Although some inhalant-induced damage to the nervous and other organ systems may be at least partially reversible when inhalant abuse is stopped, many syndromes caused by repeated or prolonged abuse are irreversible. If very severe, exposure to gasoline or gasoline vapors can cause permanent organ damage, coma, or death. The dynamic system of exposure to gasoline vapours which closely matches exposure to vapour in open air was applied in this study. The dynamic model of exposure to vapours is preferred to the static system as the latter allows the concentration of gas to build up and increase as time goes by Haschek et al [22]. However, gasoline and gasoline vapors are toxic, and chronic exposure to them can be deadly. According to the American Cancer Society, chronic or severe exposure to fuel products made from gasoline, such as diesel and benzenes, can also cause severe health complications, which may include certain types of cancer.
Neurological complications of drug abuse: pathophysiological mechanisms [Review]
Ingestion of ethylene glycol produces not only central nervous system depression, but also cardiopulmonary complications, acute renal failure, and delayed neurological sequelae [6]. Petrol fumes can be inhaled directly from a bag, saturated rag or small container either through the nose, referred to as ‘sniffing’ [3], [4], or through the mouth which is referred to as ‘baggin’ or ‘huffing’ [5], [6]. Approximately 15–20 inhalations of petrol can produce euphoria, ataxia and disorientation that can last for up to 6 h [3]. The first report of petrol sniffing as a specific form of volatile substance abuse was in the US in 1934 [7], although volatile substances have been inhaled to alter consciousness since antiquity [8]. By the 1960s, petrol sniffing was prevalent amongst adolescents of a number of indigenous populations including native Americans, Inuit Canadians, Polynesions, Maoris and Australian Aboriginals [9], [10], [11], [12], [13], [14].
Biochemical basis for the toxic effects of triethyl lead
Petrol sniffers have caused substantial damage to property and are frequently involved in robberies, often because they are hungry and in search of food [15], [29], [30]. An increased libido as a consequence of petrol sniffing has been linked to a higher incidence of sexually transmitted disease among sniffers [15], [30]. Further behavioural famous fetal alcohol syndrome adults and social problems are caused by irregular school attendance among petrol sniffers [4], [20].
Past studies, for instance, have linked altered brain connectivity to decreased working memory and work performance. Now that you know why you enjoy the smell of gasoline, read up on why the gas pump nozzle always shuts off on you and why it’s a bad idea to pump gas with the car running. And according to science, it may be less about getting a cheap buzz and more about nostalgia. If you’ve ever worked in a manufacturer’s legal department, you’re probably familiar with discussions on how to avoid liability for damages done by someone’s using products in an inappropriate manner. People have used shoes to hammer nails, attempted to pry open food cans with screwdrivers, and picked up carving knives to extend their reach for items on high shelves.
Acute cytotoxicity, genotoxicity, and apoptosis induced by petroleum VOC emissions in A549 cell line
The rats exposed to the unleaded gasoline had a significantly lower acetylcholinesterase activity as compared with the control or leaded group. No statistical changes were detected in the acetylcholinesterase activity of the leaded group as compared with the control. Serotonin content of the cerebellum was lower in the leaded gasoline group than control group, but the dopamine and norepinephrine were elevated above the control level. Data presented in tables tables33 show that the rats exposed to the two types of vapours encountered a significant decrease in the norepinephrine, dopamine and serotonin contents of the hippocampus as compared with the control group. Petrol sniffing occurs most frequently among indigenous adolescents who are from low-income, isolated communities [3], [6], [9], [20], [24], [31], [32]. The common explanation for this is that petrol is cheap, readily available and there is restricted access to other drugs of abuse that are favoured by equivalent groups in the wider community [9], [24], [32].
A person can also sustain damage to the skin, eyes, and lungs when they come into contact with gasoline liquid or the fumes or vapors of gasoline. Gasoline and its vapors are toxic, and having extended exposure, such as drinking gasoline, can seriously damage a person’s health. But don’t wait for the problem to reach that stage—by then, the damage may be irreversible.
The analysis of each individual sample was repeated three times and the average was recorded. Alkylbenzenes, including toluene and difference between helping and enabling xylene, occur naturally in small amounts in gasoline blends and standard gasoline formulations. The effects vary from severe neurological disorder (acute inhalation due to sniffing abuse) to deficits in neurobehavioural function in occupationally exposed groups. Neurobehavioural effects deriving from sub-acute exposure to toluene have been investigated in rats [20] and mice [21]. In addition to medical costs, delinquency is common among petrol sniffers and is the cause of considerable cost to the community. Petrol sniffing may promote delinquent behaviour due to its intoxicating effects that include a hunger for stimulation, proneness to violent outbursts and a need to release tension [4], [15], [29].
- In the present study, the norepinephrine level in the cerebral cortex and hypothalamus of the unleaded group was less than that in the control.
- Moreover, norepinephrine in this group was less than that in the leaded gasoline group and the dopamine was higher than that in the leaded gasoline inhaled group.
- In the cerebellum, norepinephrine level was higher in the leaded group as compared with the control group.
- People have used shoes to hammer nails, attempted to pry open food cans with screwdrivers, and picked up carving knives to extend their reach for items on high shelves.
For example, chronic abuse of volatile solvents, such as toluene or naphthalene (the volatile ingredient in mothballs), damages the protective sheath around certain nerve fibers in the brain and peripheral nervous system. This extensive destruction of nerve fibers is clinically similar to that seen with neurological diseases such as multiple sclerosis. Nitrous oxide and ether helped pioneer the discovery of medical anesthesia—because they were popular recreational inhalants among upper-class adults two centuries ago, and because it was observed that people who inhaled them felt no pain from minor injuries. Outside of a controlled environment, potential for not-so-minor injuries (to body and brain) is enormous. Effect of chronic exposure to two types of gasoline vapour on the duration of aggressive behaviour in male rats.
Furthermore, a North American study reported that 23 adolescents from a Navajo Indian reservation were hospitalised 47 times, spanning 6 years for complications secondary to petrol sniffing [20]. Data presented in tables 3 show that the rats exposed to the two types of vapours encountered a significant decrease in the norepinephrine, dopamine and serotonin contents of the hippocampus as compared with the control group. On other hand, no significant changes were found in norepinephrine and serotonin between the leaded or the unleaded gasoline, but dopamine level was lower in the unleaded gasoline than leaded gasoline groups. In the hypothalamus, data in table 2 reveal that the norepinephrine, dopamine and serotonin in the group exposed to the unleaded gasoline were lower than those of the control group. Data in table table55 reveal that Na+, K+-ATPase activity and total protein content in the two groups exposed to gasoline were lower than the control, although no significant difference was found between each other.
Effect of chronic exposure to two types of gasoline vapour on the contents of lipid peroxidation, reduced glutathione and superoxide dismutase activity of cerebral cortex in male rats. The rats of each group were subjected to aggressive behaviour tests for ten days, through the last ten days of exposure. After the completion of this test, the 15 animals of each group were decapitated and the brain was quickly removed out from each rat. The cerebral cortex was excised, from the level of the pituitary gland to the end of the olfactory lobe, for the determination of lipid peroxidation, GSH, SOD, protein, Na+, K+-ATPase, the AChE and monoamines. Hippocampus, hypothalamus and cerebellum were also excised and used for the determination of monoamines only.
This paper examines closely and compares the potential hazards of inhalation of two types of gasoline (car fuel). The first type is the commonly use leaded gasoline and the second is the unleaded type enriched with oxygenate additives as lead substituent in order to raise the octane number. Gasoline is the generic term for petroleum fuel used mainly for internal combustion engines. It is complex, volatile, and highly flammable and contains over 500 saturated or unsaturated hydrocarbons having from 3 to 12 carbon atoms. About 110 million people are exposed to gasoline constituents in the course of refueling at gasoline stations [1].
Trends in inhalant use among high school students in Illinois: 1993–1995
On the other hand, no statistical difference was found between the control and the leaded groups. Serotonin content was not affected in all the three experimental groups when comparison was made between each other. Data in table 1 show that the rats exposed to unleaded gasoline exhibited a decrease in the content of norepinephrine of the cerebral cortex in comparison with the control group. In the hypothalamus, data in table table22 reveal that the norepinephrine, dopamine and serotonin in the group exposed to the unleaded gasoline were lower than those of the control group. what is whipit Moreover, norepinephrine in this group was less than that in the leaded gasoline group and the dopamine was higher than that in the leaded gasoline inhaled group. Exposure to leaded gasoline induced a significant decrease in both dopamine and serotonin in comparison with the control group.
Major toxic risk comes from breathing exhaust fumes and evaporative and refueling emissions rather than from occasional skin contact from spills [2]. Nonetheless, after gasoline application to skin, a decrease in glutathione concentration, glutathione S -transferase activity, and lipid peroxidation was observed in liver and brain [3]. Gasoline-induced neurotoxic effects such as ataxia, tremor, acute or subacute encephalopathic syndrome were ascribable to intentional use (gasoline sniffing) and not to occupational exposure. Unfortunately, gasoline sniffing has become an increasingly rising phenomenon in the poor societies as a means for cheap mood alteration [4]. As Egypt is now in the process of transferring into the use of unleaded gasoline, this study employed the two types of gasoline currently used in Egypt and focused on comparing their impact.
