The cartridge used in this study is a newer THC cartridge that contains a ceramic heating element, a nichrome filament wire, a fibrous wick/insulation wrap through which oil was delivered to the heating element, and a stainless steel air flow tube and heating element housing that the oil remained in direct contact with. The emission of metals during the vaping process has been documented in several prior studies, but the interaction between VEA and the metal components of the vape device are still being investigated. Saliba et al. recently found that interaction between a metal heating element and PG greatly decreased the temperature required to observe PG thermal decomposition. Certain metals such as stainless steel, which is present in the cartridge used in this study, resulted in a nearly 300˚C reduction in required temperature compared to pure pyrolysis, highlighting a clear interaction between the PG decomposition and the device itself. Furthermore, a study by Jaegers et al. found that pyrolysis alone in an anaerobic environment was not able to induce thermal degradation of PG and VG at low temperatures , despite previous studies observing degradation at temperatures as low as 149˚C during vaping. However, when heated in an aerobic environment, thermal decomposition was observed at 133 and 175˚C, both without and with the addition of metal oxides Cr2O3 and ZrO2, suggesting that oxidation is a key process during vaping. In combination with the results shown here, evidence highly suggests that pure pyrolysis alone may not be the only pathway for VEA degradation. During the vaping process,cannabis grow equipment not only may VEA come into direct contact with metals that are present in the filament wire or stainless-steel body, but VEA must also come into contact with molecular oxygen in ambient air.
These interactions may promote VEA degradation at temperatures lower than predicted under pure pyrolysis conditions. Ultimately, it is then possible that compounds such as DQ or ketene may be able to form at lower temperatures than what is theoretically calculated if these interactions are considered.However, further study is required to fully understand the effects of the e-cigarette device and vaping environment on the degradation of e-liquids.There are several limitations to the study presented here that should be noted. First, this study presents a range of decomposition products that were identified using a -40˚C cold trap and GC/MS analysis. Approximately 40% of the mass of VEA consumed by the vape pen could be attributed to the compounds identified here. However, compounds with high vapor pressure, such as ketene, that have been previously reported from VEA pyrolysis may not have been efficiently captured using the cold trap method described in this study. This method is expected to better traps particle-phase compounds that are able to condense at -40˚C and are stable enough to transfer from the cold trap to collection vials at room temperature and is unable to capture highly volatile or reactive VEA vaping emission products. For example, ketene, which is expected to form during VEA pyrolysis, has an estimated boiling point of -56˚C and, as a result, was not expected to be observed in our collection. Furthermore, highly volatile and/or reactive compounds such as ketene and various low molecular weight carbonyl-containing species, etc., often require additional derivatization methods that were not used in this study to be observed using GC/MS. This study was also only able to identify compounds with mass spectra that could be found in the NIST mass spectral library. While PubChem currently reports over 111 million unique chemical structures, the NIST library used in this study contains MS fragmentation patterns for only 242,466 compounds. As such, a large portion of the TIC for each collection could not be matched to a known compound . Furthermore, several peaks were observed that were believed to be co-elution of two or more products, which prevented clear analysis of the fragmentation patterns. Several identified products, such as VEA, may also have multiple isomeric forms that have only slight differences in their retention times and mass spectra that the NIST library matching program is unable to account for.
In the case of VEA, all peaks were assumed to be and quantified as the same α form, but it is possible for VEA to exist in α, β, γ, or δ forms.Among school-aged children, ADHD is one of the most common psychiatric disorders. Estimates have placed the prevalence of ADHD as high as 3-7% of all children in the United States, with as many as 37- 85% of these cases persisting into adulthood1 . Pharmacotherapeutic treatment of ADHD typically begins when a patient is 9.8 to 10.6 years old, with a duration of 33.8 to 42 months. Treatment is most commonly prescribed to individuals that are 10-14 years old and is usually made available to the individual or to the parents of the individual until graduation from high school or college. The most-prescribed stimulant for ADHD is methylphenidate ; however, amphetamines account for about one-third of all ADHD treatment prescriptions. Biologically, methylphenidate interacts with the dopamine transporter to block dopamine reuptake, thus increasing dopamine in the synaptic cleft. Amphetamines also interact with the dopamine transporter but via an efflux mechanism, reversing the direction that the transporter conducts dopamine. Both methyphenidate and amphetamine increase the amount of dopamine in the synaptic cleft of the mesocorticolimbic system, resulting in an increased level of attentiveness that is beneficial to those with ADD or ADHD. In terms of treatment of ADHD, stimulant treatment such as methyphenidate and methamphetamine is considered to be the first line of defense in ADHD therapy. This type of treatment is frequently attempted before other methods of intervention, such as counseling or non-stimulant medication, and in the short term, stimulant treatment of ADHD has proven effective, with 73% of cases reporting treatment to be “favorable and effective” and only 22% reporting minor side effects. In combination, prescription of amphetamines has increased greatly during the past 20 years, especially among young children and those over 14.Prescription of amphetamines to two-to-four year olds increased 380% between 1990 and 1997, while prescription to those older than 14 increased 817%3 . Given the young age of treatment onset and the duration for which the drug is made available to ADHD patients, along with the prevalence of its clinical use, some critics have raised concern in scientific literature over excessive stimulant use and the long-term effects of stimulants on children.
Such concern is bolstered by the strong correlation between ADHD and Substance Use Disorder , the repeated abuse or dependence on a substance that alters the central nervous system for the purpose of obtaining its mind-altering effects or avoiding a withdrawal. For instance, adolescent tobacco use has been shown to be significantly higher amongst those with ADHD9 . Alcohol abuse is associated with as many as 17% to 45% of ADHD adults, while drug abuse is seen in 9 to 30%, suggesting that ADHD patients are ata significantly higher risk than the general population. Specifically, adolescents with ADHD have been calculated to be more than three times as likely to use marijuana when compared to the general population,mobile grow system and a striking 39.1% of ADHD patients older than 13 responded in a survey that they had abused nonprescription stimulants—mostly cocaine and methamphetamine9-11. Moreover, amphetamines are reinforcing. Following use of an amphetamine, an individual will be more likely to use the drug again if given the opportunity. This property can lead to abuse and drug-seeking behavior. It follows that amphetamine treatment may contribute to general drug-seeking behavior and substance abuse in ADHD individuals and may especially raise the risk of non-medical stimulant abuse. However, other studies have also implied that stimulant treatment, including treatment with amphetamines, may lower the likelihood of an individual with ADHD to “self-medicate,” thus lowering the potential for drug abuse in adolescence and adulthood. Based on these few population-level studies and meta-analyses, a portion of the medical community has come to the conclusion that treatment of ADD or ADHD with amphetamine is beneficial for the majority of patients. However, these studies have a number of weaknesses that will be addressed in this review.Animal studies have shown that amphetamine treatment of ADHD may increase susceptibility to substance abuse, demonstrating the abuse potential that amphetamines pose. For instance, several animal studies have demonstrated that amphetamine exposure induces drug cravings in rats. One such study illustrated that rats treated with amphetamine tended to have higher levels of self-administration of cocaine, suggesting that prescription of amphetamines may raise susceptibility to non-prescription stimulant drug abuse in human patients. A similar study concluded that self-administration of amphetamine led to sensitization of its rewarding effect, as well as to the rewarding effects of both cocaine and morphine. Since sensitization of reward may play a major role in the development of drug-craving and dependence, amphetamines, therefore, seem likely to increase a patient’s sensitization to his or her own prescription. This may then lead patients to illicit nonprescription drugs to fill the void of reward that their treatment once occupied. Thus, a patient’s prescription would increase the likelihood of abuse of both amphetamines and almost any other drug with reinforcing properties. In particular, drugs with similar stimulant properties that activate the mesocorticolimbic dopaminergic system, such as nicotine, cocaine, and methamphetamine, are strong candidates for abuse following amphetamine treatment. Moreover, abuse of non-medical stimulants may stem directly from dependence on ADHD medication. Studies of ADHD patients found that 15%-25% reported having abused their medication recently, via crushing and snorting the pills or taking a higher-than-prescription dose for recreational purposes. One group discovered that the most important factor in the development of abuse of prescription amphetamines was the abuse of other substances, implying that substance abuse may lead to abuse of medication.
However, the data in this study can be interpreted to imply reverse causation; given the sensitizing and reinforcing nature of amphetamines, patients may become dependent on their medication and turn to other substances after their medication no longer gives them satisfaction. Furthermore, the abuse of ADHD treatment seems to be much higher for amphetamines when compared to methylphenidate. Researchers have found that the most-abused medications used to treat ADHD were mixed amphetamine salts, constituting 40% of all abused ADHD medication, while long-acting amphetamines constituted an additional 12% of abused medication. Therefore, amphetamine abuse alone constituted 52% of prescription medication abuse11. Since only one-third of stimulant medication prescribed for ADHD treatment is amphetamine-based, it is apparent that amphetamines have a higher potential for abuse than other ADHD treatments. Thus, the animal and population studies detailed above both found an increase in stimulant abuse amongst ADHD patients treated with stimulants. Lastly, population studies also found that increased drug abuse following amphetamine prescription was specific to stimulant abuse. In a study that followed 21 untreated and 98 treated ADHD patients into adulthood, a significant increase in cocaine use was found amongst those treated with stimulants. Other studies found that both nicotine and cocaine use were increased amongst ADHD patients that were treated with stimulants. However, it was also found that depressants such as marijuana and alcohol showed no increase in abuse potential, supporting the hypothesis that amphetamine and/or stimulant prescription specifically raises the risk of non-medical stimulant abuse via sensitization.It has been hypothesized that stimulant treatment is increasingly protective against drug abuse in adult life the earlier the medication is prescribed in childhood. This hypothesis ties into a study that assessed “quality of life” based on measures of alcoholism, substance abuse, criminality and a questionnaire in adults with ADHD who had previously been treated with stimulants versus those that had not. This study found that ADHD patients treated as children had a higher quality of life than those treated in adolescence by the researcher’s measured index. This hypothesis – that onset of treatment at a younger age correlates with effectiveness of treatment – may indicate a link between age of prescription and likeliness to experience SUD. A younger child is much less likely to have access to any form of street drug, especially stimulants such as cocaine or methamphetamine. If prescribed at a younger age, amphetamine sensitization would occur during a time in the child’s life in which they would have no outlet through which to act on drug cravings. Since the average duration of treatment lasts between 33.8 to 42 months, the medication would likely stop before the child reaches adolescence. Withdrawal, a series of negative symptoms that occur in the absence of a drug after a prolonged period of abuse, would therefore occur when the individual would most likely have limited access to illegal stimulants.