Inhaled potential toxicities

Fillers fibreglass, silicas, calcium carbonate, powdered metal pigments some may be absorbed potential primary irritant dust inhalation low toxicity... 

Five recent studies investigated the potential toxic risk if CNTs reach the pleural cavity after inhalation exposure [6,88-91]. Three of these in vivo studies revealed that if CNTs are delivered to the abdominal cavity of mice or rats, they could induce a serious potential carcinogenic risk resembling that associated with exposure to certain asbestos fibers [6,88,89]. The other two studies described nontoxic responses [90,91]. 

Field First Aid Evacuate the Hot Zone at once when there is any release of arsine consider any victims who may have inhaled arsine to have suffered a potentially toxic dose. Although small amounts of arsine can be trapped in the victim s clothing or hair, these quantities are not likely to cause a danger for first response personnel outside the Hot Zone. Toxic effects could be delayed for up to two to twenty-four hours after exposure arsine exposure victims should all be evaluated at a medical facility. There is no specific antidote for arsine treatment is symptomatic and consists of actions to support respiratory, vascular, and renal functions. 

The Mann et al. (1985) study is limited in that too few animals were used, organs other than the liver were not adequately evaluated, and only males were studied. Although an adequate acute-duration oral study would be useful to corroborate or refute the thyroid effects seen in the Mann et al. (1985) study, this does not represent a data need, since an acute oral MRL has been derived. Ingestion of contaminated drinking water is expected to be the predominant route of exposure for individuals living in the vicinity of hazardous waste sites. However, acute-duration inhalation and dermal studies in animals are needed to assess the potential toxicity of di- -octylphthalate following exposure via these routes because there are insufficient pharmacokinetic data available to support the extrapolation of data obtained after oral administration to other routes of exposure. 

CNTs are of importance as useful bio-nanomaterials for pharmaceutical applications and biomedical engineering. However, despite the contribution of CNTs to bio-nanomaterials for pharmaceutical applications, the potential risks of CNTs about the exposure to human health have not been adequately assessed. Toxicology issues associated with CNT inhalation, dermal toxicity, pulmonary, biodistribution, biocompatibility, blood compatibility, and elimination need to be addressed prior to their pharmacological application in humans. 

However, if you link the hydroxyl group with the methane molecule rather than the ethane, you get the potentially toxic chemical called methyl alcohol, or wood spirit. Similarly, if you add what s called an aldehyde group (-CHO) instead of the hydroxyl group, you will get one of a variety of chemicals called aldehydes, of which a common one is the gas formaldehyde (HCHO), widely used in the manufacture of plastics and glues. This gas can be an irritant and potentially dangerous if inhaled. 

Bromomethane exists as a gas at ordinary temperatures, so the most likely route of human exposure is by inhalation. The hazard of this compound is increased by the fact that it has very little odor at potentially toxic levels (Alexeeff and Kilgore 1983), and effects on the body are generally delayed. Thus, people may be exposed to hazardous levels without being aware that the exposure is occurring. 

Deseriptive data are available from reports of humans exposed to 1,4-diehlorobenzene by inhalation (and possibly dermal contact). It is important to note that the case studies discussed in this section should be interpreted with caution since they reflect incidents in which individuals have reportedly been exposed to 1,4-dichlorobenzene, and they assume that there has been no other exposure to potentially toxic or infectious agents. There is usually little or no verification of these assumptions. Case studies in general are not scientifically equivalent to carefiilly designed epidemiological studies or to adequately controlled and monitored laboratory experiments. Thus, the case studies described below should be considered only as providing supplementary evidence that 1,4-dichlorobenzene may cause the reported effects. 

A reduction in total white blood cell counts to 60% of control values (p<0.05), but no changes in differential white cell counts or evidence of bone marrow damage, was found in rats intermittently exposed to 700 ppm 2-hexanone after 8 weeks during an 11-week study (Katz et al. 1980). These findings, although inconclusive, suggest that immunological effects may warrant some consideration in future assessments of the potential toxicity of inhalation exposure to 2-hexanone. 

Toxic or potentially toxic agents may be inhaled into the respiratory tract where they may cause localized effects such as irritation (e.g., ammonia, chlorine gas), inflammation, necrosis, and cancer. Chemicals may also be absorbed by the lungs into the circulatory system, thereby leading to systemic toxicity (e.g., CO, lead). 

Inhalation. The respiratory system is an important portal of entry, and for evaluation purposes animals must be exposed to atmospheres containing potential toxicants. The generation and control of the physical characteristics of such contaminated atmospheres is technically complex and expensive in practice. The alternative—direct instillation into the lung through the trachea—presents problems of reproducibility as well as stress and for these reasons is generally unsatisfactory. 

At rest, an adult human inhales 6 to 8 L of air each minute (1 L = O.OOl m3) and, during an 8-hour workday, can inhale from 5 to 20 m3 depending on the level of physical activity. The optimum size range for aerosol particles to get into the lungs and remain there is 0.5 to 5.0 [im. As instrumentation used to collect atmospheric dust have become more precise, particulate matter (PM) in the size range of 2.5 to 10 xm have come under increasing scrutiny, because many potential toxicants are adsorbed to their surfaces. These particles are inhaled and will remain in the lungs and allow the compounds to pass into the bloodstream. 

Informational needs are discussed in light of the current data that exist for both inorganic tin and organotin compounds and how additional information will help in assessing potential toxicity or human health effects after inhalation, oral, and dermal exposures. 

An advantage of the use of radioactive tracers is that uptake and elimination of a potentially toxic substance can be studied without any perceptible increase in its concentration in the body. Also, the criticism was made that the aerosols used by Kehoe and by Griffin et al. were not identical with those produced in motor exhaust. To study uptake following inhalation of exhaust lead, a method of incorporating a tracer was developed at Harwell. 

Ethylene thiourea (ETU), a potentially toxic metabolite of zineb, may be involved in thyroid effects. Occupational inhalation of zineb can lead to changes... 

Objectives of the chronic toxicity study are to characterize the profile of a chemical in any mammalian species, following prolonged and repeated exposures, through oral, dermal, or inhalation route. In this respect, the chemical toxicity should be interpreted broadly to include any change from the normal. The duration of a chronic toxicity study for effects other than neoplasia is still widely debated. Chronic toxicity testing in animals requires exposure to the test chemical by appropriate route and at an appropriate dosage for much of the test animal s lifespan, if not for the entire life. Chronic toxicity tests assess potential toxicity from long-term exposures at low levels. 

Abstract. The general alarm raised concerning the potential toxicity of inhaled nano-sized particles has moved several particle toxicology groups towards thorough investigations on the peculiar toxicity of ultrafine (nano) dusts. The new term Nanotoxicology has been proposed for these kinds of studies. An overview of the factors which may affect the toxicity of inhaled nano and micro-sized inhaled particles is herein presented. 

Iron is potentially toxic in all forms and by all routes of exposure. The inhalation of large amounts of iron dust results in iron pneumoconiosis (arc welder s lung). Chronic exposure to excess levels of iron (>50-100 mg Fe/day) can result in pathological deposition of iron in the body tissues, the symptoms of which are fibrosis of the pancreas, diabetes mellitus, and liver cirrhosis. 

SAFETY PROFILE Poison by inhalation. Potentially explosive decomposition at 200°C. Flammable when exposed to heat or flame. Explosive reaction with ammonia + heat, chlorine, concentrated nitric acid, ozone. Incompatible with oxidants. The decomposition products are hydrogen and metallic antimony. When heated to decomposition it emits toxic fumes of Sb. Used as a fumigating agent. See also ANTIMONY COMPOUNDS and HYDRIDES. 

Most studies of respiratory diseases reported for uranium involve noncancerous alveolar epithelium damage in type II cells. These changes are characterized by interstitial inflammahon of the alveolar epithelium leading eventually to emphysema or pulmonary fibrosis in acute exposures or to hyperplasia, hypertrophy, and transdifferentiation (metaplasia) in chronic exposures (Cooper et al. 1982 Dungworth 1989 Stokinger 1981 Wedeen 1992). However, the lack of significant pulmonary injury in most inhalation animal studies indicates that other potentially toxic contaminants such as inhalable dust particles, radium, or radon may contribute to these effects. 

Observe normal precautions appropriate to tbe circumstances and quantity of material bandied. Boric acid is irritating to tbe skin and is potentially toxic by inhalation. Gloves, eye protection, protective clothing, and a respirator are recommended. 

Carbon tetrabromide may be absorbed by dermal, inhalation, or oral routes. It is oxidatively metabolized by rat liver microsomes to electrophilic and potentially toxic metabolites. It is metabolized in the liver but causes primary effects on the kidneys. The electrophilic bromine derivatives formed can be excreted as such. 

Humans may be exposed to cyanide in a number of different forms. These include solids, liquids, and gases. Sources include industrial chemicals, natural products, medications, and combustion products. Inhalation of toxic fumes and ingestion of cyanide salts, cyanide-containing fruit seeds, and cyanide waste-contaminated drinking water are the most common exposure pathways. The respiratory route represents a potentially rapidly fatal type of exposure. Exposure to cyanides may also occur via the dermal route in industrial workers. 

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