LEAD POISONING AND GLUE SNIFFING INTOXICATIONS.
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Child↗
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ACUTE AND CHRONIC EFFECTS OF GLUE SNIFFING.
Fifteen boys who were habitual sniffers of the kind of glue used for assembling model airplanes were investigated in regard to the acute and chronic toxicity of the substances in the glue. The acute effects of airplane glue were measured by serial psychometric testing in eight subjects and a transitory visual motor disturbance was found. In one case there was elevated spinal fluid pressure due to intoxication with the inhaled substance. No chronic renal, hematologic or hepatic changes were observed.
Adhesives↗
CHILDHOOD AND ADOLESCENT ADDICTIVE DISORDERS.
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Adolescent↗
Headspace gas chromatographic method for the measurement of difluoroethane in blood.
OBJECTIVES: To develop a gas chromatographic assay for the analysis of difluoroethane, a volatile substance, in blood and to determine assay characteristics including linearity, limit of quantitation, precision, and specificity. SETTING: Referral toxicology laboratory RESULTS: Difluoroethane, a colorless, odorless, highly flammable gas used as a refrigerant blend component and aerosol propellant, may be abused via inhalation. A headspace gas chromatographic procedure for the identification and quantitation of difluoroethane in blood is presented. A methanolic stock standard prepared from pure gaseous difluoroethane was used to prepare whole blood calibrators. Quantitation of difluoroethane was performed using a six-point calibration curve and an internal standard of 1-propanol. The assay is linear from 0 to 115 mg/L including a low calibrator at 4 mg/L, the limit of quantitation. Within-run coefficients of variation at mean concentrations of 13.8 mg/L and 38.5 mg/L were 5.8% and 6.8% respectively. Between-run coefficients of variation at mean concentrations of 15.9 mg/L and 45.7 mg/L were 13.4% and 9.8% respectively. Several volatile substances were tested as potential interfering compounds with propane having a retention time identical to that of difluoroethane. CONCLUSIONS: This method requires minimal sample preparation, is rapid and reproducible, can be modified for the quantitation of other volatiles, and could be automated using an automatic sampler/injector system.
Administration, Inhalation↗
[Nasal osteocartilaginous necrosis caused by cocaine. Our experience with two patients].
Sinonasal osteocartilaginous necrosis induced by the abuse of inhaled cocaine must be considered in the differential diagnosis of those pathologies that produce facial midline destructions. We report two cases corresponding to women admitted in our Hospital because of such entity. There were analysed their respective clinical histories, exploration data, complementary tests, medical-surgical treatment and evolution. Cocaine is one of the drugs that has increased in last 10 years producing an elevated number of complications, as we could proved on the bibliographic review performed.
Adult↗
Death due to butane abuse--the clinical pharmacology of inhalants.
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Administration, Inhalation↗
Childhood asthma mortality: the Brooklyn experience and a brief review.
Pediatric asthma mortality is a perplexing and increasingly serious problem. Although many possible etiologic factors have been suggested, clear relationships are yet to be delineated. In addition to reviewing the literature, we studied the clinical and pathologic features of 14 local pediatric asthma deaths that occurred over a 7-year period. Thirteen of 14 children were African-American. Nine of 14 children (64.3) were older than 10 years of age, and 11 of 14 (78.6) were males. Based on a history of clinical features, 10 of the 14 children were characterized as severe asthmatics. Despite the fact that the majority of the children were regarded as severe asthmatics, only 1 of 14 had been evaluated with pulmonary function testing, and only 2 of 14 were receiving corticosteroids. Furthermore, only 2 of 14 were regarded as having good medical follow-up for their asthma. Ten of 14 children died suddenly secondary to asthma. One child was possibly abusing sympathomimetic inhalers, and none had evidence of toxic serum levels of theophylline. Six of 14 children (all adolescents) who died suddenly were negative on urine toxicology screening for cocaine, heroin, etc. Pathologic findings available for 10 children revealed mainly mucus plugging of the airways and collapse of various segments of the lungs, as well as pneumonia and pneumothorax in one child. In this group of children with sudden deaths (except for one child with pneumothorax), no other cause of death could be found.
Adolescent↗
Alcohol and drug use--is there a 'safe' amount?
All human endeavors are associated with quantifiable risks. Knowledge of the risk is essential for personal health maintenance. Nontherapeutic use of psychoactive drugs poses an important danger to individual persons and society. What are the quantitative estimates of these risks? Are they acceptable?Because the basic mechanism of the toxic effect of alcohol or other drugs is unknown, deciding on acceptable risks is difficult. Based on current information, the recreational abuse of inhalants, hallucinogens, stimulants, narcotics and sedative-hypnotic drugs poses unacceptable individual and societal risks. Groups at special risk should not consume alcohol or any drug unless they are under medical supervision. The threshold for increased morbidity from the regular use of alcohol in adults is in the range of three to five drinks per day; this rises sharply after six drinks per day. The apparent "safe" level of alcohol consumption appears to be one to two drinks per day. Further basic studies are required to refine these risk estimates.
Adult↗
Anticonvulsant and antipunishment effects of toluene.
Toluene can have striking acute behavioral effects and is subject to abuse by inhalation. To determine if its actions resemble those of drugs used in the treatment of anxiety ("anxiolytics"), two sets of experiments were undertaken. Inasmuch as prevention of pentylenetetrazol-induced convulsions is an identifying property of this class of agents, we first demonstrated that pretreatment with injections of toluene delayed the onset of convulsive signs and prevented the tonic extension phase of the convulsant activity in a dose-related manner. Injections of another alkyl benzene, m-xylene, were of comparable potency to toluene. Inhalation of toluene delayed the time to death after pentylenetetrazol injection in a manner related to the duration and concentration of exposure; at lower convulsant doses, inhalation of moderate concentrations (EC50, 1311 ppm) prevented death. Treatment with a benzodiazepine receptor antagonist (Ro 15-1788) failed to reduce the anticonvulsant activity of inhaled toluene. Anxiolytics also attenuate the reduction in response rate produced by punishment with electric shock. Toluene increased rates of responding suppressed by punishment when responding was maintained under a multiple fixed-interval fixed-interval punishment schedule of reinforcement. Distinct antipunishment effects were observed after 2 hr of exposure to 1780 and 3000 ppm of toluene; the rate-increasing effects of toluene were related to concentration and to time after the termination of exposure. Thus, toluene and m-xylene resemble in several respects clinically useful drugs such as the benzodiazepines.
Animals↗
Production of macrophage IL-1beta was inhibited both at the levels of transcription and maturation by caspase-1 following inhalation exposure to isobutyl nitrite.
Epidemiological studies have identified abuse of nitrite inhalants as an independent co-factor in HIV infection and in Kaposi's sarcoma (KS) in AIDS patients. In the present study we investigated the ability of macrophages from mice exposed to isobutyl nitrite to produce the inflammatory cytokine IL-1beta, upon stimulation with IFN-gamma and LPS. The production of IL-1beta was inhibited up to 55%. IL-1beta mRNA transcription was reduced by 35% following nitrite inhalant exposure, consistent with inhibition of activation-induced phosphorylation of macrophage mitogen-activated protein kinase p38. However, synthesis of the 31 kDa IL-1beta precursor protein was only marginally inhibited. Caspase-1, which cleaves the precursor IL-1beta into mature 17 kDa IL-1beta, was examined. Nitrite inhalant exposure blocked activation-induced increases in caspase-1 activity, consistent with a 50% reduction in 17 kDa IL-1beta shown in Western blots. Thus, exposure to nitrite inhalants reduced macrophage production of IL-1beta by reducing transcription, as well as post-translational processing mediated by caspase-1.
Acquired Immunodeficiency Syndrome↗
Acute inhalation exposure to isobutyl nitrite causes nonspecific blood cell destruction.
Abuse of nitrite inhalants is widespread among male homosexuals and has been epidemiologically correlated with seropositivity to human immunodeficiency virus (HIV) and to Kaposi's sarcoma. These drugs may act as cofactors in AIDS if they compromise the ability to resist infection or tumor growth. We have previously reported that 14 daily 45-minute exposure to 900 ppm isobutyl nitrite in an inhalation chamber did compromise the immunocompetence of mice. We now report that a single 45-minute exposure produced a transient anemia. Erythrocyte counts, hemoglobin, and hematocrit levels were reduced by 7% but rebounded to above-normal levels 24 hours later. In vitro exposure of blood to isobutyl nitrite vapors did not lyse the cells but did induce Heinz body formation and increase their binding to macrophages. Thus, it is likely that the red cells were removed by phagocytic clearance not by direct lysis. Blood leukocyte numbers were also reduced following a single exposure to the inhalant, but the cell loss was delayed until 24 hours after exposure. Recovery of peripheral blood leukocytes 72 hours after exposure coincided with a reduction in spleen cellularity, suggesting that spleen cells were mobilized to replace lost blood leukocytes.
Animals↗
Inhalation exposure to isobutyl nitrite inhibits macrophage tumoricidal activity and modulates inducible nitric oxide.
Abuse of nitrite inhalants is common among male homosexuals and a history of abuse has been correlated with seropositivity to HIV and with the incidence of Kaposi's sarcoma among AIDS patients. The present study shows that inhalation exposure of mice to 900 ppm isobutyl nitrite for 45 min/day for 14 days compromised macrophage tumoricidal activity by up to 40% and it remained compromised for at least 7 days after terminating exposures. The inhalation exposures did not affect tumor cell binding but did inhibit inducible nitric oxide (NO zero). The NO zero synthase inhibitor NG-methyl-L-arginine totally inhibited both NO zero production and cytotoxicity, suggesting that reductions in NO zero due to inhalant exposure may be responsible for the reduced cytotoxic activity. Exposure to the inhalant increased constitutive production of tumor necrosis factor-alpha (TNF-alpha). TNF-alpha has been reported to stimulate the replication of HIV and the proliferation of Kaposi's sarcoma cells in vitro.
Administration, Inhalation↗
Increased tumor growth in mice exposed to inhaled isobutyl nitrite.
Epidemiological studies have correlated the incidence of Kaposi's sarcoma (KS) in AIDS with a history of abuse of nitrite inhalants. To determine if exposure to nitrite inhalants could alter tumor growth, syngeneic PYB6 tumor cells were injected into groups of mice. Exposure of these mice to inhaled isobutyl nitrite increased both the tumor incidence and the tumor growth rate by almost 4-fold. Following only five daily exposures to the inhalant, the induction of specific T cell mediated cytotoxicity was inhibited by 36%. Similar inhalation exposures inhibited the tumoricidal activity of activated macrophages by 86%. The data suggest that exposure to abuser levels of a nitrite inhalant compromised tumor surveillance mechanisms.
Administration, Inhalation↗
Possible roles for nitric oxide in AIDS and associated pathology.
The endogenous free radical, nitric oxide (NO), plays a neurotransmitter-like role in vascular endothelium, a second-messenger role in N-methyl-D-aspartate (NMDA)-responsive neurons in the central nervous system (CNS), a neurotoxic role after its release from these neurons, and a cytotoxic role after its release by macrophages. NO also derives from exogenous sources, such as the nitrite inhalants, amyl, butyl and isobutyl nitrite. There is evidence that abuse of nitrite inhalants can affect immunomodulation, and epidemiological studies suggest that such abuse may be a cofactor in the pathogenesis of acquired immunodeficiency syndrome (AIDS). Hitherto, however, the potential role of NO in such pathogenesis has not been examined. This paper presents some current evidence that implicates both endogenous and exogenous sources of NO in AIDS and associated pathology.
Acquired Immunodeficiency Syndrome↗
NIDA technical review: nitrite inhalants.
Nitrite inhalants are commonly abused substances in the US and Europe. "Nitrite inhalants and AIDS" was a popular topic in the early 1980s when the cause of AIDS was not known. With the discovery of HIV, concern about nitrite use wained. However, nitrite inhalant use is associated with behavioral relapse and HIV transmission among gay men, with decreased lymphocyte counts and natural killer cell activity in laboratory studies, and remains a candidate "cofactor" in the pathogenesis of AIDS-related Karposi sarcoma. Discouraging nitrite use continues to be a worthwhile public health goal. Participants recommend specific research efforts.
Acquired Immunodeficiency Syndrome↗
Gas sniffing as a form of substance abuse.
The authors review the existing literature on inhalation of gasoline fumes, highlighting the acute and chronic physical and psychological effects. The clinical picture of gas sniffing includes visual hallucinations, changes in consciousness, euphoria, nystagmus, dizziness, weakness and tremors. There is the possibility of rapid recovery, sudden death or brain damage with chronic abuse. When leaded gasoline is abused then blood and urine lead levels and erythrocytic delta-aminolevulinic acid dehydrase (ALAD) levels may be helpful. Although the treatment of acute and chronic gas sniffing syndromes is often supportive and non-specific, when lead levels are high chelated therapy is indicated including British anti-lewisite, calcium disodium versenate or D-penicillamine. We also report our findings on an isolated native Indian population where intentional gas sniffing has reached epidemic proportions. Ten percent of the total population and 25% of the children between 5 and 15 years of age had been identified as gasoline inhalation abusers. In this population, the most important etiological factors included environmental, family and cultural components. The authors emphasize the need to correct the family and social deficiencies in such communities if the incidence of gas sniffing is to be decreased.
Adolescent↗