Respiratory exposure

Acute benzene poisoning results in CNS depression and is characterized by an initial euphoria followed by staggered gait, stupor, coma, and convulsions. Exposure to approximately 4000 ppm benzene results in complete loss of consciousness. Insomnia, agitation, headache, nausea, and drowsiness may persist for weeks after exposure (126). Continued inhalation of benzene to the point of euphoria has caused irreversible encephalopathy with tremulousness, emotional lability, and diffuse cerebral atrophy (125). In deaths arising from acute exposure, respiratory tract infection, hypo- and hyperplasia of sternal bone marrow, congested kidneys, and cerebral edema have been found at autopsy. 

During occupational exposure, respiratory absorption of soluble and insoluble nickel compounds is the major route of entry, with gastrointestinal absorption secondary (WHO 1991). Inhalation exposure studies of nickel in humans and test animals show that nickel localizes in the lungs, with much lower levels in liver and kidneys (USPHS 1993). About half the inhaled nickel is deposited on bronchial mucosa and swept upward in mucous to be swallowed about 25% of the inhaled nickel is deposited in the pulmonary parenchyma (NAS 1975). The relative amount of inhaled nickel absorbed from the pulmonary tract is dependent on the chemical and physical properties of the nickel compound (USEPA 1986). Pulmonary absorption into the blood is greatest for nickel carbonyl vapor about half the inhaled amount is absorbed (USEPA 1980). Nickel in particulate matter is absorbed from the pulmonary tract to a lesser degree than nickel carbonyl however, smaller particles are absorbed more readily than larger ones (USEPA 1980). Large nickel particles (>2 pm in diameter) are deposited in the upper respiratory tract smaller particles tend to enter the lower respiratory tract. In humans, 35% of the inhaled nickel is absorbed into the blood from the respiratory tract the remainder is either swallowed or expectorated. Soluble nickel compounds... 

Internal exposure (respiratory protection, hygiene, and monitoring)... 

Systemic EffectsRespiratory Effects. Nonspecific respiratory symptoms were reported in a worker involved in 1,2-dibromoethane production and presumably chronically exposed by inhalation (Kochmann 1928). One of the workers exposed in a storage tank by dermal and inhalation routes to 1,2-dibromoethane had bilateral pulmonary edema, a nonspecific agonal finding, at necropsy (Letz et al. 1984). Similar results occurred in rats exposed acutely to toxic concentrations by inhalation (Rowe et al. 1952). Abnormal respiratory effects have been well documented in experimental animals after inhalation exposure respiratory effects did not occur after dermal or oral exposure. 

Symptoms of exposure Respiratory distress, paralysis, brain damage, nausea, and vomiting (Patnaik, 1992)... 

After inhalation, respiratory and ocular effects are the first to appear, often within a few minutes after exposure. Respiratory effects include tightness in the chest and wheezing due to bronchoconstriction and excessive bronchial secretion laryngeal spasms and excessive salivation may add to the respiratory distress, and cyanosis may also occur. Ocular effects include miosis, blurring of distant vision, tearing, rhi-norrhea, and frontal headache. 

Inhalation exposure to toluene diisocyanates is irritating to the eyes and respiratory tract, and induced chronic rhinitis, interstitial pneumonia and catarrhal bronchitis after long-term exposure. Respiratory sensitization to toluene diisocyanate developed in guinea-pigs after inhalation but also after dermal exposure (lARC, 1986). 

Limited information is available on other systemic effects reported in humans and associated with benzene exposure. Respiratory effects have been noted after acute exposure of humans to benzene vapors (Avis and Hutton 1993 Midzenski et al. 1992 Winek and Collum 1971 Winek et al. 1967 Yin et al. 1987b). Cardiovascular effects, particularly ventricular fibrillation, have been suggested as the cause of death in... 

Although these studies provide some insight into the persistence of circulating toxin after parenteral administration, they do not necessarily reflect the behavior of absorbed toxin after respiratory exposure. The route of administration may not have a signiflcant impact on the behavior of toxin once absorbed into the serum and lymph, but the patterns and kinetics of absorption into the circulation might be quite different after inhalational versus parenteral exposure. Respiratory exposure could lead to a different proportion of toxin taken up into the circulation and/or lymphatics over... 

In acute exposures, respiratory disease may be limited to interstitial inflammation of the alveolar epithelium, leading eventually to emphysema or pulmonary fibrosis (Cooper et al. 1982 Dungworth 1989 Stokinger 1981 Wedeen 1992). In studies of the pulmonary effects of airborne uranium dust in uranium miners and in animals, the respiratory diseases reported are probably aggravated by the inhalable dust particles (the form in which uranium is inhaled) toxicity because most of the respiratory diseases reported in these studies are consistent with the effects of inhaled dust (Dockery et al. 1993). In some of these instances, additional data from the studies show that the workers were exposed to even more potent respiratory tract irritants, such as silica and vanadium pentaoxide (Waxweiler et al. 1983). 

Observe normal precautions appropriate to the circumstances and quantity of material handled. No occupational exposure limits have been established. Under conditions of frequent use or heavy exposure, respiratory protection may be required. When heated, lauric acid emits an acrid smoke and irritating fumes therefore, use in a well-ventilated area is recommended. 

Basic and advanced life-support measures should be implemented as necessary. Activated charcoal can be used to adsorb glutethimide if given within 1 h of exposure. Respiratory support including oxygen and ventilation should be provided as needed. There is no antidote for glutethimide. If hypotension occurs it should be treated with standard measures including... 

Available military experience indicates that less than 5% of exposed patients die from mustard exposure, although many will reqnire a long convalescence. The most likely cause of death in severely exposed patients is massive pulmonary damage, associated with pneumonia and sepsis secondary to immunosuppression. Clues to such massive exposures include symptom onset within 4h of exposure, respiratory symptoms occurring within 6h of exposure and white blood cell counts under 200 (8). 

Target tissues. Reasonable agreement was achieved between the model and experimental data for 2-butoxyacetic acid levels in the blood of rats after gavage exposure and in the urine of rats after drinking water exposure, respiratory uptake of 2-butoxyethanol, total amount metabolized, and total 2-butoxyacetic acid excreted after inhalation exposure of rats, as long as the doses were below those that caused hemolysis. In humans, reasonable agreement was achieved between the model and experimental data for respiratory uptake, the area under the curve for 2-butoxyethanol blood concentration-time, and the amount of 2-butoxyacetic acid excreted in the urine after inhalation exposure (Corley et al. 1994). 

The data describing acute lethality of common oximes (6,19,20) are summarized in the Table 1. The data show that currently used oximes, pralidoxime and obidoxime, are more toxic than methoxime as well as H oximes (HI-6 and HLp-7) regardless of the animals species and the route of exposure. Respiratory paralysis is considered to be a major factor in toxicity of pyridine aldoximes, chemicals related to the common oximes (21). Therefore, death due to respiratory paralysis is probable in oxime toxicity. 

Derris. An insecticide of plant origin. Can be used as a fish poison. Oral nausea and vomiting. Chronic exposure liver and kidney damage. Massive exposure respiratory paralysis and death. By inhalation intense respiratory stimulation and then depression, convulsions, death. Inhibits mitochondrial electron transport. 

Children may be exposed to creosote constituents brought into the home by parents or other household members who are occupationally exposed. Creosote residues may be present on clothing items and shoes of workers employed in industries where creosote-derived products are used or produced, and utility company workers who are in contact with treated wood. Exposure to children may occur through dermal contact with contaminated items. Because children are likely to be in close contact with carpet or floors, transfer of contaminated dirt from work shoes to carpeting provides a means of exposure. Respiratory exposure from contact with occupationally exposed workers is not likely to be significant. 

During occupational exposure, respiratory absorption of soluble and insoluble nickel compounds is the major route of entry, with... 

Respiratory The incidence of occupational asthma in aluminium smelters has been falling as a result of control of exposure, respiratory protection, and pre-placement medical assessment [3 ]. The incidence in 1992 in a New Zealand study was 9.46/1000/year in 2006 it was 0.36/1000 ear. 

Hypersentitivity. A hypersensitivity reaction (sometimes known as "drug fever") similar to an anaphylactoid reaction may result after repeated exposure. Respiratory difficulty and urticaria are the major clinical signs. Anaphylactoid reactions are rKinspecific. 

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