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Route of inhalation

Aerosol delivery via mechanical ventilation using nebulizers seems more complex than conventional nebulization. How should the nebulizer be powered Where in the circuit should it be connected Early studies in the ICU suggested that nebulized particles could be delivered to the lungs of intubated patients only with great difficulty. Compared to other devices such as MDIs, nebulizers were inefficient (30) and the endotracheal tube presented an additional barrier to the passage of particles into the respiratory tract (31). However, by taking the same [Pg.294]

Marcel Dekker, Inc. 270 Madison Avenue, New York, New York 10016 [Pg.294]

The filter measures inhaled mass. In the insert is a sketch of the filter configuration used to measure exhaled particles (and hence deposition) and a gamma camera for regional studies. [Pg.296]

Nebulizers can be tested in a given ventilator circuit and, as shown in Fig. 22, the choice of nebulizer can have a significant impact on drug delivery. Inhaled mass versus time is shown for a number of common nebulizers, including the devices first tested in Fig. 5. Devices shown to be efficient for spontaneously breathing patients are often even more efficient on the ventilator provided that the ventila- [Pg.296]


Bauer, M.A., M.J.Utell, P.E.Morrow, D.M.Speers, and F.R.Gibb. 1985. Route of inhalation influences airway responses to 0.30 ppm nitrogen dioxide in asthmatic subjects. Am. Rev. Respir. Dis. 131 A171. [Pg.263]

Air may enter the respiratory passages via the nose or mouth (Fig. 1), although— as a result of anatomical differences— babies rarely breathe through their mouths until at least 3-6 months of age (20,21). The route of inhalation during aerosol therapy is therefore difficult to standardize until children are old enough to use a mouthpiece, which is usually around 3 years of age. [Pg.53]

Titanium tetrachlorine (TiCI ) has a molecular weight of 189.7. NIOSH lists 10 mg/m as the lowest lethal concentration for mice by oral route of inhalation. It is highly corrosive and presents a special hazard because it reacts violently with water to liberate heat and produce hydrochloric acid. When it comes in contact with the skin, the chemical should be wiped dry. A splash of the liquid in an eye may lead to permanent eye structure damage. [Pg.103]

Hydraziae is toxic and readily absorbed by oral, dermal, or inhalation routes of exposure. Contact with hydraziae irritates the skin, eyes, and respiratory tract. Liquid splashed iato the eyes may cause permanent damage to the cornea. At high doses it can cause convulsions, but even low doses may result ia ceatral aervous system depressioa. Death from acute exposure results from coavulsioas, respiratory arrest, and cardiovascular coUapse. Repeated exposure may affect the lungs, Hver, and kidneys. Of the hydraziae derivatives studied, 1,1-dimethylhydrazine (UDMH) appears to be the least hepatotoxic monomethyl-hydrazine (MMH) seems to be more toxic to the kidneys. Evidence is limited as to the effect of hydraziae oa reproductioa and/or development however, animal studies demonstrate that only doses that produce toxicity ia pregaant rats result ia embryotoxicity (164). [Pg.288]

Health and Safety Factors. Magnesium hydroxide is not absorbed by the skin. Dry magnesium hydroxide may irritate the eyes, skin, nasal passages, and respiratory tract. Routes of body entry are skin contact, eye contact, inhalation, and ingestion. No LD q values for Mg(OH)2 are available. [Pg.351]

Inhalation is the chief route of worker exposure. Comparative data from acute or subchronic inhalation exposures with rats (98) indicate that nitromethane and nitroethane are the least toxic of the nitroparaffins by this route and do not induce methemoglobin formation. The nitropropanes are less well tolerated 2-nitropropane is more toxic than 1-nitropropane and is more likely to cause methemoglobinemia. [Pg.103]

In order to induce a toxic effect, local or systemic, the causative material must first come into contact with an exposed body surface these are the routes of exposure. In normal circumstances, and depending on the nature of the material, the practical routes of exposure are by swallowing, inhalation, and skin and eye contact. In addition, and for therapeutic purposes, it may be necessary to consider intramuscular, intravenous, and subcutaneous injections as routes of adininistration. [Pg.229]

Human incidents have been reported in workers involved in the production or uses of PCNs. In the United States as well as in Germany and Austraha, the severity of the PCN-induced toxicosis was higher after exposure to the higher chlorinated PCN mixtures. In humans the inhalation of hot vapors was the most important route of exposure and resulted in symptoms including rashes or chloracne, jaundice, weight loss, yellow atrophy of the hver, and in extreme cases, death (75,77—79). [Pg.67]

The primary routes of entry for animal exposure to chromium compounds are inhalation, ingestion, and, for hexavalent compounds, skin penetration. This last route is more important in industrial exposures. Most hexavalent chromium compounds are readily absorbed, are more soluble than trivalent chromium in the pH range 5 to 7, and react with cell membranes. Although hexavalent compounds are more toxic than those of Cr(III), an overexposure to compounds of either oxidation state may lead to inflammation and irritation of the eyes, skin, and the mucous membranes associated with the respiratory and gastrointestinal tracts. Skin ulcers and perforations of nasal septa have been observed in some industrial workers after prolonged exposure to certain hexavalent chromium compounds (108—110), ie, to chromic acid mist or sodium and potassium dichromate. [Pg.141]

Carcinogenicity of DGEBPA or DGEBPA-based resins, as measured by topical appHcation, has not been shown by a majority of the studies (45). Advanced DGEBPA resins exhibit low systemic toxicity either by dermal or oral routes and inhalation of these resins is unlikely because of low volatihty. The acute oral LD q in rats has been reported to be >2000 mg/kg (46). Acute dermal studies show these materials have alow potential for absorption through the skin in acutely toxic amounts. No evidence of carcinogenicity has been found in animals or humans for advanced DGEBPA resins (47,48). [Pg.370]

Toxic hazards may be caused by chemical means, radiation, and noise. Routes of exposure are (1) eye contact, (2) inhalation, (3) ingestion, (4) skin contact, and (5) ears (noise). An Industrial Hygiene Guide (IHG) is based on exposures for an 8-h day, 40-h week, and is not to be used as a guide in the control of health hazards. It is not to be used as a fine hne between safe and dangerous conditions. [Pg.2306]

For most ehemieals, inhalation is the main route of entry into the body. Penetration via damaged skin (e.g. euts, abrasions) should, however, be avoided. Certain ehemieals (e.g. phenol, aniline, eertain pestieides) ean penetrate intaet skin and so beeome absorbed into the body. This may oeeur through loeal eontamination, e.g. from a liquid splash, or through exposure to high vapour eoneentrations. Speeial preeautions to avoid skin eontaet are required with these ehemieals and potential exposure via skin absorption has to be taken into aeeount when assessing the adequaey of eontrol measures. [Pg.83]

Handling hazardous ehemieals has beeome part of most people s everyday living. Just eonsider gasoline, and how most people fill their own tanks. In the manufaeturing arena, ehemieals are eommonplaee. On hazardous waste sites there are a variety of unknown ehemieal substanees and other hazards that may take the form of a solid, liquid, or gas. The eflfeets of exposure to toxie ehemieals may either be immediate (e.g., aeid burns) or delayed (e.g., lung damage from inhaling asbestos). There are four routes of ehemieal exposure that exist ... [Pg.78]

Industrial environments expose individuals to a plethora of airborne chemical compounds in the form of vapors, aerosols, or biphasic mixtures of both. These atmospheric contaminants primarily interface with two body surfaces the respiratory tract and the skin. Between these two routes of systemic exposure to airborne chemicals (inhalation and transdermal absorption) the respiratory tract has the larger surface area and a much greater percentage of this surface exposed to the ambient environment. Or dinary work clothing generally restricts skin exposures to the arms, neck, and head, and special protective clothing ensembles further limit or totally eliminate skin exposures, but breathing exposes much of the airway to contaminants. [Pg.195]

As stated earlier, inhalation is the main route of absorption for occupational exposure to chemicals. Absorption of gaseous substances depends on solubility ifi blood and tissues (as presented in Sections 2.3.3-2.3.5), blood flow, and pulmonary ventilation. Particle size has an important influence on the absorption of aerosols (see Sections 2.3.7 and 3.1.1). [Pg.263]

Another difficulty comes from the consideration of the route of entry (sf the contaminant, as chemicals can enter the body by various routes and the human body responds to the action of a toxic agent primarily on the basis of the rate and route of exposure. Without any doubt, the most important route of exposure at the workplace is inhalation, and this should be the route used to set OELs. However, if there is a threat of significant exposure by other routes, such as cutaneously (including mucous membranes and the eyes), either by contact with vapors or by direct skin contact w ith the substance, additional recommendations may be necessary. [Pg.365]

Route of entry Path by which toxins and other substances may enter the human body. These include inhalation, ingestion, and absorption through the skin. Less common routes include injection and absorption through moist surfaces surrounding the eyes and ear canal. [Pg.1473]

To help public health professionals and others address the needs of persons living or working near hazardous waste sites, the information in this section is organized first by route of exposure (inhalation, oral, and dermal) and then by health effect (death, systemic, immunological, neurological, reproductive, developmental, genotoxic, and carcinogenic effects). These data are discussed in terms of three exposure periods acute (14 days or less), intermediate (15-364 days), and chronic (365 days or more). [Pg.39]

Estimates of exposure levels posing minimal risk to humans (Minimal Risk Levels or MRLs) have been made for methyl parathion. An MRL is defined as an estimate of daily human exposure to a substance that is likely to be without an appreciable risk of adverse effects (noncarcinogenic) over a specified duration of exposure. MRLs are derived when reliable and sufficient data exist to identify the target organ(s) of effect or the most sensitive health effect(s) for a specific duration within a given route of exposure. MRLs are based on noncancerous health effects only and do not consider carcinogenic effects. MRLs can be derived for acute, intermediate, and chronic duration exposures for inhalation and oral routes. Appropriate methodology does not exist to develop MRLs for dermal exposure. [Pg.40]

Deaths following exposure to methyl parathion occurred in children (two sisters, aged 4 and 11 years). Exposure was by multiple routes including inhalation of methyl parathion that was sprayed inside a house from a solution containing 4% methyl parathion (1.25% methyl parathion was recommended by a manufacturer for field spraying). Thirteen days after spraying, the house air contained 0.041 mg/m, ... [Pg.41]

Figure 3-5 graphically depicts the information that currently exists on the health effects of methyl parathion in humans and animals by various routes of exposure. The available literature reviewed concerning the health effects of methyl parathion in humans described case reports of longer-term studies of pesticide workers and case reports of accidental or intentional ingestion of methyl parathion. The occupational exposure is believed to be via the dermal and inhalation routes. The information on human exposure is limited in that the possibility of concurrent exposure to other pesticides or other toxic substances cannot be quantified. [Pg.120]


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See also in sourсe #XX -- [ Pg.71 ]




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