines for sample collection postmortem. Toxicol Rev. 24:63–71. 18 Also have to consider postmortem redistribution of the drug, discussed in the next section below. See also: Skopp G (2004) Preanalytic aspects in postmortem toxicology. Forensic Sci Int. 142:75–100. 19 For an excellent article on PMR by a leading expert in the area, see Drummer and his colleagues, e.g. Gerostamoulos D, Beyer J, Staikos V, Tayler P, Woodford N, and Drummer OH (2012) The effect of the postmortem interval on the redistribution of drugs: a comparison of mortuary admission and autopsy blood specimens. Forensic Sci Med Pathol.8:373–379. 20 Obviously there are some caveats in comparing levels of a postmortem drug in a legal case and drug concentrations reported in forensic studies. For example, most drugs have quite a large lethal blood concentration range which can provide little information in comparing a single value from a real case. 21 Drug-craving cues like the numerous mentions of alcohol in this book are based on actual data. Neuroimaging shows that craving areas of the brain become activated (“light up”) in response to pictures of crack cocaine in abstinent users, another proof that addictive drug use alters the brain.
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samples.22 These studies show that the ratio of vitreous fluid alcohol to femoral blood alcohol is highly variable. Some cases show a high ratio of vitreous fluid alcohol to femoral blood alcohol, other the opposite, with a low ratio of vitreous fluid alcohol to femoral blood alcohol. The ratio of vitreous ethanol to blood BAC is highly variable when the level of ethanol in the blood is less than 0.10% BAC. The concentration of ethanol in the vitreous fluid is typically higher than that in femoral blood; however, the relationship between vitreous fluid and heart blood is not clear.23 An early study made a mathematical model to prediction of blood alcohol concentration (BAC) from the alcohol concentration in the vitreous fluid but concluded that “the prediction interval is too wide to be of real practical use.”24 They continued that previous authors provided simple conversion factors to estimate BAC from vitreous alcohol “without taking into account the uncertainty of the prediction for an individual subject.” Another study of 62 deceased subjects found that ethanol concentrations in the vitreous fluid did not have a significant correlation to peripheral BAC.25 Expert authors in the field suggested more studies are needed before vitreous fluid ethanol can make reliable predictions of BAC.26 They outlined the studies needed: a large population of cases where the time and amount of alcohol consumed before death was known, the time of death, and the time of postmortem sampling was known. Other authors found that the ratio between vitreous ethanol concentration and blood BAC is so variable that a rule-of-thumb practice is to take half the vitreous alcohol concentration to estimate the BAC.27 In the present chapter case of the drowned corpse, the insurance company denied benefits largely based on the alcohol level from a single sample of vitreous fluid. From a single determination of 0.12% vitreous fluid alcohol, the insurance company claimed the decedent’s BAC was greater than 0.08% and that he was intoxicated. This violated the no intoxication clause of the life insurance policy. The claim of intoxication was made by the insurance company in spite of both the report from the medical examiner and the official death certificate note an accidental death by drowning with no contributing factor or other significant factor of alcohol intoxication.
Postmortem redistribution of alcohol Postmortem redistribution of drugs and ethanol results when the drug or ethanol diffuses from higher concentrations to areas of lower concentrations in the corpse following the disruption of cellular membranes.28 Postmortem redistribution of drugs and ethanol makes it impossible to determine with certainty the actual drug or ethanol content in the person before they died. It is well established in the forensic pharmacology literature that ethanol undergoes postmortem redistribution.29 Postmortem redistribution of ethanol is also caused by trauma to the deceased in the manner of death. Traumatic injuries to the torso are known to increase BAC.30 Other studies show that specimen site variability (e.g., heart blood versus femoral blood) is due to postmortem redistribution of ethanol.31
Postmortem production of ethanol After a person dies, a process of accelerated microbe growth begins in many tissues of the body. These microbes, mostly bacteria, yeast, and fungi, have been identified in postmortem tissues and are known to produce alcohol as part of their natural metabolism.32 This process is called the “postmortem production of ethanol” or “endogenous ethanol production” (inside the body, as opposed to exogenous ethanol from a few drinks). Ethanol synthesis by microbes is observed in the early stages of decomposition or putrefaction.33 Postmortem production of ethanol can lead to ethanol level as high as 22
Caplan YH, Levine B (1990) Vitreous humor in the evaluation of postmortem blood ethanol concentrations. J Anal Toxicol. 14:305–307; Kugelberg FC, Jones AW (2007) Interpreting results of ethanol analysis in postmortem specimens: a review of the literature. Forensic Sci Int. 165:10–29. 23 Honey D et al. (2005) Comparative alcohol concentrations in blood and vitreous fluid with illustrative case studies. J Anal Toxicol. 29:365–369. 24 Pounder DJ, Kuroda N (1994) Vitreous alcohol is of limited value in predicting blood alcohol. Forensic Sci Int. 65:73–80. 25 Mackey-Bojack S et al. (2000) Cocaine, cocaine metabolite, and ethanol concentrations in postmortem blood and vitreous humor. J Anal Toxicol. 24:59–65. 26 Sylvester PA et al. (1998) Op cit. 27 Jones AW, Holmgren P (2001) Uncertainty in estimating blood ethanol concentrations by analysis of vitreous humour. Clin Pathol. 54:699–702. 28 Kugelberg FC, Jones AW (2007) Op cit.; Pélissier-Alicot AL et al. (2006) Op cit.; Drummer OH (2004) Postmortem toxicology of drugs of abuse. Forensic Sci Int. 142:101–113. 29 Kugelberg FC, Jones AW (2007) Op cit.; Iwasaki Y et al. (1998) On the influence of postmortem alcohol diffusion from the stomach contents to the heart blood. Forensic Sci Int. 94:111–118. 30 Winek et al. (1995) The role of trauma in postmortem alcohol determination. Forensic Sci Int. 71:1–8. 31 Can et al. (2012) Importance of sampling sites for postmortem evaluation of ethyl alcohol. Forensic Res. 3:7. 32 Lewis RJ et al. (2004) Ethanol formation in unadulterated postmortem tissues. Forensic Sci Int. 146:17–24. 33 Boumba VA et al. (2008) Biochemical pathways generating post-mortem volatile compounds co-detected during forensic ethanol analyses. Forensic Sci Int. 174:133–151.
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0.22 g/dL (0.22% BAC).34 Postmortem production of ethanol is not rare but common. All 9 accident victims showed postmortem production of ethanol in an FAA-investigation accident.35 Importantly, this study also showed that postmortem production of ethanol can occur in bodies stored at 4°F, as is commonly done in the morgue. It is often stated that a vitreous humor fluid sample is less likely to undergo postmortem production of ethanol due to its isolated location in the eyeball.36 However, research shows that fluid samples from the vitreous fluid can show evidence of postmortem production of ethanol.37 Through postmortem redistribution, any microbial production of ethanol elsewhere would also be freely available to distribute to the vitreous humor fluid. Drug concentrations have been noted to undergo postmortem increases in the vitreous humor fluid samples, which was attributed to dehydration.38 Additionally, the vitreous humor contains glucose (a sugar) which is known to be used for the postmortem production of ethanol by microbes.39 Also, there are a number of other substrates besides glucose that microbes can use for the postmortem production of ethanol including amino acids, fatty acids, and glycerol.40 According to some investigators, postmortem BAC analysis has an unacceptable high rate of specimen site variability.41 Vitreous fluid alcohol concentration did not correlate well without high variability when compared to BAC obtained from femoral and heart blood samples. There is high variability in the value of BAC depending on where the blood is sampled from the body. Studies show that even the left side of the heart may yield significantly different BAC values than the right side of the heart in postmortem determinations of ethanol concentration.42
Postmortem redistribution of methamphetamine One study measured antemortem (while subject was still alive) and postmortem levels of methamphetamine and amphetamine in blood samples. Methamphetamine and amphetamine concentrations in peripheral blood samples were 1.5 to 2 times greater in the postmortem samples compared to the antemortem samples.43 In this study, antemortem samples were taken 7–22 min prior to a declaration of death at the hospital, and the postmortem samples 5–30 h after death at autopsy. As mentioned earlier, obtaining samples after death for forensic analysis for drugs is confounded by postmortem redistribution (PMR) of drugs. Methamphetamine undergoes extensive PMR and methamphetamine is concentrated in the liver. Human and primate studies with direct imaging show that the liver and kidneys are organs with the highest uptake of methamphetamine. In humans, about a quarter (23%) of the total methamphetamine dose was concentrated in the liver in live imaging studies.44
Fetal Remains and Maternal Drug Use Estimates of illicit drug use45 during pregnancy vary widely in the medical literature. Maternal use of illicit drugs is selfreported by about 5%–10% of pregnant women. However, universal drug testing in high-risk populations (low socioeconomic status) reveals a higher rate of 10%–40% illicit drug use during pregnancy.46 In general, maternal use of illicit drugs during pregnancy may place the fetus at risk for problems including low birth weight, small head circumference, increased preterm delivery, and other developmental complications.47 With the use of illicit drugs, the evidence or data is insufficient or too variable to ascertain with certainty drugs that produce ill effects on the fetus and at what drug concentrations. Furthermore, clinical studies that take into account the confounding factors such 34
Skopp G (2004) Preanalytic aspects in postmortem toxicology. Forensic Sci Int. 142:75–100. Lewis et al. (2004) Op. cit. 36 de Martinis BS et al. (2006) Alcohol distribution in different postmortem body fluids. Hum Exp Toxicol. 25:93–97. 37 de Lima IV, Midio AF (1999) Origin of blood ethanol in decomposed bodies. Forensic Sci Int. 106:157–162. 38 Skopp G (2004), Op. cit. 39 Kugelberg FC, Jones AW (2007) Interpreting results of ethanol analysis in postmortem specimens: a review of the literature. Forensic Sci Int. 165:10–29. 40 Boumba VA et al. (2008) Biochemical pathways generating post-mortem volatile compounds co-detected during forensic ethanol analyses. Forensic Sci Int. 174:133–151. 41 Sylvester PA et al. (1998) Unacceptably high site variability in postmortem blood alcohol analysis. J Clin Pathol. 51:250–252. 42 Pélissier-Alicot AL et al. (2006) Comparison of ethanol concentrations in right cardiac blood, left cardiac blood and peripheral blood in a series of 30 cases. Forensic Sci Int. 156:35–39. 43 McIntyre IM et al (2013) Antemortem and postmortem methamphetamine blood concentrations: three case reports. J Anal Toxicol. 37:386–389. 44 Volkow ND et al. (2010) Distribution and pharmacokinetics of methamphetamine in the human body: clinical implications. PLoS One 5:e15269. 45 Includes the abuse of prescription drugs, like opioids, as well as the standard drugs like marijuana, coke, etc. 46 Farst KJ et al. (2011) Drug testing for newborn exposure to illicit substances in pregnancy: pitfalls and pearls. Int J Pediatr. 2011:951616. doi: 10.1155/2011/951616. 47 Rayburn WF (2007) Maternal and fetal effects from substance use. Clin Perinatol. 34:559–571. 35
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as poverty, poor nutrition, lack of prenatal care, and so on, from actual drug use-related factors are limited, sometimes inconsistent, or does not exist in the few studies that were done. A study from 2009 examined admission at federally funded drug treatment centers and found that in 1994, methamphetamine use accounted for 8% of admitted pregnant women.48 In 2006 treatment for methamphetamine was the reason given by 24% of pregnant women. While the increase in the meth-using mothers reporting for treatment may have been due to the success and growth of the treatment program in targeting methamphetamine users, the use of methamphetamine during pregnancy remains a significant health issue. The next section reviews clinical studies with respect to methamphetamine use and adverse drug effects on the fetus.
Methamphetamine effects on the fetus In a comprehensive clinical study of all pregnancies in California from 2005 to 2008, the medical records of 8542 women who used methamphetamine during pregnancy were compared with over 2 million women who did not use methamphetamine.49 Preterm birth, defined as delivery of less than 37 weeks, was present in 23.4% of meth users compared to 8.9% in the control group of nonuser pregnancies. However, there was not a significant increase in preterm death of the neonate, occurring in 2.1% of meth-using mothers and in 1.6% in nonusing mothers. Two important conclusions come from this study: preterm death is not increased by maternal use of methamphetamine and that earlier delivery that occurs due to methamphetamine use is not reflected in a greater death rate of preterm neonates. These data also show that even with methamphetamine use, 76.6% of neonates are born at full-term, proving that methamphetamine is more likely to have no effect on the fetus. Finally, the data show that preterm death or intrauterine fetal demise (IUFD) occurs at a rate essentially the same in the meth-exposed and non-meth-exposed fetus, and is rare at only 2.1% of meth using mothers and 1.6% of nonusing mothers. The previous study also noted that methamphetamine use may have been protective against gestational diabetes. Other studies note an increase in preterm births and low birth weight of neonates born to mothers who used methamphetamine during pregnancy.50 As noted in this paper, when assessing the impact of illicit drug exposure during pregnancy, there are numerous other confounding factors to take into consideration and rule out before the effects can be attributed solely to the drug action. These include concurrent use of tobacco and alcohol, use and access to prenatal care, polydrug exposure, prescription drugs, insurance coverage, nutrition, and socioeconomic status to name a few. These other factors are associated with methamphetamine use per se. A large clinical study of methamphetamine effects on intrauterine growth of neonates exposed to methamphetamine during pregnancy was done using a target group of 204 mothers who used methamphetamine compared to 3501 mothers who did not.51 This study employed a sophisticated multivariate analysis that factored in the covariates of neonate gender, prenatal care visits, household income, socioeconomic status, mother’s weight gain, mother’s age, partner status, and race. Additionally, cooccurrence of methamphetamine and maternal tobacco, alcohol, and marijuana use was considered. In the final analysis, there was a significant decrease in the overall size of neonates at birth in meth-using mothers than nonusing control group. However, there were no significant differences in average birth weight of babies from meth users or control mothers. The researchers found no instances of IUFD attributed to the use of methamphetamine in meth-using mothers. Surprisingly, in this chapter’s third case, no blood or urine samples were obtained from the accused mother for drug testing after she was apprehended. Hair samples from the mother would have been ideal in that drug use during the time of pregnancy could have been analyzed. Without evidence of maternal use of methamphetamine during the pregnancy, it is not possible to conclude with certainty that prenatal exposure of methamphetamine was a contributing factor in the intrauterine fetal demise.
Methamphetamine in fetal liver samples There are few studies of fetal liver tissue and methamphetamine. One study examined the incidence of fetal drug exposure in Alabama from 2004 to 2011 using toxicological records from the Alabama Department of Forensic Sciences.52 The
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Terplan M et al. (2009) Methamphetamine use among pregnant women. Obstet Gynecol. 113:1285–1291. Gorman MC et al. (2014) Outcomes in pregnancies complicated by methamphetamine use. Am J Obstet Gynecol. 211:429.e1–7. 50 Ladhani NN et al. (2011) Prenatal amphetamine exposure and birth outcomes: a systematic review and meta-analysis. Am J Obstet Gynecol. 205:219. e1–7. 51 Nguyen D et al (2010) Intrauterine growth of infants exposed to prenatal methamphetamine: results from the infant development, environment, and lifestyle study. J Pediatr. 157:337–339. 52 Kalin JR (2014) Incidence of fetal drug exposure in Alabama: 2004-2011. J Forensic Sci. 59:1029–1035. 49
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authors found that out of 15,600 total fatalities (all ages) with postmortem toxicology screens, only 39 cases were from fetal or neonate deaths. Of these 39 cases, 22 were positive for any drug and only 7 were positive for methamphetamine or amphetamine. Liver samples were available from 2 cases with methamphetamine levels of 1.2 μg/g and 2.3 μg/g. However, in the first positive meth case, five other drugs were detected, including the opioid hydrocodone. In the second positive meth case, the conclusion was that the manner of death was undetermined. The authors concluded that placental insufficiency, miscarriage, and IUFD are natural occurring events (unrelated to drug use) and that fetal/neonate death “is often deemed drug-related only by virtue of a positive toxicological finding.” A small forensic report examining 8 cases of maternal methamphetamine use and fetal demise reported only a single case of intrauterine fetal demise (IUFD) where fetal liver samples were obtained. In this one case, a toxicology analysis reported a methamphetamine level of 0.52 μg/g and amphetamine level of 0.04 μg/g in the fetal liver sample. In that single case the manner of death was given as “IUFD, with findings consistent of asphyxia in the presence of maternal methamphetamine abuse.”53 However, there were no supporting studies to confirm the pathologist’s finding and no physical evidence of asphyxia. The detection of amphetamines in the liver samples is not that uncommon. The liver concentrates methamphetamine and amphetamine, and other drugs, as the liver is the site of drug metabolism. There are also binding sites for methamphetamine and amphetamines on the cells of the liver tissue.54 In postmortem studies, liver tissues were found to have 6–7 times higher concentrations of methamphetamine and amphetamine than peripheral blood.55 In another study, liver concentrations of methamphetamine ranged from about 2 to 9 times that of peripheral blood.56 A forensic study in apparent suicides by drug overdose examined amphetamines found in adult liver samples.57 The authors noted that in 6 out of 13 postmortem liver samples, false positive concentrations of amphetamines were found in liver samples that were not found in blood or other biological samples of the deceased. This could be the result of a large number of other drugs and medicines that can give a false positive methamphetamine result. The authors also state that it is known that amphetamines can be generated spontaneously from body substances in the liver and that this can occur in decomposing liver tissue. All the previous studies were done in adult postmortem tissue samples. There are no studies comparing blood to liver methamphetamine concentrations in a fetus or neonate. One study examined illicit drug and metabolites found in maternal hair samples in conjunction with drugs and metabolites found in fetal tissue remains in a group of 60 women undergoing elective abortion.58 There was not a good correlation between maternal use of illicit drugs as reflected in the hair samples and levels of illicit drugs found in the fetal tissue samples. The authors also noted that there is a large variability in the movement of drugs through the placenta and placental metabolism of drugs. Placentopharmacology and the workings of the placenta are still not well understood. A single measurement of the concentration of methamphetamine from liver samples which may be from 2 days to 1 week or more in a decomposing fetus does not support a determination of death due to methamphetamine toxicity. There are no such toxic levels known for methamphetamine in liver samples in adults and certainly no studies of possible toxic levels of methamphetamine in liver tissue samples obtained from fetal remains. At present, there is no scientific basis for asserting that a certain amount of methamphetamine in the decayed liver sample of the fetal tissues was the cause of death of the discarded fetus.
The Toxicologist and the Pharmacologist Drug Expert Toxicology is the study of the toxic effects of drugs, chemicals, or other substances on living organisms. A toxicologist may have an undergraduate, masters, or PhD degree. The label of “toxicologist” is therefore broader than the label of “pharmacologist” which was adjudicated59 to be indicative of a person holding a PhD in Pharmacology, that is, a Professor of Pharmacology. Not that there is anything wrong with being a toxicologist, some of my best friends are toxicologists. It’s just that the level of training and experience, and therefore expertise on drugs, can vary drastically in a toxicologist drug
53
Stewart JL, Meeker JE (1997) Fetal and infant deaths associated with maternal methamphetamine abuse. J Anal Toxicol. 21:515–517. Jones AL, Simpson KJ (1999) Review article: mechanisms and management of hepatotoxicity in ecstasy (MDMA) and amphetamine intoxications. Aliment Pharmacological Ther. 13:129–133. 55 McIntyre IM (2015) A “theoretical” post-mortem redistribution factor (Ft) as a marker of post-mortem redistribution. Eur J Forensic Sci. 2:24–26. 56 McIntyre IM et al. (2011) Postmortem methamphetamine distribution. J Forensic Res 2:122–125. 57 Sutlovic D et al. (2017) Amphetamine in post-mortem liver sample? Peertechz J Forensic Sci Tech. 3:1–4. 58 Falcon M et al. (2012) Maternal hair testing for the assessment of fetal exposure to drug of abuse during early pregnancy: Comparison with testing in placental and fetal remains. Forensic Sci Int. 218:92–96. 59 See Chapter 14, section entitled “The Pharmacist versus the Pharmacologist Drug Expert.” 54
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expert in contrast to the solid, lumbering, and extensive multiyear training (including toxicology) for the PhD pharmacologist drug expert.60 Of course, a PhD level Toxicologist would be no less acceptable than a PhD pharmacologist, and may be a better choice depending on the toxic drug issue at hand. It is important to recognize the different types of toxicologists that the drug expert or attorney may encounter in various cases. The toxicologist who signs off on investigative reports and is director of the state forensic laboratories in my home state is a PhD Toxicologist with a PhD in Toxicology from a pharmacology and toxicology program. The head of the Tulsa police forensics laboratory is a Toxicologist with a Master’s Degree in Toxicology. The lab technician at the largest medical toxicology lab in town is an undergraduate with a major in Toxicology and a bachelor’s degree. All three persons are commonly referred to as a toxicologist and have the title of “Toxicologist” next to their name, but their levels of expertise, skill sets, and areas of knowledge vary widely. The type of a degree that the expert witness earned rightly matters to attorneys as shown in sociological studies carried out by surveys and experimental legal cases.61 Experimental case results show that type of degree, as well as the actual testimony, years of experience, and testifying history are among the top four characteristics that attorneys assess in deciding to employ an expert witness. The number of publications and the expert’s fee are lesser ranked considerations. In the survey data, particular aspects underlying expert witness credibility that were ranked most important by attorneys were, in order, perceived trustworthiness, communication skills, and conclusions to be offered in testimony and report. The toxicologist in the chapter case on fetal remains detected methamphetamine and amphetamine in a liver sample from the fetal remains and opined that use of methamphetamine by the mother caused fetal death. He did not present any report or evidence from the medical literature to support his testimony. The drug expert wrote a detailed report with over thirty references from clinical research and forensic studies. The drug expert concluded that there is no reliable data to compare the level of detected methamphetamine in a decayed fetal liver sample to a toxic level in the blood that would kill a fetus. [Narrative continued] The drug expert researched several journal articles on the postmortem distribution of alcohol and findings from other forensic cases. It was found that estimates of alcohol levels and impairment from analysis of postmortem vitreous humor is unable to predict blood levels at the time of the accident. There was only one sample and that was obtained 72 h after the accident. Additionally, a literature search showed that the correlation of ethanol levels between vitreous humor samples and blood samples was not established. The judge found the drug expert’s testimony persuasive and made a judgment against the insurance company. Eventually, after many requests from their attorney, the parents of the decedent received full benefit from the insurance company. In the second case of the putrefied liver, there were two prescription drugs and one OTC drug detected and quantified from decayed liver samples. There was no evidence from pharmacy records that the prescription drugs were being abused. The OTC drug was relatively non-toxic, containing the antihistamine diphenhydramine. The drug expert concurred with the medical examiner in that there was no toxicological evidence to assert that the woman’s death was nothing but accidental. After a long delay, the dead woman’s mother received the death benefits from the insurance company. In the third chapter case with the fetal remains, the drug expert found that false positives of methamphetamine and amphetamine are not rare due to other drug cross-reactions on the assay, that the liver concentrates methamphetamine, and that there were no conclusive studies of fetal methamphetamine and toxicity. There was no evidence that the mother used methamphetamine while she was pregnant. Methamphetamine toxicity to the fetus leading to intrauterine demise (IUFD) is not clearly established in the literature of forensic or clinical studies. Largely due to the drug expert’s report, the second degree murder charge was dismissed. The mother still has charges pending related to the stillbirth and her drug use during pregnancy.
60
After a 4-year undergraduate biology degree and a 3-year American Peace Corps in Nepal tour-of-duty, I spent 3 years at U of IL at Chicago for my M.S. in Biomedical Sciences, 4 years for Ph.D. in Pharmacology at Mayo Clinic, and 2 years postdoc at U of MN before finally getting my first job as Assistant Professor of Pharmacology here at OSU. That was 30 years ago. 1 6 Wechsler HJ et al. (2015) Attorney beliefs concerning scientific evidence and expert witness credibility. Int J Law Psychiatry 41:58–66.
Dead Men Tell No Tales: Drug levels in a drowned, a decayed, and a dumpster corpse Insurance Claims and Drug Use Drug Detection in Fluid From the Eyeballs and Other Places Postmortem Detection of Alcohol and Methamphetamine Fetal Remains and Maternal Drug Use The Toxicologist and the Pharmacologist Drug Expert
[Narrative] John Plano was a 23-year old college grad from a well-to-do family in South Tulsa. One weekend at Grand Lake, he rented a speedboat and met his friends on the lake. After tying up to a flotilla of moored vessels, he stepped across to the next boat to meetup with his friends. He soon returned to his boat and took a dive into the waters from the bow. His friends became worried, then very agitated when they didn’t see him surface. They called the Grand Lake Water Patrol who responded within 10 min and began searching the waters. After 4 h of searching and darkness approaching, the search crews stopped for the night. Three days later, a fisherman reported a dead body floating in a cove near the scene of the accident. The decedent, Mr. Plano, was identified as the corpse from dental records and autopsy. The toxicological results showed that alcohol and THC was present in fluid samples from the eyeball (vitreous humor) but none from samples of heart or liver. On the basis of this finding, the insurance company refused payment of the decedent’s life insurance policy, on the grounds that the insured party was impaired by drugs at the time of the accident. The parents of the insured sued the insurance company with the assistance of a private law firm. The law firm consulted with a local drug expert regarding the detection of alcohol in vitreous fluid, and the insurance company’s denial due to drug impairment based on these results. In a separate case, the decayed body of a woman was discovered in an apartment by the manager after a neighbor complained of a foul odor. A full autopsy was done with no signs of trauma or obvious pathology. Toxicology was done on putrefied liver samples and the amounts of two prescription drugs and one OTC drug were quantified. On the basis of this toxicology report, the deceased life insurance company refused to pay the death benefit to her mother due to alleged suicide of the insured. The mother sought legal assistance and her attorney contacted a local drug expert to interpret the findings of the toxicology report. In a third case, a shoebox containing fetal remains was discovered in a dumpster by a homeless person. Toxicology of the fetal remains was limited to a decayed liver sample which gave methamphetamine and amphetamine levels in the fetal liver samples. The mother was tracked down and arrested for murder. A national organization for legal rights of pregnant women contacted a local drug expert to opine on the interpretation of the methamphetamine and amphetamine levels found in the fetal remains.
Insurance Claims and Drug Use Private life insurance and accidental death insurance arose as a response to the Industrial Revolution, and primarily the new transportation network of railroads.1 One of the first accident death insurance companies was formed in response to accidents and injuries that occurred with railroad travel in England. In 1863 the Travelers Insurance Company was the 1
Scales AF (2000) Man, God and the Serbonian bog: the evolution of accidental death insurance. 86 Iowa L. Rev. 173.
The Drug Expert. https://doi.org/10.1016/B978-0-12-800048-9.00019-5 © 2020 Elsevier Inc. All rights reserved.
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first company to issue accident policies in the United States.2 The name “Travelers Insurance” is apt and points out to the moorings of the present life insurance and accidental death and dismemberment (AD&D) policy stemming from the special case of persons using the modern conveyances of the time. Nowadays, life insurance is packaged with AD&D policies and coverage is continuous and independent of traveling or not.3 While any death results in the same outcome to the deceased and surviving loved ones (i.e., the insured is dead) all manner of death does not automatically trigger the death benefit. For example, life insurance companies cannot pay out claims from a husband who takes out a large policy on himself with his wife as beneficiary, then kills himself so his wife can live comfortably the rest of her life. Like all insurance companies, life insurance companies do not want to pay any death benefits if they don’t have to; such is the case in every for-profit industry.4 For that reason, there are a number of circumstances when death benefits are excluded. For example, the group Life Insurance and AD&D plan5 offered to employees of the OSU Medical School in Tulsa lists the following death benefit exclusions (bold added):
Accidental Death and Dismemberment Exclusions ReliaStar Life does not pay benefits for loss directly or indirectly caused by any of the following: ● Suicide or intentionally self-inflicted injury, while sane or insane. ● Physical or mental illness. ● Bacterial infection or bacterial poisoning. Exception: Infection from a cut or wound caused by an accident. ● Riding in or descending from an aircraft as a pilot or crew member. ● Any armed conflict, whether declared as war or not, involving any country or government. ● Injury suffered while in the military service for any country or government. ● Injury which occurs when you commit or attempt to commit a felony. ● Use of any drug, narcotic or hallucinogenic agent – – unless prescribed by a doctor. – which is illegal. – not taken as directed by a doctor or the manufacturer. ● Your intoxication. Intoxication means your blood alcohol content meets or exceeds the legal presumption of intoxication under the laws of the state where the accident occurred.
Because the use of alcohol, prescription drugs, OTC drugs, and/or illegal drugs is so common among insured individuals (as it is in all people, see Chapter 1), life insurance companies will often deny death benefits if there is any sign of drug use in the deceased. It is often the job of the drug expert to assist the insurance companies (rarely) and the plaintiffs filing suit against them (commonly), when issues of drug use in the deceased arise.
Drug Detection in Fluid From the Eyeballs and Other Places The ideal postmortem sample for detection of drug use is a vial of femoral blood. Blood is the easiest to use, as the methodology for blood sampling in the living can be applied to blood sampling in the dead. Peripheral bold samples, such as from the femoral vein, also give the best comparison of drug levels between the living and the dead. Nearly every drug, if taken by humans, has a research paper or two on the pharmacokinetics of that drug and corresponding blood levels and time course of those levels. Most drugs approved by the FDA in the last few decades also include peak blood concentration of a drug in the full prescribing information.
Vitreous humor fluid samples for postmortem detection of drugs When femoral blood cannot be obtained from a corpse due to decapitation, dismemberment, or fractionation, there is one place in the body that contains fluid encapsulated in a sealed container: the eyeball. The eyeball holds its shape due to the vitreous humor. Humor is an old word for fluid, as in the four humors of the body.6 Vitreous humor is a clear, colorless fluid 2
Travelers Insurance Company, with its iconic red umbrella logo, is still going strong today. For instance it is said that most home accidents occur in the bathroom. The insured in that case is would not be considered in a state of conveyance from one place to another, i.e., travelling. 4 Like health care, perhaps insurance companies should be embedded in a nonprofit structure. 5 Your Group Life Insurance Plan, for OSU employees, from ReliaStar Insurance Company, subsidiary of the Dutch ING financial group. 6 Early Greek medicine identified the four humors of the body as blood, yellow bile, black bile, and phlegm. 3
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filling the main chamber of the eye. Vitreous humor can be sampled by using a syringe and needle and inserting about 1 cm into the eyeball and slowly withdrawing the vitreous fluid.7 Because of its blood supply, the vitreous humor also reflects a drug’s concentration in the peripheral blood, although the relationship between vitreous fluid and blood levels of a drug is not clear (see later). For this reason, vitreous humor samples are often used for forensic analysis, especially in decayed or decomposing human bodies.8 Studies comparing the use of vitreous fluid or femoral blood samples for use in routine drug screening showed that drug screens in femoral blood resulted in twice as many positive drug tests in blood than vitreous fluid.9 This suggests that vitreous fluid, either by its restricted blood flow and lower drug concentrations or other biological processes, is not as good as blood for routine drug detection in postmortem samples. The vitreous fluid sample taken from the drowned man in the first narrative case of this chapter yielded a vitreous alcohol concentration of 0.10%, which was the basis of the insurance company denial of death benefits to the parents of the dead man. There were no other samples obtained in that case.
Liver samples for postmortem detection of drugs The liver could easily qualify as the number one internal organ in the abdomen. It is the only internal organ that can regenerate itself, and among its many roles, acts as the gatekeeper of all foreign substances that enter the body. Food and drugs taken orally are absorbed in the stomach and small intestine and immediately enter a special blood vessel pathway called the hepatic portal system. Drugs that are given by the IV route, directly in the bloodstream, quickly end up in the liver due to its large blood flow. The liver is also the number one site for drug metabolism. Putrefied liver tissue taken from the decedent described in the second chapter case was analyzed by GC-MS and three drug substances were detected and quantified.10 The toxicology report from the Medical Examiner’s Office reported zolpidem (Ambien®) at 4.5 μg/g (micrograms per gram of liver tissue), carisoprodol (Soma®) at 200 μg/g, and diphenhydramine (Benadryl®) at 30 μg/g in the putrefied liver samples of the decedent. On the basis of these findings, the insurance company denied benefits to the dead woman’s spouse, asserting that the presence of these drugs showed that the decedent purposely overdosed on these medications and committed suicide. Decomposed liver samples from the fetal remains found in third chapter case were also sampled and tested for drugs. The fetal liver tissue had a methamphetamine concentration of 3.0 μg/g and amphetamine was detected but not quantified. On the basis of this finding, the state’s toxicologist opined that the mother’s use of methamphetamine caused intrauterine fetal demise.
Other tissue sources for postmortem drug detection The kidney, brain, and muscle are also used for postmortem drug detection.11 These samples are often used when blood cannot be obtained. Samples can be used from these tissues but they also contain large amounts of lipids (fats) which interfere with the analytic methods used in toxicology. However, there is limited data to compare postmortem and premortem drug concentrations to aid in interpretation of results from these samples. More rarely, bone, hair, and fingernail samples are used for the postmortem detection of drugs, especially in decomposed corpses. Bone tissues are especially useful if the body has undergone severe decomposition, exsanguination, or skeletonization.12 Examination of bone tissue in a completely skeletonized corpse revealed significant levels of the opioid fentanyl. The amount of fentanyl was found to be dependent on the type of bone tissue examined (legbone vs. vertebrae) and area of the bone (outer tissue vs. bone marrow).13 Hair sampling for drug detection is noninvasive and can be obtained in the living and the dead. As discussed in Chapter 6 Hairs of the Innocent, drug detection in hair has a long window of detection as drugs in hair are interwoven into the hair matrix as the hair grows. In postmortem hair samples, depending on the length of the hair, 7
Yee L et al. (2000) Chiral high-performance liquid chromatographic analysis of fluoxetine and norfluoxetine in rabbit plasma, urine, and vitreous humor using an acetylated beta-cyclodextrin column. J Anal Toxicol. 24:651–655. 8 Metushi IG et al. (2016) Assessment and comparison of vitreous humor as an alternative matrix for forensic toxicology screening by GC-MS. J Anal Toxicol. 40:243–247. 9 Metushi IG et al. (2016) Ibid. 10 Gas chromatography-mass spectrometry, the standard method for identifying and quantifying forensic drug samples. See Chapter 5. 11 Margalho C et al. (2011) Illicit drugs in alternative biological specimens: A case report. J Forensic Legal Med. 18:132e135. 12 Orfanidis A et al. (2018) Alprazolam and zolpidem in skeletal tissue of decomposed body confirms exposure. J Forensic Sci. http://dx.doi.org/ 10.1111/1556-4029.13890. 13 Lafrenière NM, Watterson JH (2009) Detection of acute fentanyl exposure in fresh and decomposed skeletal tissues. Forensic Sci Internat. 185:100–106.
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exposure to drugs in the deceased may be determined for the past 6 months or longer. However, this precludes use of hair samples to ascertain immediate or acute drug effects in the deceased. Hair is also an ideal matrix for drug detection in ancient humans, like cocaine metabolites found in Northern Chilean mummies dating back to 2000 BCE.14 In a more recent case, antipsychotic drugs were detected in the fingernails and toenails of an unidentified and bloated corpse.15 Drug testing helped investigators determine the identity of the corpse as it narrowed their search to a long-term user of antipsychotic medicines. As mentioned, liver, kidney, brain, and most of the other tissues samples noted before, as well as vitreous fluid samples from the eye, cannot be obtained in living patients. Therefore the data from toxicological tests using these postmortem samples cannot be directly compared to reference data of drug and alcohol levels measured in living subjects. The drug expert is often the person to make this key point in the trial to avoid the overinterpretation by other experts. Existing data correlating any drug levels obtained postmortem from drug levels in living beings is extremely limited.
Postmortem Detection of Alcohol and Methamphetamine Postmortem blood samples are ideally taken from a peripheral site, with the femoral vein in the leg considered the “gold standard” in medicolegal and forensic research.16 In analytical toxicology guidelines, it is stated that drug levels from postmortem blood samples are most reliable when the interval between death and postmortem sampling is short, and blood samples are collected from a peripheral site, preferably the femoral vein.17 Under ideal conditions, because postmortem blood samples can be compared to peripheral blood samples obtained in living patients, an attempt at correlating therapeutic and toxic (or intoxicating) levels of drugs and ethanol can be made.18 As introduced in Chapter 8, postmortem redistribution (PMR) of drugs occurs when a drug’s concentration in the blood is different before and after death. This is important as nearly all of the data on the blood level of a drug and any adverse or toxic effects are based on blood levels in living subjects (antemortem samples). Depending on the drug, PMR can artificially increase blood concentrations when postmortem processes draw drugs from tissues in to the blood. Conversely, the process of PMR can decrease blood levels of a drug after death by the stoppage of blood circulation and drug absorption into fat tissue. For many drugs, PMR processes can be negligible with no change in antemortem and postmortem levels.19 In any event, in many cases the drug expert only has postmortem drug concentration data and is asked to form an opinion. Some opinions can be made when the drug levels are in extremis, for example, super-high levels of a drug might easily relate to drug concentrations found in forensic studies of documented suicides using the drug at issue.20 Many cases yield astonishing low levels of drug in postmortem samples, supporting a nonexistent role of acute drug use in the decedent.
Vitreous fluid sample for alcohol determination With all the instances of alcohol mentioned in this book, the reader might be tempted to leave the coffee shop and head to a nearby bar.21 However, the postmortem redistribution of alcohol is an important topic to bring up because so many people drink alcohol and drive, or jump off a boat, and end up dead that reports of postmortem alcohol levels often find their way to the drug expert’s desk. Because a femoral blood sample is considered the most reliable site of sampling for forensic interpretation (see earlier), much forensic research compares the ethanol concentration from vitreous fluid to ethanol concentration from femoral blood 14
Cocaine metabolites were found in these hair specimens. Baez H et al. (2000) Drugs in prehistory: chemical analysis of ancient human hair. Forensic Sci Internat. 108:173–179. 15 Chen H et al. (2014) Determination of clozapine in hair and nail: the role of keratinous biological materials in the identification of a bloated cadaver case. J Forensic Leg Med. 22:62–67. 16 Launiainen T, Ojanperä I (2014) Drug concentrations in post-mortem femoral blood compared with therapeutic concentrations in plasma. Drug Test Anal. 6:308–316. 17 Flanagan RJ, Connally G, Evans JM (2005) Analytical toxicology: guidelines for sample collection postmortem. Toxicol Rev. 24:63–71. 18 Also have to consider postmortem redistribution of the drug, discussed in the next section below. See also: Skopp G (2004) Preanalytic aspects in postmortem toxicology. Forensic Sci Int. 142:75–100. 19 For an excellent article on PMR by a leading expert in the area, see Drummer and his colleagues, e.g. Gerostamoulos D, Beyer J, Staikos V, Tayler P, Woodford N, and Drummer OH (2012) The effect of the postmortem interval on the redistribution of drugs: a comparison of mortuary admission and autopsy blood specimens. Forensic Sci Med Pathol.8:373–379. 20 Obviously there are some caveats in comparing levels of a postmortem drug in a legal case and drug concentrations reported in forensic studies. For example, most drugs have quite a large lethal blood concentration range which can provide little information in comparing a single value from a real case. 21 Drug-craving cues like the numerous mentions of alcohol in this book are based on actual data. Neuroimaging shows that craving areas of the brain become activated (“light up”) in response to pictures of crack cocaine in abstinent users, another proof that addictive drug use alters the brain.
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samples.22 These studies show that the ratio of vitreous fluid alcohol to femoral blood alcohol is highly variable. Some cases show a high ratio of vitreous fluid alcohol to femoral blood alcohol, other the opposite, with a low ratio of vitreous fluid alcohol to femoral blood alcohol. The ratio of vitreous ethanol to blood BAC is highly variable when the level of ethanol in the blood is less than 0.10% BAC. The concentration of ethanol in the vitreous fluid is typically higher than that in femoral blood; however, the relationship between vitreous fluid and heart blood is not clear.23 An early study made a mathematical model to prediction of blood alcohol concentration (BAC) from the alcohol concentration in the vitreous fluid but concluded that “the prediction interval is too wide to be of real practical use.”24 They continued that previous authors provided simple conversion factors to estimate BAC from vitreous alcohol “without taking into account the uncertainty of the prediction for an individual subject.” Another study of 62 deceased subjects found that ethanol concentrations in the vitreous fluid did not have a significant correlation to peripheral BAC.25 Expert authors in the field suggested more studies are needed before vitreous fluid ethanol can make reliable predictions of BAC.26 They outlined the studies needed: a large population of cases where the time and amount of alcohol consumed before death was known, the time of death, and the time of postmortem sampling was known. Other authors found that the ratio between vitreous ethanol concentration and blood BAC is so variable that a rule-of-thumb practice is to take half the vitreous alcohol concentration to estimate the BAC.27 In the present chapter case of the drowned corpse, the insurance company denied benefits largely based on the alcohol level from a single sample of vitreous fluid. From a single determination of 0.12% vitreous fluid alcohol, the insurance company claimed the decedent’s BAC was greater than 0.08% and that he was intoxicated. This violated the no intoxication clause of the life insurance policy. The claim of intoxication was made by the insurance company in spite of both the report from the medical examiner and the official death certificate note an accidental death by drowning with no contributing factor or other significant factor of alcohol intoxication.
Postmortem redistribution of alcohol Postmortem redistribution of drugs and ethanol results when the drug or ethanol diffuses from higher concentrations to areas of lower concentrations in the corpse following the disruption of cellular membranes.28 Postmortem redistribution of drugs and ethanol makes it impossible to determine with certainty the actual drug or ethanol content in the person before they died. It is well established in the forensic pharmacology literature that ethanol undergoes postmortem redistribution.29 Postmortem redistribution of ethanol is also caused by trauma to the deceased in the manner of death. Traumatic injuries to the torso are known to increase BAC.30 Other studies show that specimen site variability (e.g., heart blood versus femoral blood) is due to postmortem redistribution of ethanol.31
Postmortem production of ethanol After a person dies, a process of accelerated microbe growth begins in many tissues of the body. These microbes, mostly bacteria, yeast, and fungi, have been identified in postmortem tissues and are known to produce alcohol as part of their natural metabolism.32 This process is called the “postmortem production of ethanol” or “endogenous ethanol production” (inside the body, as opposed to exogenous ethanol from a few drinks). Ethanol synthesis by microbes is observed in the early stages of decomposition or putrefaction.33 Postmortem production of ethanol can lead to ethanol level as high as 22
Caplan YH, Levine B (1990) Vitreous humor in the evaluation of postmortem blood ethanol concentrations. J Anal Toxicol. 14:305–307; Kugelberg FC, Jones AW (2007) Interpreting results of ethanol analysis in postmortem specimens: a review of the literature. Forensic Sci Int. 165:10–29. 23 Honey D et al. (2005) Comparative alcohol concentrations in blood and vitreous fluid with illustrative case studies. J Anal Toxicol. 29:365–369. 24 Pounder DJ, Kuroda N (1994) Vitreous alcohol is of limited value in predicting blood alcohol. Forensic Sci Int. 65:73–80. 25 Mackey-Bojack S et al. (2000) Cocaine, cocaine metabolite, and ethanol concentrations in postmortem blood and vitreous humor. J Anal Toxicol. 24:59–65. 26 Sylvester PA et al. (1998) Op cit. 27 Jones AW, Holmgren P (2001) Uncertainty in estimating blood ethanol concentrations by analysis of vitreous humour. Clin Pathol. 54:699–702. 28 Kugelberg FC, Jones AW (2007) Op cit.; Pélissier-Alicot AL et al. (2006) Op cit.; Drummer OH (2004) Postmortem toxicology of drugs of abuse. Forensic Sci Int. 142:101–113. 29 Kugelberg FC, Jones AW (2007) Op cit.; Iwasaki Y et al. (1998) On the influence of postmortem alcohol diffusion from the stomach contents to the heart blood. Forensic Sci Int. 94:111–118. 30 Winek et al. (1995) The role of trauma in postmortem alcohol determination. Forensic Sci Int. 71:1–8. 31 Can et al. (2012) Importance of sampling sites for postmortem evaluation of ethyl alcohol. Forensic Res. 3:7. 32 Lewis RJ et al. (2004) Ethanol formation in unadulterated postmortem tissues. Forensic Sci Int. 146:17–24. 33 Boumba VA et al. (2008) Biochemical pathways generating post-mortem volatile compounds co-detected during forensic ethanol analyses. Forensic Sci Int. 174:133–151.
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0.22 g/dL (0.22% BAC).34 Postmortem production of ethanol is not rare but common. All 9 accident victims showed postmortem production of ethanol in an FAA-investigation accident.35 Importantly, this study also showed that postmortem production of ethanol can occur in bodies stored at 4°F, as is commonly done in the morgue. It is often stated that a vitreous humor fluid sample is less likely to undergo postmortem production of ethanol due to its isolated location in the eyeball.36 However, research shows that fluid samples from the vitreous fluid can show evidence of postmortem production of ethanol.37 Through postmortem redistribution, any microbial production of ethanol elsewhere would also be freely available to distribute to the vitreous humor fluid. Drug concentrations have been noted to undergo postmortem increases in the vitreous humor fluid samples, which was attributed to dehydration.38 Additionally, the vitreous humor contains glucose (a sugar) which is known to be used for the postmortem production of ethanol by microbes.39 Also, there are a number of other substrates besides glucose that microbes can use for the postmortem production of ethanol including amino acids, fatty acids, and glycerol.40 According to some investigators, postmortem BAC analysis has an unacceptable high rate of specimen site variability.41 Vitreous fluid alcohol concentration did not correlate well without high variability when compared to BAC obtained from femoral and heart blood samples. There is high variability in the value of BAC depending on where the blood is sampled from the body. Studies show that even the left side of the heart may yield significantly different BAC values than the right side of the heart in postmortem determinations of ethanol concentration.42
Postmortem redistribution of methamphetamine One study measured antemortem (while subject was still alive) and postmortem levels of methamphetamine and amphetamine in blood samples. Methamphetamine and amphetamine concentrations in peripheral blood samples were 1.5 to 2 times greater in the postmortem samples compared to the antemortem samples.43 In this study, antemortem samples were taken 7–22 min prior to a declaration of death at the hospital, and the postmortem samples 5–30 h after death at autopsy. As mentioned earlier, obtaining samples after death for forensic analysis for drugs is confounded by postmortem redistribution (PMR) of drugs. Methamphetamine undergoes extensive PMR and methamphetamine is concentrated in the liver. Human and primate studies with direct imaging show that the liver and kidneys are organs with the highest uptake of methamphetamine. In humans, about a quarter (23%) of the total methamphetamine dose was concentrated in the liver in live imaging studies.44
Fetal Remains and Maternal Drug Use Estimates of illicit drug use45 during pregnancy vary widely in the medical literature. Maternal use of illicit drugs is selfreported by about 5%–10% of pregnant women. However, universal drug testing in high-risk populations (low socioeconomic status) reveals a higher rate of 10%–40% illicit drug use during pregnancy.46 In general, maternal use of illicit drugs during pregnancy may place the fetus at risk for problems including low birth weight, small head circumference, increased preterm delivery, and other developmental complications.47 With the use of illicit drugs, the evidence or data is insufficient or too variable to ascertain with certainty drugs that produce ill effects on the fetus and at what drug concentrations. Furthermore, clinical studies that take into account the confounding factors such 34
Skopp G (2004) Preanalytic aspects in postmortem toxicology. Forensic Sci Int. 142:75–100. Lewis et al. (2004) Op. cit. 36 de Martinis BS et al. (2006) Alcohol distribution in different postmortem body fluids. Hum Exp Toxicol. 25:93–97. 37 de Lima IV, Midio AF (1999) Origin of blood ethanol in decomposed bodies. Forensic Sci Int. 106:157–162. 38 Skopp G (2004), Op. cit. 39 Kugelberg FC, Jones AW (2007) Interpreting results of ethanol analysis in postmortem specimens: a review of the literature. Forensic Sci Int. 165:10–29. 40 Boumba VA et al. (2008) Biochemical pathways generating post-mortem volatile compounds co-detected during forensic ethanol analyses. Forensic Sci Int. 174:133–151. 41 Sylvester PA et al. (1998) Unacceptably high site variability in postmortem blood alcohol analysis. J Clin Pathol. 51:250–252. 42 Pélissier-Alicot AL et al. (2006) Comparison of ethanol concentrations in right cardiac blood, left cardiac blood and peripheral blood in a series of 30 cases. Forensic Sci Int. 156:35–39. 43 McIntyre IM et al (2013) Antemortem and postmortem methamphetamine blood concentrations: three case reports. J Anal Toxicol. 37:386–389. 44 Volkow ND et al. (2010) Distribution and pharmacokinetics of methamphetamine in the human body: clinical implications. PLoS One 5:e15269. 45 Includes the abuse of prescription drugs, like opioids, as well as the standard drugs like marijuana, coke, etc. 46 Farst KJ et al. (2011) Drug testing for newborn exposure to illicit substances in pregnancy: pitfalls and pearls. Int J Pediatr. 2011:951616. doi: 10.1155/2011/951616. 47 Rayburn WF (2007) Maternal and fetal effects from substance use. Clin Perinatol. 34:559–571. 35
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as poverty, poor nutrition, lack of prenatal care, and so on, from actual drug use-related factors are limited, sometimes inconsistent, or does not exist in the few studies that were done. A study from 2009 examined admission at federally funded drug treatment centers and found that in 1994, methamphetamine use accounted for 8% of admitted pregnant women.48 In 2006 treatment for methamphetamine was the reason given by 24% of pregnant women. While the increase in the meth-using mothers reporting for treatment may have been due to the success and growth of the treatment program in targeting methamphetamine users, the use of methamphetamine during pregnancy remains a significant health issue. The next section reviews clinical studies with respect to methamphetamine use and adverse drug effects on the fetus.
Methamphetamine effects on the fetus In a comprehensive clinical study of all pregnancies in California from 2005 to 2008, the medical records of 8542 women who used methamphetamine during pregnancy were compared with over 2 million women who did not use methamphetamine.49 Preterm birth, defined as delivery of less than 37 weeks, was present in 23.4% of meth users compared to 8.9% in the control group of nonuser pregnancies. However, there was not a significant increase in preterm death of the neonate, occurring in 2.1% of meth-using mothers and in 1.6% in nonusing mothers. Two important conclusions come from this study: preterm death is not increased by maternal use of methamphetamine and that earlier delivery that occurs due to methamphetamine use is not reflected in a greater death rate of preterm neonates. These data also show that even with methamphetamine use, 76.6% of neonates are born at full-term, proving that methamphetamine is more likely to have no effect on the fetus. Finally, the data show that preterm death or intrauterine fetal demise (IUFD) occurs at a rate essentially the same in the meth-exposed and non-meth-exposed fetus, and is rare at only 2.1% of meth using mothers and 1.6% of nonusing mothers. The previous study also noted that methamphetamine use may have been protective against gestational diabetes. Other studies note an increase in preterm births and low birth weight of neonates born to mothers who used methamphetamine during pregnancy.50 As noted in this paper, when assessing the impact of illicit drug exposure during pregnancy, there are numerous other confounding factors to take into consideration and rule out before the effects can be attributed solely to the drug action. These include concurrent use of tobacco and alcohol, use and access to prenatal care, polydrug exposure, prescription drugs, insurance coverage, nutrition, and socioeconomic status to name a few. These other factors are associated with methamphetamine use per se. A large clinical study of methamphetamine effects on intrauterine growth of neonates exposed to methamphetamine during pregnancy was done using a target group of 204 mothers who used methamphetamine compared to 3501 mothers who did not.51 This study employed a sophisticated multivariate analysis that factored in the covariates of neonate gender, prenatal care visits, household income, socioeconomic status, mother’s weight gain, mother’s age, partner status, and race. Additionally, cooccurrence of methamphetamine and maternal tobacco, alcohol, and marijuana use was considered. In the final analysis, there was a significant decrease in the overall size of neonates at birth in meth-using mothers than nonusing control group. However, there were no significant differences in average birth weight of babies from meth users or control mothers. The researchers found no instances of IUFD attributed to the use of methamphetamine in meth-using mothers. Surprisingly, in this chapter’s third case, no blood or urine samples were obtained from the accused mother for drug testing after she was apprehended. Hair samples from the mother would have been ideal in that drug use during the time of pregnancy could have been analyzed. Without evidence of maternal use of methamphetamine during the pregnancy, it is not possible to conclude with certainty that prenatal exposure of methamphetamine was a contributing factor in the intrauterine fetal demise.
Methamphetamine in fetal liver samples There are few studies of fetal liver tissue and methamphetamine. One study examined the incidence of fetal drug exposure in Alabama from 2004 to 2011 using toxicological records from the Alabama Department of Forensic Sciences.52 The
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Terplan M et al. (2009) Methamphetamine use among pregnant women. Obstet Gynecol. 113:1285–1291. Gorman MC et al. (2014) Outcomes in pregnancies complicated by methamphetamine use. Am J Obstet Gynecol. 211:429.e1–7. 50 Ladhani NN et al. (2011) Prenatal amphetamine exposure and birth outcomes: a systematic review and meta-analysis. Am J Obstet Gynecol. 205:219. e1–7. 51 Nguyen D et al (2010) Intrauterine growth of infants exposed to prenatal methamphetamine: results from the infant development, environment, and lifestyle study. J Pediatr. 157:337–339. 52 Kalin JR (2014) Incidence of fetal drug exposure in Alabama: 2004-2011. J Forensic Sci. 59:1029–1035. 49
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authors found that out of 15,600 total fatalities (all ages) with postmortem toxicology screens, only 39 cases were from fetal or neonate deaths. Of these 39 cases, 22 were positive for any drug and only 7 were positive for methamphetamine or amphetamine. Liver samples were available from 2 cases with methamphetamine levels of 1.2 μg/g and 2.3 μg/g. However, in the first positive meth case, five other drugs were detected, including the opioid hydrocodone. In the second positive meth case, the conclusion was that the manner of death was undetermined. The authors concluded that placental insufficiency, miscarriage, and IUFD are natural occurring events (unrelated to drug use) and that fetal/neonate death “is often deemed drug-related only by virtue of a positive toxicological finding.” A small forensic report examining 8 cases of maternal methamphetamine use and fetal demise reported only a single case of intrauterine fetal demise (IUFD) where fetal liver samples were obtained. In this one case, a toxicology analysis reported a methamphetamine level of 0.52 μg/g and amphetamine level of 0.04 μg/g in the fetal liver sample. In that single case the manner of death was given as “IUFD, with findings consistent of asphyxia in the presence of maternal methamphetamine abuse.”53 However, there were no supporting studies to confirm the pathologist’s finding and no physical evidence of asphyxia. The detection of amphetamines in the liver samples is not that uncommon. The liver concentrates methamphetamine and amphetamine, and other drugs, as the liver is the site of drug metabolism. There are also binding sites for methamphetamine and amphetamines on the cells of the liver tissue.54 In postmortem studies, liver tissues were found to have 6–7 times higher concentrations of methamphetamine and amphetamine than peripheral blood.55 In another study, liver concentrations of methamphetamine ranged from about 2 to 9 times that of peripheral blood.56 A forensic study in apparent suicides by drug overdose examined amphetamines found in adult liver samples.57 The authors noted that in 6 out of 13 postmortem liver samples, false positive concentrations of amphetamines were found in liver samples that were not found in blood or other biological samples of the deceased. This could be the result of a large number of other drugs and medicines that can give a false positive methamphetamine result. The authors also state that it is known that amphetamines can be generated spontaneously from body substances in the liver and that this can occur in decomposing liver tissue. All the previous studies were done in adult postmortem tissue samples. There are no studies comparing blood to liver methamphetamine concentrations in a fetus or neonate. One study examined illicit drug and metabolites found in maternal hair samples in conjunction with drugs and metabolites found in fetal tissue remains in a group of 60 women undergoing elective abortion.58 There was not a good correlation between maternal use of illicit drugs as reflected in the hair samples and levels of illicit drugs found in the fetal tissue samples. The authors also noted that there is a large variability in the movement of drugs through the placenta and placental metabolism of drugs. Placentopharmacology and the workings of the placenta are still not well understood. A single measurement of the concentration of methamphetamine from liver samples which may be from 2 days to 1 week or more in a decomposing fetus does not support a determination of death due to methamphetamine toxicity. There are no such toxic levels known for methamphetamine in liver samples in adults and certainly no studies of possible toxic levels of methamphetamine in liver tissue samples obtained from fetal remains. At present, there is no scientific basis for asserting that a certain amount of methamphetamine in the decayed liver sample of the fetal tissues was the cause of death of the discarded fetus.
The Toxicologist and the Pharmacologist Drug Expert Toxicology is the study of the toxic effects of drugs, chemicals, or other substances on living organisms. A toxicologist may have an undergraduate, masters, or PhD degree. The label of “toxicologist” is therefore broader than the label of “pharmacologist” which was adjudicated59 to be indicative of a person holding a PhD in Pharmacology, that is, a Professor of Pharmacology. Not that there is anything wrong with being a toxicologist, some of my best friends are toxicologists. It’s just that the level of training and experience, and therefore expertise on drugs, can vary drastically in a toxicologist drug
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Stewart JL, Meeker JE (1997) Fetal and infant deaths associated with maternal methamphetamine abuse. J Anal Toxicol. 21:515–517. Jones AL, Simpson KJ (1999) Review article: mechanisms and management of hepatotoxicity in ecstasy (MDMA) and amphetamine intoxications. Aliment Pharmacological Ther. 13:129–133. 55 McIntyre IM (2015) A “theoretical” post-mortem redistribution factor (Ft) as a marker of post-mortem redistribution. Eur J Forensic Sci. 2:24–26. 56 McIntyre IM et al. (2011) Postmortem methamphetamine distribution. J Forensic Res 2:122–125. 57 Sutlovic D et al. (2017) Amphetamine in post-mortem liver sample? Peertechz J Forensic Sci Tech. 3:1–4. 58 Falcon M et al. (2012) Maternal hair testing for the assessment of fetal exposure to drug of abuse during early pregnancy: Comparison with testing in placental and fetal remains. Forensic Sci Int. 218:92–96. 59 See Chapter 14, section entitled “The Pharmacist versus the Pharmacologist Drug Expert.” 54
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expert in contrast to the solid, lumbering, and extensive multiyear training (including toxicology) for the PhD pharmacologist drug expert.60 Of course, a PhD level Toxicologist would be no less acceptable than a PhD pharmacologist, and may be a better choice depending on the toxic drug issue at hand. It is important to recognize the different types of toxicologists that the drug expert or attorney may encounter in various cases. The toxicologist who signs off on investigative reports and is director of the state forensic laboratories in my home state is a PhD Toxicologist with a PhD in Toxicology from a pharmacology and toxicology program. The head of the Tulsa police forensics laboratory is a Toxicologist with a Master’s Degree in Toxicology. The lab technician at the largest medical toxicology lab in town is an undergraduate with a major in Toxicology and a bachelor’s degree. All three persons are commonly referred to as a toxicologist and have the title of “Toxicologist” next to their name, but their levels of expertise, skill sets, and areas of knowledge vary widely. The type of a degree that the expert witness earned rightly matters to attorneys as shown in sociological studies carried out by surveys and experimental legal cases.61 Experimental case results show that type of degree, as well as the actual testimony, years of experience, and testifying history are among the top four characteristics that attorneys assess in deciding to employ an expert witness. The number of publications and the expert’s fee are lesser ranked considerations. In the survey data, particular aspects underlying expert witness credibility that were ranked most important by attorneys were, in order, perceived trustworthiness, communication skills, and conclusions to be offered in testimony and report. The toxicologist in the chapter case on fetal remains detected methamphetamine and amphetamine in a liver sample from the fetal remains and opined that use of methamphetamine by the mother caused fetal death. He did not present any report or evidence from the medical literature to support his testimony. The drug expert wrote a detailed report with over thirty references from clinical research and forensic studies. The drug expert concluded that there is no reliable data to compare the level of detected methamphetamine in a decayed fetal liver sample to a toxic level in the blood that would kill a fetus. [Narrative continued] The drug expert researched several journal articles on the postmortem distribution of alcohol and findings from other forensic cases. It was found that estimates of alcohol levels and impairment from analysis of postmortem vitreous humor is unable to predict blood levels at the time of the accident. There was only one sample and that was obtained 72 h after the accident. Additionally, a literature search showed that the correlation of ethanol levels between vitreous humor samples and blood samples was not established. The judge found the drug expert’s testimony persuasive and made a judgment against the insurance company. Eventually, after many requests from their attorney, the parents of the decedent received full benefit from the insurance company. In the second case of the putrefied liver, there were two prescription drugs and one OTC drug detected and quantified from decayed liver samples. There was no evidence from pharmacy records that the prescription drugs were being abused. The OTC drug was relatively non-toxic, containing the antihistamine diphenhydramine. The drug expert concurred with the medical examiner in that there was no toxicological evidence to assert that the woman’s death was nothing but accidental. After a long delay, the dead woman’s mother received the death benefits from the insurance company. In the third chapter case with the fetal remains, the drug expert found that false positives of methamphetamine and amphetamine are not rare due to other drug cross-reactions on the assay, that the liver concentrates methamphetamine, and that there were no conclusive studies of fetal methamphetamine and toxicity. There was no evidence that the mother used methamphetamine while she was pregnant. Methamphetamine toxicity to the fetus leading to intrauterine demise (IUFD) is not clearly established in the literature of forensic or clinical studies. Largely due to the drug expert’s report, the second degree murder charge was dismissed. The mother still has charges pending related to the stillbirth and her drug use during pregnancy.
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After a 4-year undergraduate biology degree and a 3-year American Peace Corps in Nepal tour-of-duty, I spent 3 years at U of IL at Chicago for my M.S. in Biomedical Sciences, 4 years for Ph.D. in Pharmacology at Mayo Clinic, and 2 years postdoc at U of MN before finally getting my first job as Assistant Professor of Pharmacology here at OSU. That was 30 years ago. 1 6 Wechsler HJ et al. (2015) Attorney beliefs concerning scientific evidence and expert witness credibility. Int J Law Psychiatry 41:58–66.