Inhalation Of Crack Cocaine Research Articles

Individuals Reporting Past 3-month Smoked Stimulant Use Are Placed at Risk for Infection and Injury Amid COVID-19.

Smoking stimulants, such as methamphetamine and "crack" cocaine, can spread infections, including hepatitis C and COVID-19, and lead to injuries, particularly when individuals share or use makeshift pipes. The purpose of the study was to assess the practices of people who inhale ("smoke") stimulants to guide future clinical harm reduction efforts. Anonymous surveys were administered to participants reporting inhalation of crack cocaine and/or methamphetamine in the past 3 months. Participants were eligible if they sought services from an outreach team staffed by a municipal syringe service program (SSP) or if they were patients at a low-threshold substance use disorder treatment program, the Massachusetts General Hospital Bridge Clinic. The survey was administered to 68 total participants, 30% of whom were recruited in the Massachusetts General Hospital Bridge Clinic and 70% through SSP outreach. Unsafe smoking practices were reported by 93% of participants. Among the 46% of participants surveyed who both smoked and injected stimulants, 61% of those participants stated that they injected instead of smoked stimulants because of lack of access to pipes. Amid COVID-19, 35% of participants adopted safer smoking practices. Most participants reported that they would be more likely to attend an SSP or health center if pipes were provided. Inhalational practices that place participants at risk of injury and illness are common. Providing safer smoking equipment may promote health and engage individuals in care.

Impairment of spatial working memory and oxidative stress induced by repeated crack cocaine inhalation in rats

Crack cocaine is a highly toxic drug with great potential to induce addiction. It produces more intense effects than cocaine powder, with its use having grown worldwide. However, few studies have focused on the cognitive and biochemical consequences that result from crack cocaine inhalation. This study examined the effects of direct crack cocaine inhalation on spatial working memory and brain oxidative stress parameters in rats. Male adult Wistar rats, well-trained in an eight-arm radial maze (8-RM), underwent five sessions of crack cocaine inhalation (crack cocaine group) once a day or inhalation simulation (sham group), being tested in 1-h delayed tasks 24 h after the last inhalation. An additional inhalation session was carried out the following day, with the prefrontal cortex, hippocampus and striatum being removed five minutes afterwards in order to assess oxidative damage such as lipid peroxidation, thiobarbituric acid-reactive species (TBARS) levels, and advanced oxidation protein products (AOPP), as well as the activity of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx). Animals from the crack cocaine group showed more errors (p < 0.01) in the 1-h post-delay performance in the 8-RM when compared to the sham group. The crack cocaine group showed decreased (p < 0.05) lipid peroxidation in the hippocampus and increased (p < 0.001) levels of AOPP and SOD activity (p < 0.05) in the striatum when compared to the sham group. Therefore, the repeated inhalation of crack cocaine impaired long-term spatial working memory and elicited oxidative stress in the hippocampus and striatum of rats.

Crack cocaine inhalation induces schizophrenia-like symptoms and molecular alterations in mice prefrontal cortex

Crack cocaine (crack) addiction represents a major social and health burden, especially seeing as users are more prone to engage in criminal and violent acts. Crack users show a higher prevalence of psychiatric comorbidities – particularly antisocial personality disorders – when compared to powder cocaine users. They also develop cognitive deficits related mainly to executive functions, including working memory. It is noteworthy that stimulant drugs can induce psychotic states, which appear to mimic some symptoms of schizophrenia among users. Social withdraw and executive function deficits are, respectively, negative and cognitive symptoms of schizophrenia mediated by reduced dopamine (DA) tone in the prefrontal cortex (PFC) of patients. That could be explained by an increased expression of D2R short isoform (D2S) in the PFC of such patients and/or by hypofunctioning NMDA receptors in this region. Reduced DA tone has already been described in the PFC of mice exposed to crack smoke. Therefore, it is possible that behavioral alterations presented by crack users result from molecular and biochemical neuronal alterations akin to schizophrenia. Accordingly, we found that upon crack inhalation mice have shown decreased social interaction and working memory deficits analogous to schizophrenia's symptoms, along with increased D2S/D2L expression ratio and decreased expression of NR1, NR2A and NR2B NMDA receptor subunits in the PFC. Herein we propose two possible mechanisms to explain the reduced DA tone in the PFC elicited by crack consumption in mice, bringing also the first direct evidence that crack use may result in schizophrenia-like neurochemical, molecular and behavioral alterations.

Behavioural, biochemical and molecular changes induced by chronic crack-cocaine inhalation in mice: The role of dopaminergic and endocannabinoid systems in the prefrontal cortex

Crack-cocaine addiction has increasingly become a public health problem worldwide, especially in developing countries. However, no studies have focused on neurobiological mechanisms underlying the severe addiction produced by this drug, which seems to differ from powder cocaine in many aspects. This study investigated behavioural, biochemical and molecular changes in mice inhaling crack-cocaine, focusing on dopaminergic and endocannabinoid systems in the prefrontal cortex. Mice were submitted to two inhalation sessions of crack-cocaine a day (crack-cocaine group) during 11 days, meanwhile the control group had no access to the drug. We found that the crack-cocaine group exhibited hyperlocomotion and a peculiar jumping behaviour (“escape jumping”). Blood collected right after the last inhalation session revealed that the anhydroecgonine methyl ester (AEME), a specific metabolite of cocaine pyrolysis, was much more concentrated than cocaine itself in the crack-cocaine group. Most genes related to the endocannabinoid system, CB1 receptor and cannabinoid degradation enzymes were downregulated after 11-day crack-cocaine exposition. These changes may have decreased dopamine and its metabolites levels, which in turn may be related with the extreme upregulation of dopamine receptors and tyrosine hydroxylase observed in the prefrontal cortex of these animals. Our data suggest that after 11 days of crack-cocaine exposure, neuroadaptive changes towards downregulation of reinforcing mechanisms may have taken place as a result of neurochemical changes observed on dopaminergic and endocannabinoid systems. Successive changes like these have never been described in cocaine hydrochloride models before, probably because AEME is only produced by cocaine pyrolysis and this metabolite may underlie the more aggressive pattern of addiction induced by crack-cocaine.

Repeated inhalation of crack-cocaine affects spermatogenesis in young and adult mice

To investigate the effects of repeated crack-cocaine inhalation on spermatogenesis of pubertal and mature Balb/c mice, ten young (Yex) and ten adult (Aex) Balb/c mice were exposed to the smoke from 5 g of crack with 57.7% of pure cocaine in an inhalation chamber, 5 days/week for 2 months. The young (Yc) and adult (Ac) control animals (n = 10) were kept in a specially built and controlled animal house facility. The morphologic analysis of both testes of all animals included the analysis of quantitative and qualitative histologic parameters to assess the effect of crack-cocaine on spermatogenesis and Leydig cells. Apoptosis was determined by immunolabeling with caspase-3 antibodies. Compared to the Yc animals, Yex animals showed a significant reduction in the number of stage VII tubules per testis (p = 0.02), Sertoli cells (p < 0.001) and elongated spermatids (p = 0.001). Comparisons between the Yex and Aex groups identified a significant reduction in the number of Sertoli cells (p < 0.001) and round spermatids (p < 0.001) in the Yex group and a significant increase in apoptotic Leydig cells (p = 0.04) in the Aex group. The experimental results indicate that crack-cocaine smoke inhalation induced spermatogenesis disruption in chronically exposed mice, particularly in pubertal mice.

Effects of Chronic Exposure to Crack Cocaine on the Respiratory Tract of Mice

Smoked cocaine (crack cocaine) causes several forms of injury to the respiratory tract, including asthma exacerbations, lung edema and hemorrhage, and nasal mucosal alterations. Few studies, however, have assessed respiratory tract pathology in habitual users of crack cocaine. Here, we describe the histological alterations in the respiratory tract of mice caused by chronic inhalation of crack cocaine. Twenty 2-month-old BALB/c mice were exposed to the smoke of 5 g crack cocaine in an inhalation chamber once a day for two months and compared to controls (n = 10). We then morphometrically analyzed nose and bronchiolar epithelial alterations, bronchiolar and alveolar macrophage cell density, alveolar hemosiderin content, and in addition determined the vasoconstriction index and the wall thickness of pulmonary arteries. The serum cocaine level was 212.5 ng/mL after a single inhalation. The mucus content of the nasal epithelium increased in crack-exposed animals, and the nasal and bronchial epithelium thickness decreased significantly. The alveolar hemosiderin content and the alveolar and bronchiolar macrophage cell density increased in animals exposed to crack. The vasoconstriction index increased in the pulmonary arteries of the exposed group. Chronic crack cocaine inhalation causes extensive histological changes along the entire respiratory tract.

Noninjection drug use: an under‐appreciated risk factor for hepatitis C virus transmission

Noninjection drug use: an under‐appreciated risk factor for hepatitis C virus transmission

Pulmonary Complications from Cocaine and Cocaine-based Substances: Imaging Manifestations

Cocaine is the illicit drug whose abuse most often results in cardiopulmonary symptoms and emergency treatment. Habitual smoking of alkaloidal cocaine ("freebase," "crack") has replaced nasal insufflation as the most common method of abuse. Smoking of cocaine exposes the lung directly to the volatilized drug as well as to the other combustion products of the smoked mixture, thereby increasing the risk of adverse pulmonary effects. A wide variety of pulmonary complications including interstitial pneumonitis, fibrosis, pulmonary hypertension, alveolar hemorrhage, asthma exacerbation, barotrauma, thermal airway injury, hilar lymphadenopathies, and bullous emphysema may be associated with the inhalation of crack cocaine or of associated substances such as talc, silica, and lactose. Cocaine abuse represents one of the most serious medical and social problems of our time. Radiologists should be familiar with the various pleuropulmonary complications associated with the abuse of illicit drugs in general and of cocaine in particular to ensure correct diagnosis and appropriate treatment planning in patients with respiratory manifestations associated with such abuse.

Inhalation of crack cocaine can mimic pulmonary embolism.

Inhaled cocaine has been associated with a number of pulmonary manifestations including pulmonary edema, hypersensitivity pneumonitis, bronchospasm, obliterative bronchiolitis, alveolar hemorrhage, and pneumomediastinum. However, the effects of cocaine on pulmonary vasculature have been poorly described. The authors report a patient with a history of cocaine inhalation presenting with high clinical suspicion for pulmonary embolism and a high probability ventilation-perfusion lung scan. A pulmonary angiogram revealed no pulmonary embolism. The authors believe this syndrome was caused by intense pulmonary artery vasospasm secondary to cocaine inhalation. A pulmonary angiogram may be required to establish the correct diagnosis and avoid unnecessary anticoagulation in such patients.

Adult Supraglottitis Subsequent to Smoking Crack Cocaine

Supraglottitis is one possible complication of smoking crack cocaine. From 1992 through 2001, our institution treated nine patients for thermal supraglottitis secondary to crack cocaine inhalation. In this article, we describe two of these cases, and we briefly review what is known about this entity and the mechanism of injury. We also provide our recommendations for management.

Cocaine-induced acute renal failure, hemolysis, and thrombocytopenia mimicking thrombotic thrombocytopenic purpura

Acute renal failure (ARF) can occur as a complication of cocaine abuse. We present a case of microangiopathic hemolytic anemia, ARF, and thrombocytopenia after inhalation of crack cocaine in a 38-year-old woman. Her renal failure ultimately required dialysis. She underwent renal biopsy because of persistent renal failure, hematuria, and thrombocytopenia. The biopsy findings consisted of thrombotic microangiopathy and glomerular ischemia. After treatment with fresh frozen plasma, her platelet count and bleeding resolved. The possible mechanisms involved in cocaine-induced thrombotic microangiopathy include: (1) endothelial injury, (2) vasoconstriction and/or impairment of vasodilatation, (3) procoagulant activity, and (4) antiplatelet activity. Although our patient survived after hemodialysis and transfusion of fresh frozen plasma, she continued to have residual renal insufficiency. One month later, the patient again used cocaine and presented with worsening ARF, anemia, and thrombocytopenia.

Bronchoscopy in Crack Lung

We describe the bronchoalveolar lavage appearance in a patient presenting with chest pain, cough, shortness of breath, and diffuse interstitial infiltrates after the inhalation of crack cocaine. There was a gradual darkening of the aspirated fluid reflecting increased recovery of carbonaceous material introduced into the lung during deep inhalation of ignited crack. This emphasizes the importance of early bronchoscopy as a diagnostic tool for this entity and for the recognition of potential complications of thermal injury, a component of crack lung syndrome.

Thoracic aortic dissection secondary to crack cocaine ingestion

Thoracic aortic dissection is a rare but recognized complication of crack cocaine inhalation. It is thought to be triggered in some cases by transient severe elevations in blood pressure, causing a shear effect on the thoracic aorta. Unrecognized, it can result in high morbidity and mortality. A case of an unusual presentation of thoracic aortic dissection following crack cocaine ingestion is reported.