Route of entry inhalation

Route Dependent Toxicity. The toxicity of trichloroethylene does not seem to be heavily dependent upon its route of entry. Inhalation and ingestion are the primary exposure routes, and the liver, heart, and central nervous system are the primary targets for both routes (Candura and Faustman 1991). Renal toxicity results principally from oral exposure, and dermal exposure generally confines its toxic effects to the skin, although broad systemic effects can be induced imder conditions of high exposure (Bauer and Rabens 1974). Attributing such effects solely to dermal exposure, however, is difficult because inhalation exposure is often a factor in these cases as well. 

Total human exposure Accounts for all exposures a person has to a specific contaminant, regardless of environmental medium or route of entry (inhalation, ingestion and dermal absorption). Sometimes, total exposure is used incorrectly to refer to exposure to all pollutants in an environment. Total exposure to more than one pollutant should be stated explicitly as such (NRC, 1991). 

Exposure or exposed means that an employee is subjected to a hazardous chemical in the course of employment through any route of entry (inhalation, ingestion, skin contact or absorption, etc.), and includes potential (e.g. accidental or possible) exposure. 

Exposure or exposed means that an employee is subjected to a toxic substance or harmful physical agent in the course of employment through any route of entry (inhalation, ingestion, skin contact or absorption, etc.) and includes past exposure and potential (e.g., accidental or possible) exposure, but does not include situations where the employer can demonstrate that the toxic substance or harmful agent is not used, handled, stored, generated, or present in the workplace in any manner different from typical non-occupational situations. 

The route of entry section describes the primary pathway by which the chemical enters the body. There are three principal routes of entry inhalation, skin, and ingestion. 

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. 

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. 

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. 

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. 

Where sufficient toxicologic information is available, we have derived minimal risk levels (MRLs) for inhalation and oral routes of entry at each duration of exposure (acute, intermediate, and chronic). These MRLs are not meant to support regulatory action but to acquaint health professionals with exposure levels at which adverse health effects are not expected to occur in humans. They should help physicians and public health officials determine the safety of a community living near a chemical emission, given the concentration of a contaminant in air or the estimated daily dose in water. MRLs are based largely on toxicological studies in animals and on reports of human occupational exposure. 

L-l is a vesicant (blister agent) also, it acts as a systemic poison, causing pulmonary edema, diarrhea, restlessness, weakness, subnormal temperature, and low blood pressure. In order of severity and appearance of symptoms, it is a blister agent, a toxic lung irritant, absorbed in tissues, and a systemic poison. When inhaled in high concentrations, it may be fatal in as short a time as 10 min. L-1 is not detoxified by the body. Common routes of entry into the body include ocular, percutaneous, and inhalation. 

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... 

All these entry routes are controlled by the application of proper industrial hygiene techniques, summarized in Table 2-1. These control techniques are discussed in more detail in chapter 3 on industrial hygiene. Of the four routes of entry, the inhalation and dermal routes are the most significant to industrial facilities. Inhalation is the easiest to quantify by the direct measurement of airborne concentrations the usual exposure is by vapor, but small solid and liquid particles can also contribute. 

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