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Respiratory system occupational

Respiratory System. Occupational exposure to metals in the form of metal dust makes the respiratory system a likely target. Acute exposure may cause irritations and... [Pg.50]

As is the case with the skin, the lungs are in constant contact with the external environment [16]. Exposure to the toxins in cigarette smoke is one of the most common causes of congestive, obstructive damage in the respiratory system. Occupational exposure to asbestos and medically necessary exposure to drugs such as cyclophosphamide and carmustine can also cause lung injury. Inhalations of coal dust and cotton fibers are other occupational hazards to the lungs. [Pg.9]

In a nested case-control study of cancers associated with chemical exposures in the wood industry, Kauppinen et al. (1986) found a significantly increased risk of respiratory system cancer associated with exposure to phenol and phenol in wood dust. As is often the case in occupational settings, these exposures were confounded by smoking and exposures to other materials like pesticides. The increased risk observed for exposure to phenol was almost 5-fold (odds ratio of 4.94), but showed no dose-related increase. This risk dropped to 4-fold with adjustments for smoking history, and to less than 3-fold (and non-significant) when workers exposed to both phenols and pesticides were excluded from the analysis. [Pg.53]

Some occupational situations, if inadequately controlled, can create opportunities for damage to the respiratory system. Exposure to certain forms of the metals nickel and cadmium, ordinarily as airborne particulates, can cause cellular damage, edema, and, if sustained for sufficiently long periods, emphysema. Many other metals, usually only in some of their many chemical forms, can produce emphysema upon subchronic or chronic exposure. [Pg.109]

Heuper, W. C. (1966). Occupational and Environmental Cancer of the Respiratory System. Springer-Verlag, New York. [Pg.156]

Hueper, W.C. Occupational and Environmental Cancers of the Respiratory System. (Recent Results in Cancer Research, v. 3) New York Springer-Verlag. 1966. p. 103-105. [Pg.130]

Kazuyuki 0, Higashi T, Nakadate T, et al. 1992. Fom year follow-up of effects toluene diisocyanate exposure on the respiratory system in polyurethane foam manufacturing worker. Int Arch Occup Environ Health 63 565-569. [Pg.173]

The LD50 (rat, oral) of sodium carbonate peroxohydrate is 1034 mg/kg. The occupational exposure limit is 10 mg/m3 per 40-hour week. The compound is a skin and eye irritant inhalation of dust can cause irritation to the mucous membranes and the respiratory system. Decomposition in the presence of organic material can be rapid and highly exothermic. [Pg.1229]

Mercury exists in the environment in three main chemical forms elemental mercury (Hg°), inorganic mercurous (Hg+) and mercuric (Hg2+) salts, and organic methylmer-cury (CH3Hg) and dimethylmercury (CH3HgCH3) compounds. Elemental mercury, in the form of mercury vapor, is almost completely absorbed by the respiratory system, whereas ingested elemental mercury is not readily absorbed and is relatively harmless. Once absorbed, elemental mercury can cross the blood-brain barrier into the nervous system. Most exposure to elemental mercury tends to be from occupational sources. [Pg.52]

Occupational exposure to chromium(VI) compounds in a number of industries has been associated with increased risk of respiratory system cancers, primarily bronchogenic and nasal. Among the industries investigated in retrospective mortality studies are chromate production, chromate pigment production and use, chrome plating, stainless steel welding, ferrochromium alloy production, and leather tanning. [Pg.80]

Table 9-2 also presents data from occupational and epidemiologic studies that indicate that the respiratory system is the primary target for sulfur dioxide. There was variability in the study findings that probably resulted from a lack of adequate analytical measurements (use of area sampling rather than personnel monitoring) the multiplicity of confounding, concurrent exposures to other chemicals and participates and the study indices investigated. However, some reasonable correlations between effects reported and exposure bounds can be determined. [Pg.289]

Several in vivo and in vitro studies conclusively demonstrate that benzene can be absorbed through human skin (Blank and McAuliffe 1985 Franz 1984 Susten et al. 1985 Tsuruta 1989). In general, skin absorption is considered a minor source of concern in the occupational environment as it occurs at a much lower rate and extent compared with benzene absorption through the respiratory system (OSHA 1989). However, benzene absorption through the skin as a result of benzene contamination in rubber solvents is a major route of exposure in tire building operations (Susten et al. 1985). Benzene is an irritant to the skin and, by defatting the keratin layer, may cause erythema, vesiculation, and dry and scaly dermatitis... [Pg.191]

Toxicity and health effects Prolonged occupational exposure to sec-butyl acetate affects health. The symptoms of toxicity include irritation of the skin and eyes. Exposure to high concentrations of sec-butyl acetate irritates the nose and throat, causing coughing and respiratory distress, headache, nausea, vomiting, dizziness, drowsiness, and coma. After prolonged exposure to sec-butyl acetate, industrial workers show symptoms of severe irritation to eyes, headache, drowsiness, dryness in the upper respiratory system and skin, and narcosis. [Pg.57]

Chronic occupation-related exposure is associated with significant excess mortality from cancer of the respiratory system and of the prostate. Depending on the segment of the population considered, the respiratory cancer risk for coke oven workers was as high as 4.5 times the risk for nonoven workers. To evaluate a biologically effective exposure dose in human biomonitoring studies, DNA carcinogen adduct analysis is frequently used. [Pg.637]

Furfural can cause skin sensitization and has been shown to cause irritant dermatitis which may become eczematous. It can be absorbed through the skin or by inhalation and it is an irritant to the eyes, skin, and respiratory system. No throat or eye irritation was noted in humans exposed to 10 ppm for 8h or 20 ppm for 4h. No data are available relative to reproductive or developmental effects in humans exposed to furfural. When air concentrations reach from 2 to 14 ppm, headaches, itching of the throat, and red/weeping eyes occurred in exposed humans. If exposures are severe, respiratory tract irritation can progress to acute respiratory distress syndrome, which may be delayed in its onset by up to 72 h. The National Institute for Occupational Safety and Flealth has indicated that 100 ppm in air is a concentration immediately dangerous to life or health. [Pg.1206]

Acute NP exposure, such as may occur in occupational settings, can produce severe irritation to the eye, skin, and respiratory system. Symptoms of such acute toxicity include a burning sensation, cough, labored breathing, sore throat, unconsciousness, abdominal pain, diarrhea, nausea, skin irritation, and burns. Other than these acute effects, there is no conclusive evidence that typical exposure to NP causes adverse health effects in humans. [Pg.1846]

Results of an epidemiological study indicated that chronic, occupational exposure to vinyl acetate at concentrations below 22 ppm is not likely to result in irritation of the upper respiratory system. In addition, no chronic adverse effects were reported for chronic exposures to concentrations between 5 and 10 ppm. Chronic exposures to moderate and high doses have been shown to produce damage and... [Pg.2825]

Fly ash from municipal waste and industrial waste incinerators contains polychlorinated dibenzo-p-dioxins (PCDDs), including tetrachlorodibenzo-/j-dioxin (TCDD) and polychlorinated dibenzofurans (PCDFs), which are lipophiles, and heavy metals, including chromium, copper, manganese, vanadium, and lead, which are hydrophilesJ29-31 These chemicals have multiple toxicities and are known to impact the human liver, immune system, respiratory system, thyroid, male reproductive function, and CNS J32 34l Several are human carcinogensJ32 35 Enhanced toxic effects are observed in the mixtures of some of theseJ21,22 36 The mixtures of toxicants present in fly ash are complex and the mechanisms for their action on the human body are largely unknown. It is known that occupational exposure to fly... [Pg.202]

Some occupational situations, if inadequately controlled, can create opportunities for similar damage to the respiratory system. Exposures... [Pg.54]

Acute-Duration Exposure. Sufficient information is available from occupationally exposed humans to identify the respiratory system as a target organ following acute inhalation exposure (Levy et al. [Pg.47]

No MRLs were derived for inhalation exposure to selenium because of insufficient quantitative data concerning both human and animal exposures. Data on the health effects of inhaled selenium in humans are derived from studies of occupationally exposed workers. These studies suggest that the respiratory system is the most sensitive end point for inhaled selenium dust, but they do not provide quantitative measurements of exposure and are frequently confounded by concurrent exposure to other chemicals. Animal studies support the respiratory system as the target of selenium toxicity, but these are acute studies of exposure to high concentrations of selenium that also produced serious health effects and death. [Pg.35]

Respiratory Effects. In humans, the respiratory system is the primary site of injury after inhalation of elemental selenium or selenium compounds. The largest number of reported human exposures occurred in occupational settings, especially in industries that extract, mine, treat, or process seleniumbearing minerals and in industries that use selenium or selenium compounds in manufacturing. The... [Pg.45]

Ventilated- faceplate Series of individual respiratory systems (or masks) serviced by a common filter. Clean working area subject to inadvertent entry of contamination. High work rate, reduced breathing resistance. Frequent entry and exit movements. Brief inside occupation. Infantry fighting vehicles. Seif-propeiied howitzers. [Pg.103]

Inhalation is a prominent pathway for radiation dose contributions from environmental or occupational intake of radioactive iodine. The ability to model and predict the kinetics of iodine in the body can be used for internal dosimetric assessments that predict the radiation dose delivered to various tissues. These assessments may be used to assess risk to the individual from inhalation intakes of radioactive iodine, which may occur through two distinct processes depending on its physical form. Iodine bound to particulates may be deposited in the respiratory tract, and iodine gas may be taken up by various tissues in the respiratory system during the breathing cycle. Inhalation models are necessary for estimates of iodine uptake and deposition that may result in radiation dose to workers or members of the public. [Pg.260]


See other pages where Respiratory system occupational is mentioned: [Pg.97]    [Pg.236]    [Pg.22]    [Pg.129]    [Pg.652]    [Pg.123]    [Pg.48]    [Pg.55]    [Pg.288]    [Pg.242]    [Pg.43]    [Pg.78]    [Pg.69]    [Pg.427]    [Pg.2265]    [Pg.264]    [Pg.47]    [Pg.662]    [Pg.463]    [Pg.254]    [Pg.801]    [Pg.18]   


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Respiratory system

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