Drug overdose is now the leading cause of unintentional death nationwide, driven by increased prescription opioid overdoses. To better understand urban opioid overdose deaths, this paper examines geographic, demographic, and clinical differences between heroin-related decedents and prescription opioid decedents in San Francisco from 2010 to 2012. During this time period, 331 individuals died from accidental overdose caused by opioids (310 involving prescription opioids and 31 involving heroin). Deaths most commonly involved methadone (45.9 %), morphine (26.9 %), and oxycodone (21.8 %). Most deaths also involved other substances (74.9 %), most commonly cocaine (35.3 %), benzodiazepines (27.5 %), antidepressants (22.7 %), and alcohol (19.6 %). Deaths were concentrated in a small, high-poverty, central area of San Francisco and disproportionately affected African-American individuals. Decedents in high-poverty areas were significantly more likely to die from methadone and cocaine, whereas individuals from more affluent areas were more likely die from oxycodone and benzodiazepines. Heroin decedents were more likely to be within a younger age demographic, die in public spaces, and have illicit substances rather than other prescription opioids. Overall, heroin overdose death, previously common in San Francisco, is now rare. Prescription opioid overdose has emerged as a significant concern, particularly among individuals in high-poverty areas. Deaths in poor and affluent regions involve different causative opioids and co-occurring substances.

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Cannabinoids are often excluded from postmortem toxicology screens due to their ubiquitous nature, interpretative difficulties and unanswered questions regarding their postmortem redistribution. In this study, we review 30 postmortem cases where a drug screen gave a positive cannabinoids result and a confirmation identified Δ⁹-tetrahydrocannabinol (THC), 11-hydroxy-Δ⁹-tetrahydrocannabinol (11-OH-THC), and/or 11-nor-9-carboxy-Δ⁹-tetrahydrocannabinol (THC-COOH) in peripheral (BL-P) or cardiac/central blood (BL-C) and/or urine (UR). Had cannabinoids not been included in these toxicologic evaluations, incomplete or erroneous inferences would have been drawn in a substantial number of cases regarding cause/manner of death. THC was detected in 28 BL-C and in all 30 BL-P. THC and THC-COOH were confirmed present in 2 and 23 UR, respectively. 11-OH-THC was detected in 4 BL-C, 6 BL-P, and 0 UR. The mean THC concentrations in BL-C and BL-P were 8.0 and 15.8 ng/mL, respectively. The mean THC-COOH concentrations in BL-C and BL-P were 55.2 and 60.6 ng/mL, respectively. The mean 11-OH-THC concentrations in BL-C and BL-P were 17.0 and 12.5 ng/mL, respectively. Postmortem interval (PMI) for each case was determined and evaluated in relation to BL-C/BL-P concentration ratios with THC-COOH exhibiting a possible trend. This study is the first of its kind and demonstrates the usefulness of cannabinoid analyses as part of death investigations. Furthermore, it provides distribution data that will improve the ability of toxicologists and pathologists to evaluate cannabinoid concentrations in human postmortem specimens.

The case of a 22-year-old male Caucasian driver is presented. He was involved in a traffic collision. At the roadside, he displayed blank stare and mellow speech with a barely audible voice. A DRE found low body temperature, rigid muscle tone, normal pulse, lack of horizontal and vertical gaze nystagmus, nonconvergence of the eyes, dilated pupil size, and normal Pupillary reaction to light. A standard toxicology DUID protocol was performed on the driver's whole blood including ELISA and GC-MS drug screens with negative results. Additional drug screening was undertaken for bath salts and synthetic cannabinoid receptor agonists by LC-MS/MS by a commercial laboratory and identified the synthetic cannabinoid receptor agonist XLR-11 in the driver's blood. XLR-11 was subsequently quantified at 1.34 ng/mL. This is the first documented case involving a driver operating a motor vehicle under the influence of the synthetic cannabinoid receptor agonist XLR-11.