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Deaths Due to Asphyxiant Gases
Published in Sudhir K. Gupta, Forensic Pathology of Asphyxial Deaths, 2022
Decontamination is the prime part of the treatment. Withdraw the patient from the site of exposure and remove the clothing and accessories and prevent the inhalation exposure. Dermal decontamination can be done by washing the exposed area with water. Gastrointestinal decontamination is helpful if some form of cyanide may have prolonged absorption kinetics. For patients presenting within 1 hr of ingestion, it is advisable to perform orogastric lavage and administering activated charcoal in attempt to retrieve any amount of the cyanide.13 One gram of activated charcoal binds to only 35 milligram of cyanide.14
Experimental Lung Carcinogenesis by Intratracheal Instillation
Published in Joan Gil, Models of Lung Disease, 2020
Details of the IT instillation technique and a survey of major carcinogenicity studies in which the technique has been used will be provided in this chapter. Since inhalation is a method comparable to IT instillation, studies using inhalation exposure will also be reviewed.
Chemical injuries
Published in Jan de Boer, Marcel Dubouloz, Handbook of Disaster Medicine, 2020
Organophosphate compounds are commonly used as pesticides but can also be used as chemical warfare agents. The toxicity seen with these agents is due to inhibition of acetylcholinesterase, which causes accumulations of acetylcholine at cholinergic synapses, accounting for a cholinergic crisis with a variety of central and peripheral neurologic manifestations. Increased muscarinic activity produces activation of all the exocrine glands causing lacrimation, salivation, perspiration and excessive secretion by the bronchial and intestinal glands and stimulation of the pancreas, bronchospasm, sinus bradycardia, miosis and involuntary contractions of the muscles of the gastrointestinal tract causing abdominal cramps, vomiting, diarrhea and involuntary urination. Pulmonary symptoms are most marked after an inhalation exposure. Nicotine effects include those involving the skeletal muscles, including the muscles of the respiratory system as reflected by fasciculations and fibrillation and weakness followed by paralysis but also hypertension and tachycardia. Central nervous system effects are confusion, anxiety, restlessness, agitation, insomnia, ataxia, drowsiness, convulsions, coma and paralysis of respiratory centres10,13,21,23. Both central respiratory depression and the ventilatory compromise produced by bronchospasm, hypersecretion and respiratory muscle weakness are the most life-threatening manifestations13,21,23.
Modeling of clearance, retention, and translocation of inhaled gold nanoparticles in rats
Published in Inhalation Toxicology, 2022
A. Krikas, P. Neofytou, G. P. Gakis, I. Xiarchos, C. Charitidis, L. Tran
The present model aims to describe the ADME and biodistribution of inhaled AuNPs (without surface coatings) in rats. The model is developed using three existing in vivo experimental datasets (Han et al. 2015; Kreyling et al. 2018). The inhalation exposure details regarding each experimental dataset are summarized in Figure 1. In the first study, Sprague–Dawley rats were exposed to a nose-only inhalation of AuNPs, and studied the time dependent biodistribution of the NPs to the different organs. The rats were exposed to AuNPs for six hours a day for five consecutive days (six hour exposure followed by 18 hour post exposure for each day). Then, a post exposure period of 1, 3, and 28 days was used to study the long-term biodistribution. Two sets of experiments were conducted: one for 105 nm diameter NPs exposure (henceforth 105 nm dataset), and one for 13 nm (henceforth 13 nm dataset) Au NPs (Han et al. 2015).
Analyzing pesticides and metal(loid)s in imported tobacco to Saudi Arabia and risk assessment of inhalation exposure to certain metals
Published in Inhalation Toxicology, 2022
Mohammed A. Al Mutairi, Hatim A. Al Herbish, Rakan S. Al-Ajmi, Hatim Z. Alhazmi, Reham A. Al-Dhelaan, Abdullah M. Alowaifeer
Besides metals, mainstream cigarette smoke contains other carcinogens, such as aldehydes, aromatic amines, heterocyclic compounds, polycyclic aromatic hydrocarbons, N-nitrosamines, phenolic compounds, nitrohydrocarbons, and miscellaneous organic compounds. Based on smoke machine-generated data, smokers are exposed to 1400–22 000 ug/of these compounds per cigarette (IARC 2004). Aromatic amines, polycyclic aromatic hydrocarbons, and N-nitrosamines are the strongest of them but are found in relatively lower concentrations (0.004–0.3 ug/cigarette). On the contrary, acetaldehyde and isoprene are weaker carcinogens but are found at higher levels (700–1000 ug/cigarette). Nonetheless, toxicological inhalation exposure studies are predominantly conclusive in that smokers are at an increased risk of developing cancer.
Grouping of nanomaterials to read-across hazard endpoints: a review
Published in Nanotoxicology, 2019
L. Lamon, K. Aschberger, D. Asturiol, A. Richarz, A. Worth
Oosterwijk et al. (2016) propose a conceptual framework for inhalation exposure, that can be updated and validated once more information on the property–toxicity relationships and on the NMs mechanism of action become available. The hazard module computes different scores according to the accumulation fractions of NMs in different respiratory regions (nasal, tracheobronchial, and pulmonary region) and according to local or systemic toxicity that is considered in the alveolar region. PC properties such as net charge, size, hydrophobicity/hydrophilicity, solubility and ion toxicity, and conduction band energy are computed to classify the NMs into four hazard classes. Drew et al. (2017) proposed a quantitative framework to group NMs and bulk materials through a set of properties including density, surface area, and diameter that were most predictive of the potency to elicit neutrophilic pulmonary inflammation (acute exposure).C.,