Lungs chronic toxicity

Recycling of printer circuit boards is deemed as the most important source of heavy metals to the ambient environment. These heavy metals may be entering into human body from various exposure routes such as ingestion, inhalation, and dermal absorption. Exposure to high levels of heavy metals can lead to acute and chronic toxicity, such as damage to central and peripheral nervous systems, blood composition, lungs, kidneys, liver, and even death [14],... 

In summary, fires represent a particularly complex problem for toxicologists. The exposure atmospheres are a mixture of many substances, and no two fires are alike. One aspect of the mixture that has received relatively little attention is the particulate component of smokes. From studies on carbon black and on soot in diesel exhaust we now have information on the chronic toxicity of soot. An area in which we need additional information is the potential for fire-generated soot to adsorb toxic materials, and then to deposit and desorb such materials in the lung. For this information we must await the results of future research. 

According to Stokinger, at least three effects of long-term exposure to ozone have been recc ized effects on morphology and function of the lung, lung-tumor acceleration, and aging. An additional effect, the development of tolerance after exposure to low concentrations of ozone, may also be related to chronic toxicity. 

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. 

Talc Lung tumors in female rats Related to high dose level and resulting chronic toxicity [57]... 

In chronic toxicity studies, liver and kidneys were the principal target organs. Exposure to 1,2-dichloroethane by gavage for 78 weeks induced a significant increase in the incidence of tumors at several sites in both rats and mice. Inhalation exposure of rats or mice did not show significant increases in tumor incidence. However, repeated dermal or intraperitoneal application of 1,2-dichloroethane resulted in an increase in lung tumors in mice. 

Chronic toxicities following exposure include shortness of breath and pulmonary edema, which may progress to respiratory infections, reduction in the blood s oxygen carrying capacity, lung disorders, eye damage, and digestive disorders. 

Chronic toxicity of Telone II following gavage dosing (3 times/week) for two years in Fischer 344 rats and/or B6C3Fi mice included neoplasms (forestomach, liver, lung, urinary bladder), epithelial hyperplasia (forestomach, urinary bladder) and hydronephrosis (43,46,47). 

Waalkes MP and Rehm S (1994) Chronic toxic and carcinogenic effects of cadmium chloride in male DBA/2NCr and NFS/NCr mice strain-dependent association with tumors of the hematopoietic system, injection site, liver, and lung. Fundam Appl Toxicol 23 21-31. 

Chronic Toxicity. According to the U.S. Department of the Army (DA 1990b), chronic exposure to HT can cause sensitization and chronic lung impairment (cough, shortness of breath, chest pain) however, epidemiological data or experimental animal data to evaluate dose-response functions for such effects were not found in the available literature. 

Chronic Toxicity. According to the U.S. Department of the Army (DA 1990b), chronic exposure to HT can cause sensitization and chronic lung impair-... 

Przybylowski, J., Zajusz, K., Chronic Toxic Action of Leaded Gasoline 78 Vapors. 2. Changes in the Lungs and Heart, Biul. Sluzby Sanit. Epidemiol. Wojewodztwa Katowickiego 17 [1973] 47/50 C.A. 81 [1974] No. 146499. 

For a health hazard to exist, there must be a contaminant pathway from the soil to the biota. Firstly the contaminant must reach the location of the target biota, and secondly, it must be able to enter the target biota. Both mobility and bioavailability depend strongly on chemical speciation (the chemical form in which the contaminant metal is present). Hazard via aqueous pathways will be low where contaminants are only released slowly from particles, or in non-bioavailable dissolved forms. However, poorly soluble metal compounds are often chronically toxic by inhalation, because particles have a long residence time in the lungs. 

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