Assessment and management of acute poisoning by petroleum products.
ABSTRACT Petroleum products are highly complex chemical mixtures consisting predominantly of hydrocarbons. Their composition varies with source and intended use of the product. Virtually all are blended products that come into contact with man in a wide range of circumstances. Their toxicity for man is generally low and the use of additives rarely affects the toxicity of the final product. Because products are blended to meet performance, and not chemical specifications, their composition varies significantly. Management of toxicity benefits from simplified guidelines that consider the product by its type. Management in most cases is symptomatic, but the doctor needs to be aware of the potential for development of sequelae such as aspiration pneumonia and central nervous system (CNS) depression. Local and systemic effects of exposure to hydrocarbons are reviewed, as are immediate assessment and recommended management of acute exposure to petroleum products. Because of the large scope of this subject, this paper limits itself to acute toxicity of petroleum products encountered inthe public domain. It does not address topics such as chronic toxicity, solvent abuse, petrochemicals, or pesticides.
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ABSTRACT: Abstract Biocides are added to biodiesels to prevent degradation resulting from microbial growth. A 28-day repeated oral dose study was conducted to assess a potential risk arising from ingestion of isothiazolinone biocides in biodiesels. A mixture of 5-chloro-2-methyl-4-isothiazolin-3-one and 2-methyl-4-isothiazolin-3-one (CMIT/MIT) diluted in corn oil was administered by gavage to male and female rats at 0, 0.26, 0.78, 2.33 and 7.0 mg/kg body weight per day. Rat water and food consumption was monitored. At the end of the dosing period, organs were weighed and histological examinations performed. Hematology, serum clinical chemistry and biomarkers of inflammation were assessed. Reduction of serum triglyceride levels in males and induction of hepatic phase 1 xenobiotic metabolizing enzymes in females accompanied by subtle histological changes in the liver were observed at the highest CMIT/MIT exposure. These changes were more indicative of an adaptive, reversible response than overt toxicity. Based on recommended levels for the control of microbial growth in fuels, CMIT/MIT contained in accidentally ingested biodiesels is not expected to represent a significant health risk.Drug and Chemical Toxicology 10/2013; · 1.29 Impact Factor
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ABSTRACT: Contamination of soil and groundwater by petroleum-based products is an extremely widespread and important environmental problem. Here we have tested a simple optical approach for detecting and identifying such industrial contaminants in soil samples, using a set of fluorescent DNA-based chemosensors in pattern-based sensing. We used a set of diverse industrial volatile chemicals to screen and identify a set of five short oligomeric DNA fluorophores on PEG-polystyrene microbeads that could differentiate the entire set after exposure to their vapors in air. We then tested this set of five fluorescent chemosensor compounds for their ability to respond with fluorescence changes when exposed to headgas over soil samples contaminated with one of ten different samples of crude oil, petroleum distillates, fuels, lubricants and additives. Statistical analysis of the quantitative fluorescence change data (as Δ(R,G,B) emission intensities) revealed that these five chemosensors on beads could differentiate all ten product mixtures at 1000 ppm in soil within 30 minutes. Tests of sensitivity with three of the contaminant mixtures showed that they could be detected and differentiated in amounts at least as low as one part per million in soil. The results establish that DNA-polyfluorophores may have practical utility in monitoring the extent and identity of environmental spills and leaks, while they occur and during their remediation.Chemical Science 08/2013; 4(8):3184-3190. · 8.31 Impact Factor
Article: Hydrocarbon toxicity: A review.[Show abstract] [Hide abstract]
ABSTRACT: Abstract Context. Clinical effects of hydrocarbon exposure have been reported since 1897. These substances are ubiquitous, and their exposures are common. The specific hydrocarbon and route of exposure will determine the clinical effect, and an understanding of this is helpful in the care of the hydrocarbon-exposed patient. Objective. To complete a comprehensive review of the literature on hydrocarbon toxicity and summarize the findings. Methods. Relevant literature was identified through searches of Medline (PubMed/OVID) and Cochrane Library databases (inclusive of years 1975-2013), as well as from multiple toxicology textbooks. Bibliographies of the identified articles were also reviewed. Search terms included combinations of the following: hydrocarbons, inhalants, encephalopathy, coma, cognitive deficits, inhalant abuse, huffing, sudden sniffing death, toluene, renal tubular acidosis, metabolic acidosis, arrhythmia, dermatitis, and aspiration pneumonitis. All pertinent clinical trials, observational studies, and case reports relevant to hydrocarbon exposure and published in English were reviewed. Chronic, occupational hydrocarbon toxicity was not included. Results. Exposure to hydrocarbons occurs through one of the following routes: inhalation, ingestion with or without aspiration, or dermal exposure. Inhalational abuse is associated with central nervous system depression, metabolic acidosis, and arrhythmia. The exact mechanism of the CNS depression is unknown, but experimental evidence suggests effects on NMDA, dopamine, and GABA receptors. Chronic toluene inhalation causes a non-anion gap metabolic acidosis associated with hypokalemia. Halogenated hydrocarbon abuse can cause a fatal malignant arrhythmia, termed "sudden sniffing death". Individuals who regularly abuse hydrocarbons are more likely to be polysubstance users, exhibit criminal or violent behavior, and develop memory and other cognitive deficits. Heavy, long-term use results in cerebellar dysfunction, encephalopathy, weakness, and dementia. Neuroimaging may demonstrate leukoencephalopathy in these cases. Acute exposures improve with cessation of exposure. Electrolyte and fluid replacement will improve metabolic acidosis. Arrhythmias are precipitated via catecholamine surge, and beta blockers are presumed protective. Aspiration of hydrocarbons causes a potentially fatal pneumonitis. Symptoms may include cough, wheezing respiratory distress, and hypoxia. Bilateral interstitial infiltrates may be delayed for several hours after the development of pneumonitis. Treatment consists of supportive care, supplemental oxygen, and may require intubation and admission to an intensive care unit in severe cases. Unfortunately, aspiration pneumonitis remains a leading cause of poisoning mortality in children. Dermal exposure can cause dermatitis, chemical burns, and defatting injury. Oral exposure can cause local irritation as well as vomiting, diarrhea, and abdominal pain. Conclusion. Acute hydrocarbon exposure can result in a wide array of pathology, such as encephalopathy, pneumonitis, arrhythmia, acidosis, and dermatitis. Intentional inhalational and accidental ingestion exposures with aspiration lead to the greatest morbidity and mortality.Clinical toxicology (Philadelphia, Pa.). 06/2014; 52(5):479-489.