Sunday, October 25, 2015

Severe Toxicity after Synthetic Cannabinoid Exposure in an Infant (NACCT 2015)

This case report from Hawkins et al. and the Louisiana Poison Center and Louisiana State University Health Sciences Center in Shreveport, LA was published in Clinical Toxicology as an abstract presented at the 2015 Annual Meeting of the North American Congress of Clinical Toxicology (NACCT), 53:7, 639-777.

Severe Toxicity after Synthetic Cannabinoid Exposure in an Infant
J.A. Hawkins, M.L. Ryan, T.C. Arnold

In summary:

A 10 month old child presented to a Louisiana emergency department after ingesting herbal potpourri. The child had consumed the potpourri several hours prior to arrival and was suffering from altered mental status including unresponsiveness, moaning, and rigidity.

At presentation, the child’s blood pressure was 108/71 mm Hg, pulse was 71 beats per minute (bradycardia), respiration was 22 breaths per minute, and rectal temperature was 90.4 F (hypothermia). Glucose was 162 mg/dL. Blood urea nitrogen was 32 mg/dL. Lactic acid in serum was 3.6 mmol/L.

The child was intubated on admission due to prolonged apnea/oxygen desaturation and extubated on hospital day two. He recovered fully and was discharged on the third day and allowed to return home.

Analysis of the product consumed by the child was positive for the synthetic cannabinoid MAB-CHMINACA. Toxicological analysis on the admission serum specimen was positive for the presence of MAB-CHMINACA and a metabolite of said compound.

I have covered a bit about MAB-CHMINACA here at TDMTP over the last year or so.

Thursday, October 15, 2015

New Reports of Synthetic Cannabinoid Deaths (TIAFT 2015)

The International Association of Forensic Toxicologists (TIAFT) held their annual meeting in Florence, Italy during September 2015.

There were three presentations in which synthetic cannabinoid-related deaths were reported. The synthetic cannabinoids involved included MMB-CHMINACA, PB-22, and 5F-PB-22.

MMB-CHMINACA Blood Concentrations in Recreational Users and Fatal Intoxications
R. Kronstrand, E. Tyrkko*, D. Lindstedt, M. Roman

Tyrkko et al. report that during 2014 in Sweden, the synthetic cannabinoid MMB-CHMINACA was detected in six postmortem cases. Two of the six cases were certified as fatal intoxications with MMB-CHMINACA with blood concentrations equal to 0.001 and 0.003 mcg/g. In both cases, autopsy findings were unremarkable.

Three Deaths Involving Synthetic Cannabinoid PB-22
M.G. Pricone*, S. Yap, D. Gerostamoulos, O.H. Drummer, N.W. Woodford

Pricone et al. report that in Australia in 2014 during a four month period three deaths occurred where the synthetic cannabinoid PB-22 was identified as the main toxicological finding. Individuals were 19, 23, and 33 years of age. The blood concentrations of PB-22 were 0.2, 0.5, and 3 ng/mL.  Causes of death in two of the cases were certified as PB-22 associated. The cause of death in one of the cases remains undetermined.

Death After Consumption of New Synthetic Cannabinoids and Alcohol
A. Ewald*, N. Schaefer, B. Peters, P. Schmidt

Ewald et al. reported a case out of Germany of a 33 year old male who was found deceased in his friend’s house.  He had last  been seen alive by a friend a few hours prior to being discovered. The deceased individual had a history of ethanol and synthetic cannabinoid consumption. Findings at autopsy included visceral edema/congestion and a respiratory tract infection. Toxicological findings of peripheral blood were 5F-PB-22 (0.85 ng/mL) and ethanol (0.265%). Cause of death was determined to be combined intoxication of PB-22 and ethanol.

* It is important to note that MMB-CHMINACA was the first purported name of the compound as it was sold as such by chemical vendors. But, the actual compound is not an indazole carboxamide, it is an indole carboxamide and a more suitable name is MDMB-CHMICA. Just more alphabet soup synthetic cannabinoids! Also just lends credence to the line of thinking that you cannot (or should not) completely trust research chemical vendors. According to Shevyrin et al., true MMB-CHMINACA had not been found on the market as of January 2015.

Thursday, September 24, 2015

DXM to be age restricted?

Here is a bill I completely missed.

H.R. 3250 was introduced into the United States House of Representatives on July 28, 2015 and is titled "DXM Abuse Prevention Act of 2015". The PDF version of the bill is located here. The sponsor is Rep. Bill Johnson (R-OH).

The aim of this bill is to set a mandatory minimum age requirement for purchase of Dextromethorphan (DXM) at 18 years. No one 17 years of age or younger will be allowed to purchase DXM or DXM-containing products. The only exception to the age requirement is if the purchaser is an active member of the United States military.

On July 31, 2015, the bill was referred to the Energy and Commerce's subcommittee on Health. No further movement on the bill has occurred.


Wednesday, September 23, 2015

What do Etizolam, Zopiclone, O-Desmethyltramadol, and Salvinorin A all have in common?

As an addendum to the blog post from yesterday discussing the Synthetic Drug Control Act of 2015, roinonsteroids and other fine folks over at have outlined the identity of other substances on the list.

Interestingly, the five benzodiazepines listed are etizolam, zopiclone, and “3 benzos that have never appeared on the research chemical market”.
As mentioned earlier, etizolam is not a benzodiazepine; it is a thienodiazepine. I guess it could be listed as a benzodiazepine derivative.
Zopiclone is also not a benzodiazepine. In fact, more often than not, it is described as a non-benzodiazepine hypnotic. Zopiclone is not available in the USA, but the S-enantiomer (eszopiclone) is marketed as Lunesta and is currently found in Schedule IV of the CSA.
Salvinorin A, one of the terpenoid compounds found in the Salvia divinorum plant, as well as O-desmethyltramadol, the active metabolite of the drug tramadol, are included in the 13 opioids/opioid-like substances.
Image from
One wonders how the legislators constructed this list?
Is this just a grab bag of chemical names from research chemical websites? Or did actual chemists and toxicologists construct this list?
Considering that the folks at Reddit/r/researchchemicals and Reddit/r/drugs believe that a  large amount of these substance have never appeared on the market or aren't very common at all, this piece of legislation seems very Draconian.
Knowing that it they are on the DEA's Drugs and Chemicals of Concern list, I'm honestly surprised that mitragynine/7-hydroxymitragyine (alkaloids found in the plant Mitragyna speciosa or Kratom) isn't listed anywhere.

Tuesday, September 22, 2015

Doing the same thing over and over and expecting different results is...

New legislation has been introduced into the United States House of Representatives entitled "Synthetic Drug Control Act of 2015". It is a long piece of legislation for one reason...

The folks who wrote this thing have included a humongous amount of additional substances to be added to Schedule I of the Controlled Substances Act.

From my count, the bill includes:

121 phenylalkylamines
117 cannabimimetics
16 arylcyclohexamines
26 tryptamines 
8 benzylpiperidines
5 benzodiazepines
13 opioids and opioid-like substances
8 piperazines
2 tropane alkaloids


316 Schedule I controlled substances listed in those drug classes.

As a comparison, if you include the recently announced scheduling of MAB-CHMINACA, there are currently 25 synthetic cannabinoids/cannabimimetics classified as Schedule I controlled substances at the Federal level. This legislation increases that number to 117 substances, which is a 368% increase in number of controlled synthetic cannabinoids.

What are we doing here?

Doing the same thing over and over again and expecting different results is insanity.

This is insanity.

And to make matters worse for the non-chemist, the initial text of the bill, contains only chemical names - there are no common names included. There are no JWH-xxx or AB-XXXXXX or Alpha-XXX listed.  I am not going to go through the list line-by-line at the moment and detail what exactly is included, but here are two examples of drugs that are to be newly scheduled if this legislation is passed and signed.

Methoxetamine is listed as its chemical name 2-(ethylamino)-2-(3-methoxyphenyl)cyclohexanone. There is no mention that this substance is commonly known as Methoxetamine.

Etizolam is listed under the Benzodiazepines designation (even though it is not a benzodiazepine; it is a thienodiazepine) as 4-(2-chlorophenyl)-2-ethyl-9-methyl-6H-thieno-[3,2-f][1,2,4]triazolo[4,3-a][1,4]diazepine. There is no mention of the name etizolam.

Oh joy. The cat and mouse games of the government continue.

Schedule hundreds of compounds thereby making them illegal to possess and use and eventually (pretty quickly I might add) hundreds more compounds with completely unknown pharmacology and toxicology will flood the market. Great plan.



To all the crime labs out there who test for Schedule I controlled substances, if this legislation passes, your life is about to become more complex because now you have to include these in your testing panels. That's job stability and security, I guess.

The PDF version of H.R.3537 can be found here.

Wednesday, September 16, 2015

Notice of Intent: MAB-CHMINACA to be placed into Schedule I

The United States DEA has filed a notice of intent to place the synthetic cannabinoid MAB-CHMINACA into Schedule I of the Controlled Substances Act. The pre-publication text of the notice can be found here. The official notice will be published on 9/16 here.

MAB-CHMINACA is also known as ADB-CHMINACA. The chemical name is
N-(1-Amino-3,3-Dimethyl-1-oxoButan-2-yl)-1-(CycloHexylMethyl)-1H-INdAzole-3-CarboxAmide. The alphabet soup naming convention is shown by red-colored bold uppercase font.

I've covered this compound previously here and here.

As you can see from the chemical structures detailed above, ADB-CHMINACA is closely related to many other synthetic cannabinoids, namely AB-CHMINACA, which was placed into Schedule I about 8 months ago. The difference between the two compounds is a tert-butyl moiety vs. an isopropyl moiety.

When this compound is officially scheduled (probably around a month from now, so around October 15th), it will be the 25th synthetic cannabinoid explicitly scheduled by the US Federal Government in approximately 4.5 years (since 3/2011).

The current list of Federally controlled synthetic cannabinoids is (in alphabetical order):
CP-47,497-C8 homologue
Well, as history has shown, a new synthetic cannabinoid will now reign supreme and we'll still continue to see hospitalizations and potential fatalities. And rest assured, it'll be a substance with unknown pharmacology and toxicology.
Next research chemical up!

My vote is for 5F-AMB.
"And the beat goes on, the beat goes on
Drums keep pounding a rhythm to the brain..."


Saturday, August 29, 2015

Unintentional exposure to AB-PINACA and more...

This case report from Thornton et al. published in the Annals of Emergency Medicine's most recent issue describes an 10 month old child's unintentional exposure to a synthetic cannabinoid substance.

Thornton, S.L., Akpunonu, P., Glauner, K., Sarah Hoehn, K., Gerona, R. (2015) Unintentional pediatric exposure to a synthetic cannabinoid (AB-PINACA) resulting in coma and intubation, Annals of Emergency Medicine, 66, 343-344.

In summary:
A 10 month old female chewed on a synthetic cannabinoid-containing cigarette and was taken to the emergency department by her mother within thirty minutes of being found. Body temperature was 97.9 F.
Pulse rate 132 beats/minute
Blood pressure was 106/69 mm Hg
Respiratory rate was 34 breaths/minute
Oxygen saturation was 97% on room air.
Normal mental status was documented.

Within 90 minutes, the child's response to verbal and physical stimuli stopped.
The child developed respiratory depression which required intubation.

The child was admitted to the hospital and later tested positive for influenza A.

The child was intubated for 36 hours but recovered fully.

Serum was collected at hospital admission and was analyzed for the presence of drugs  by liquid chromatography with quadrupole time of flight mass spectrometry (LC/qToF). Analysis was positive for the synthetic cannabinoid AB-PINACA (42 ng/mL) and its metabolite AB-PINACA  N-pentanoic acid (345 ng/mL). No other compounds were detected in the toxicological analyses.

In addition to this Annals of Emergency Medicine report, this case appeared in Clinical Toxicology (Philadelphia) journal as part of the proceedings of the annual meeting of the North American Congress on Clinical Toxicology (NACCT). Here is the citation and link:

Thornton et al. (2015) Severe symptoms from an unintentional pediatric exposure to AB-PINACA with laboratory confirmation. Clinical Toxicology, 53, 7: Abstract 184.

We covered a little bit about AB-PINACA here at TDMTP when it was originally placed into Schedule I in December 2014, but as with most new psychoactive substances, at emergence, very little is known about a substance's pharmacological or toxicological profile. But now we do know a little more about AB-PINACA.
In a 2015 paper, Wiley et al. reported that AB-PINACA had binding affinity (Ki) equal to 2.87 nM at the CB1 receptor and 0.88 nM at the CB2 receptor.  EC50 was 71 nM at CB1 and 14.9 nM at CB2 (1). AB-PINACA is considered a high efficacy CB1 and CB2 receptor agonist.
The National Forensic Laboratory Information System (NFLIS) midyear report for 2014 listed AB-PINACA as the 3rd most commonly detected synthetic cannabinoid in drug seizures in the USA. The United States Federal government officially placed AB-PINACA into Schedule I of the Controlled Substances Act in January 2015 (2).
1. Wiley, JL, Marusich, JA, Lefever TW, Antonazzo KG, Wallgren MT, Cortes RA, Patel PR, Grabenauer M, Moore KN, Thomas BF (2015) AB-CHMINACA, AB-PINACA, and FUBIMINA: Affinity and potency of novel synthetic cannabinoids in producing delta-9-tetrahydrocannabinoil like effects in mice. Journal of Pharmacology and Experimental Therapeutics. Article in Press, doi: 10.1124/jpet.115.225326
2. Drug Enforcement Administration (2015) Schedules of controlled substances: temporary placement of three synthetic cannabinoids into Schedule I. Final Order. Federal Register. Vol. 80, 5042-5047.

Tuesday, August 4, 2015


Cocaine is a song written by J.J.  Cale in 1976 but made famous when Eric Clapton covered it in 1977 and put it on his 1980 Slowhand album. I enjoy the JJ Cale version better that Clapton's. It's a little more relaxed and chill. But, my favorite cover of the song is from the Canadian glam-rock band Brighton Rock (off their Love Machine album). I'd love to see Halestorm cover this song sometime.

The song is supposedly an anti-drug song. Looking at the lyrics (below), I definitely see that. What do you think?

 J.J. Cale's version of Cocaine from 1976

Eric Clapton's version of Cocaine from 1980
Brighton Rock's version of Cocaine from 1991
If you wanna hang out you've got to take her out.
If you wanna get down, down on the ground.

She don't lie, she don't lie, she don't lie; Cocaine.

If you got bad news, you wanna kick them blues.
When your day is done and you wanna run.

She don't lie, she don't lie, she don't lie; Cocaine.

If your thing is gone and you wanna ride on.
Don't forget this fact, you can't get it back.

She don't lie, she don't lie, she don't lie; Cocaine.
She don't lie, she don't lie, she don't lie; Cocaine.

- Cocaine by J.J. Cale

Sunday, August 2, 2015

Sandra Bland's Toxicology Report: THC

Sandra Bland’s toxicology report was released several days ago. The toxicology laboratory ran a basic "drugs of abuse panel" for several drug classes. The only results reported were blood THC concentration (18±4 ng/mL) and blood THC-COOH concentration (120±27 ng/mL). On a side note, the lab used GC/MS/MS to quantify THC, which is pretty cool to me. We don't see much gas chromatography tandem mass spectrometry in forensic toxicology.

I’m not going to interpret the blood concentration and offer an opinion on the matter because I do not have any additional information about the case. I do not have the facts and do not have a true context in which to place the toxicological findings. Currently, it is difficult to establish a relationship between a person’s THC blood concentration and impairing effects and it is not recommended to try and predict said effects based on blood THC concentrations alone.

But, I read a piece published by neuropsychopharmacologist Dr. Carl Hart, on the matter the other day and I found a few things that need clarified.

In his piece (found here), a few quotes were pretty bold. And a couple that were just wrong. I discuss these below. When I asked for a citation to the general Twitterati regarding Dr. Hart’s statements, Dr. Hart provided me with a citation to a paper by Cooper and Haney titled Comparison of Subjective, Pharmacokinetic, and Physiologic Effects of Marijuana Smoked as Joints and Blunts, published in the journal Drug and Alcohol Dependence. The full text paper can be found here open access.

The paper discusses plasma THC concentrations of subjects smoking marijuana. As mentioned before I’m not entertaining a discussion on actual concentrations or an opinion on the matter, but it is crucial to note the paper discusses THC plasma concentrations. The blood samples collected by the medical examiner were femoral and subclavian blood. They were not plasma. The reported blood to plasma ratio of THC is approximately 0.55 (range is 0.5-0.6). That is to say, blood concentrations should be approximately 55% of what plasma levels will be.

   A THC plasma level at 1 ng/mL is equivalent to 0.3 ng/mL in whole blood.
   A THC plasma level at 5 ng/mL is equivalent to 2.75 ng/mL in whole blood.
   A THC plasma level at 10 ng/mL is equivalent to 5.5 ng/mL in whole blood.
   A THC plasma level at 20 ng/mL is 11 ng/mL in whole blood.

Now, this is postmortem blood. It isn't antemortem blood. But taken at face value, a THC blood concentration of 18 ng/mL would equate to 32.8 ng/mL in plasma.

“Simply put, Waller County officials exaggerated Bland’s THC amounts.”

No, they did not exaggerate the amounts. They did [eventually] release the reports. They reported the correct values that were found. 18±4 ng/mL THC. Now, the interpretation of said results are a completely separate matter.

“Furthermore, the levels are far below the 150 nanograms per milliliter limit set by the World Anti-Doping Agency to indicate marijuana-induced performance alterations.”

The comparison of a postmortem whole blood THC concentration to the World Anti-Doping Agency’s (WADA) mandated THC-carboxylic acid metabolite concentration reporting threshold (150 ng/mL) is illogical and invalid. By doing this, one is not simply comparing apples to oranges. This is comparing apples to cats.

“It is disappointing that the county officials did not require him [Officer Encinia] to provide a urine sample for drug testing…”

It may or may not be protocol to do this. I do not know. But, even if it were, a urine drug test is negligible. It will more than likely provide little-to-no information about what was going on pharmacologically (if anything) in the officer’s body at the time of the traffic stop and eventual arrest. The detection of drugs in urine is typically measured in days. As an example, methamphetamine/amphetamine is detected in urine for approximately 1-5 days after administration. Heroin is detectable in urine as 6-acetylmorphine for up to 18-24 hours and as morphine for 1-4 days after administration. If you want more information on approximate drug detection windows, you can find it here. If one wanted to get a better picture or snapshot of what exactly was going on in the officer’s body at the time of the incident, then blood, not urine, would be the matrix to analyze.

One thing that wasn’t discussed in Dr. Hart’s piece, but I did see discussed in another article (with quotes from forensic toxicologists Dr. Bruce Goldberger and Dr. Nikolas Lemos) was postmortem redistribution (PMR).PMR is a phenomenon that occurs after death when drugs stored in tissues and organs diffuse back into the blood stream. This diffusion can falsely elevate the blood level at autopsy and may not be representative of the drug concentration at the actual time of death. THC can undergo PMR. In a series of 19 deaths, heart:femoral blood concentration ratios average 1.5 (range, 0.3-3.1) for THC. (Holland et al., 2010). In this case, femoral blood was analyzed, so PMR should be minimized, but it still can occur. If resuscitation was attempted (and I do not know if it was), then this could have also played a role in movement of blood from central to peripheral sites or even release of drug from tissues into blood creating a false elevation in blood drug concentration. Did PMR occur in this case? Unless a central blood sample was also analyzed (and quantified) for THC, we’ll never know. But it is something that must be taken into consideration when interpreting the postmortem blood THC concentration.
In postmortem toxicology, the entire case must be considered before offering an opinion on a matter. In the end, Sandra Bland did not die from a THC "overdose" or did not die from "THC intoxication". The blood THC findings do not change the ruled cause of death. All of this is just food for thought and things I thought should be clarified.



Thursday, July 30, 2015

Case Report: Synthetic cannabinoids as a cause for black carbonaceous bronchoalveolar lavage

Biswas,A., Patel, V., Jantz, M., Mehta, H.J. (2015) Synthetic cannabinoids as a cause for black carbonaceous bronchoalveolar lavage. BMJ Case Reports,  doi: 10.1136/bcr-2015-211391

A direct link to the PDF paper is here.

The authors are from the Department of Pulmonary, Critical Care and Sleep Medicine at the University of Florida (Gainesville, FL) and the Department of Pulmonary and Critical Care Medicine of Saint Joseph Heart and Lung Institute (Phoenix, AZ).

I am neither a pathologist nor a medical doctor of any kind, so I won’t go into detail about the pathology other than some general documented findings the authors observed.

This case is of a 44 year old woman  who is an ex-smoker (quit 10 years ago), but currently uses cocaine and cannabis. She has HIV and has had past mycobacterial and pneumocystis infections. The woman presented to hospital with subacute fever (5 day duration). She had a cough with productive yellow sputum, which eventually developed into a dry cough. Chest x-ray was suggestive of pneumonia. According to the authors the patient’s clinical, radiographic, and histopathology “was consistent with respiratory bronchiolitis-associated interstitial lung disease (RB-ILD). Bronchoalveolar lavage fluid was colored black.

Interestingly, in the "Learning Points" section, the authors state:

Pulmonary complications may result from impurities inhaled during the process of cocaine smoking. We propose that synthetic cannabinoids can do the same by a similar mechanism.

Other than the title of the paper, this is the only time “synthetic cannabinoids” are mentioned.

What am I missing here? How are synthetic cannabinoids involved in this case report? I’m confused.  The title of this case report is "Synthetic cannabinoids as a cause...". That leads one to believe that synthetic cannabinoids or use of associated products were involved in some fashion, but I’m not sure where they actually fit it other than a possible undiscussed hypothesis from the authors. Synthetic cannabinoids aren't even mentioned at at all in the patient's history, so why throw that hypothesis out there?!?

Thursday, July 9, 2015

Hyperthermia and rhabdomyolysis caused by a synthetic cannabinoid? Maybe. Maybe not.

B. Sweeney, S. Talebi, D. Toro, K. Gonzalez, J.P. Menoscal, R. Shaw, G.W. Hassen (2015) Hyperthermia and severe rhabdomyolysis from synthetic cannabinoids. American Journal of Emergency Medicine. Article in Press. doi: 10.1.16/j.ajem.2015.05.052
This case is reported about of the Department of Emergency Medicine at the New York Metropolitan Hospital Center in New York City, New York. The case consists of a 27 year old man who was brought to the hospital for agitation and disruptive behavior. He was found by law enforcement “eating the grass of a local soccer field”. Witnesses reported that he was smoking “K2”. The man had a history of schizophrenia and medication noncompliance.
While in the hospital, he was combative and aggressive, so medical staff sedated him with midazolam (Versed) and haloperidol (Haldol). He was hyperthermic (106.1°F) and tachycardic (173 beats per minute). Treatment to decrease his core temperature was undertaken by using ice packs and evaporative cooling. After an hour, his temperature was 101.7°F.
Initial hospital admission testing revealed creatine (2.2 mg/dL), lactate (4.1 mmol/L), and creatinine phosphokinase (1341 IU/L). The hospital lab performed a urine drug screen; the urine was positive for benzodiazepines.
Once he became alert , the man admitted to smoking “Mr. Big Shot”. He was admitted to the hospital for monitoring, hydration, and a psych consult.
While being monitored, creatinine phosphokinase levels continued to increase (5867 > 14950 > 29580 IU/L). Liver enzymes also saw this marked increase. The man was transferred to ICU for management of rhabdomyolysis. Peak creatinine phosphokinase was 57050 IU/L. After two days in ICU, creatinine phosphokinase and liver enzymes decreased. The man was transferred out of ICU on the fourth day of admission where he still exhibited episodes of psychosis and agitation. Haloperidol and olanzapine (Zyprexa) were used. On the tenth day of admission, the man was transferred to psych for management of schizophrenia.
A nice case report on the surface. But missing one major aspect. Analytical confirmation of drug.
The patient admitted use of a “K2” product. But what substance or substances were in that product? Was it a synthetic cannabinoid? Was it a cathinone or other type of stimulant? Who knows. I don’t and the authors don't either. The patient didn't know. No one knows. It has been documented that herbal incense and potpourri products can contain substances other than synthetic cannabinoids. I’m sure there was some blood drawn during the hospital admission process. Why wasn't a synthetic cannabinoid test attempted?
The authors state that a urine drug screen was completed. At least that's something, but it's a test that has very little value (if any) because of the overall windows of detection for drugs and drug metabolites in urine (hours to days to possibly weeks). In acute overdosages, it is quite possible to have a sky high level of drug in blood, but very little drug excreted into the urine. Blood/serum/plasma should be the matrix of choice when doing toxicological analyses.
To report that a specific symptom or effect is associated with or related to “synthetic cannabinoid” use, one must ascertain if a synthetic cannabinoid was actually consumed.  A witness report or patient statement is circumstantial evidence, but not proof of synthetic cannabinoid presence or identification. The title of the case report is "Hyperthermia and severe rhabdomyolysis from synthetic cannabinoids", but the authors have not shown synthetic cannabinoids to be involved. It could have easily been a smoking blend contaminated with a random substituted cathinone du jour or methamphetamine.
This is my main concern with case reports such as this one. Not all laboratories are set up to monitor for these substances. That’s a given - and  it's the reason why reference laboratories exist. But to not attempt this confirmation AND to take the time  and effort to publish the case as hyperthermia induced by a very specific cause – synthetic cannabinoids – is negligent at worst and sloppy at best. To publish this case report without analytical confirmation is shoddy science. I would never publish a case report as a fatality associated with substance Y without at least detecting the substance in blood, tissue, etc. Why is this any different for clinical toxicology or medicine?
I leave you with a question to ask yourselves…
Why are manuscript reviewers and journal editors and peers in the field not questioning this lack of analytical confirmation? Why are we as toxicologists and chemists (and generally as scientists) not questioning this type of work?

We should be questioning it.

Monday, June 15, 2015

Alcohol and the Alleged Profession?

As much as I rail against the media (or the alleged profession?) for their reporting on new psychoactive substances as well as the more established drugs out there, I have to say that I absolutely love this article that appeared on Vox today, titled Imagine if the media covered alcohol like other drugs. It is written by German Lopez (@germanrlopez). I'm not sure it can be considered satire, because it is 100% true.

A fabulous beginning quote from the article:

"The widespread use of a substance called "alcohol" - also known as "booze" - has been linked to erratic and even dangerous behavior, ranging from college students running naked down public streets to brutal attacks and robberies."

Now go read it in its entirety.

H/T @infectiouschris

Increase in Reported Adverse Effects Related to Synthetic Cannabinoid Use - USA

On June 12, 2015, the CDC released some information via the Morbidity and Mortality Weekly Report (Notes from the Field: Increase in Reported Adverse Health Effects Related to Synthetic Cannabinoid Use – US , January – May 2015) on the recent increase in synthetic cannabinoid-related hospitalizations, illnesses, and deaths that has occurred during the first five months of 2015.

Digital image of Kickass herbal incense taken by ForensicToxGuy (2014)

If you’re a normal reader of this blog, then you’ll know exactly of which I am talking.

Here's my last take on this noted increase in hospitalizations:

Some information from the CDC release in MMWR:
  • For the time range, there were 3,572 synthetic cannabinoid-related phone calls made to poison centers in the US. This is a 229% increase from the same period of time for 2014. Almost 81% of phone calls were regarding males. Median age was 26 years, with a range of 7 months – 72 years.
  • The most common adverse effects included agitation (35% of cases), tachycardia (29% of cases), and drowsiness/tiredness (26.3% of cases).
  • In 11.3% of the 2,961 phone calls for which a medical outcome was reported, 11.3% of cases (335 total) had a major adverse effects, which essentially means that there were life threatening signs or symptoms or a result of residual disability or disfigurement).
  • Fifteen deaths were reported. Fourteen of the fifteen deaths (93.3%) were single substance acute intoxications. One death involved poly-substance use.
  • 92.7% of reported use was intentional exposure.
  • Most common other substances used in combination with synthetic cannabinoids were ethanol (23% of cases), marijuana (16.5% of cases), and benzodiazepines (11.0%).
Note: The report did not include any discussion of case history surrounding the exposures resulting in adverse effects, toxicology results from any of the reported cases or even information that the drug of interest was analytically confirmed in a biological matrix, and microscopic and macroscopic findings at autopsy. All of this is important information that makes a complete case report.

If you’ve followed this blog for any length of time, you should not be surprised at any of these findings.  I’ll end by repeating what I did in the blog post cited above…

Synthetic cannabinoids have been and will continue to be a major issue in the US. They are public health nightmares. These recent hospitalizations (and the now noted increase in poison center calls) are not surprising to me and should not be surprising to anyone that follows this subject. These adverse effects are the norm. The vast majority of people using these substances and products are consuming substances of unknown identity with unknown pharmacological and toxicological profiles in unknown combinations at unknown dosages. This reckless and dangerous behavior will result in serious adverse health effects.

Monday, June 8, 2015


Black Sabbath's Snowblind. Tremendous song.

And it's all about our friend - cocaine.

It has been said that during the recording of Sabbath's Vol. 4, the substances abuse issues were prevalent. Speakers full of cocaine were being delivered to the studio; massive amounts of drugs were being consumed daily while recording the music. Snowblind was intended to be the real title for what would eventually become Vol. 4, but the music execs mandated a change.

Also, I've never seen this personally, but in the liner notes of the album, Sabbath thanks "the great Coke-cola".

Here's a great performance from 1975. Hope you enjoy the music as much as I do.



Friday, May 29, 2015

Thought for the Day

I've always thought the following would make good toxicology themed names for a rock/metal/punk band:

Gastric Lavage

Postmortem Redistribution

The Iliacs


The LD50s

Serotonin Syndrome

Happy Friday all!



Wednesday, May 27, 2015


Gordon Lightfoot's "Sundown" was released in 1974 and is one of my favorite songs. 

It was theorized that he wrote the song about former girlfriend/mistress Cathy Smith. Lightfoot has gone on to expand on this in interviews and has actually corroborated that he wrote the song and its lyrics with her on his mind.

Also, if you're a music fan and a drug history fan, you are probably thinking that the name Cathy Smith is familiar to you. It should be. Cathy Smith was a rock music groupie and drug dealer back in the 1970s. She dealt drugs to Keith Richards and Ron Wood of the Rolling Stones when they toured as The New Barbarians. Later on, she was the person who injected John Belushi with the fatal speedballs of cocaine and heroin (supposedly 11 total) in 1982. She served 15 months in US prison for that episode and was deported back to Canada after her release.
Image of John Belushi in Animal House is from

Anyway, Sundown is a song with haunting lyrics, if you put them in perspective of the tumultuous time and relationship between Lightfoot and Smith.



Tuesday, May 26, 2015

Another day, another flakka story

A new article centered on flakka was published on today. And some of it just makes me shake my head. Blatant misinformation as usual in a few aspects.
But like “bath salts”, a group of related synthetic drug that were banned in 2012…
No. “Bath salts” weren’t banned in 2012. Three components commonly found in “bath salts” products were banned by 2012. These were MDPV, Mephedrone, and Methylone. More "bath salts" compounds, including alpha-PVP, were banned in 2014.

A small overdose of the drug, which can be smoked, injected, snorted or injected, can lead to a range of extreme symptoms: “excited delirium,” as experts call it, marked by violent behavior; spikes in body temperature (105 degrees and higher, Hall said); paranoia.

Stimulant psychosis. Not excited delirium.

Probably what has brought flakka the most attention is that it gives users what feels like the strength and fury of the Incredible Hulk.

Strength and fury? Nice, but, no, you won't be meeting this guy after taking a dose of flakka (alpha-PVP).
Image from
But it [flakka] does have one advantage over its predecessor: it has not been banned – yet.

Yes, it has. Alpha-PVP has been considered a Schedule I controlled substance since March 7, 2014. It is banned in the USA.
It will probably take several years to get the data necessary to put a federal ban on flakka, he added.

No. It is currently considered a federal Schedule I controlled substance and it isn't coming off that list in any way, shape, or form.

Journalists, there are people out there that could help you, if you'd ask. Please do ask.