Toxic chemicals organism

Many of the factors that can affect organisms adversely are inherent stressors, including availability of nutrition, water quality, temperature and other climatic extremes, disease, and predation. It is important to be able to separate effects of inherent stressors from those of toxic chemicals. There are often important synergistic relationships between inherent stressors and the effects of toxic chemicals. Organisms that are under stress from inherent stressors are likely to be more susceptible to the effects of xenobiotic toxicants. 

For organic toxic chemicals and their degradation products the number of possibilities is very high. The environmental samples composition usually is very complicated. Unambiguous identification needs serial-pai allel strategy of analysis with many-stage crosschecking of data. 

In nonindustrial settings, MCS substances are the cause of indoor air pollution and are the contaminants in air and water. Many of the chemicals which trigger MCS symptoms are known to be irritants or toxic to the nervous system. As an example, volatile organic compounds readily evaporate into the air at room temperature. Permitted airborne levels of such contaminants can still make ordinary people sick. When the human body is assaulted with levels of toxic chemicals that it cannot safely process, it is likely that at some point an individual will become ill. For some, the outcome could be cancer or reproductive damage. Others may become hypersensitive to these chemicals or develop other chronic disorders, while some people may not experience any noticeable health effects. Even where high levels of exposure occur, generally only a small percentage of people become chemically sensitive. 

Creosote is a complex mixture of toxic chemicals, which can have both immediate and chronic effects on exposed organisms. PIC of creosote are of particular concern due to long half-lives of some chemicals, and because of multiple pathways to the environment from ash and soot. 

Inhalation is the most rapid route, immediately introducing toxic chemicals to respiratory tissues and the bloodstream. Once admitted to the blood through the lungs, these chemicals are quickly transported throughout the body to contact all organs. In many cases, chemicals accumulate in a target organ. 

Professional society of persons conducting research in occupational safety and health or responsible for implementing industrial hygiene programs in governmental and industrial organizations. Establishes exposure limits for toxic chemicals used in the workplace. 

Hazardous chemicals is a broad categoiy that includes chemicals that may be toxic, flammable, corrosive, explosive, or luirmful to tlie environment. A toxic chemical is one type of a hazardous chemical. Toxic chemicals cause adverse health effects, such as severe illness or deatli, when ingested, inltaled, or absorbed by a lii ing organism. 

G.24 The concentration of toxic chemicals in the environment is often measured in parts per million (ppm) or even parts per billion (ppb). A solution in which the concentration of the solute is. 1 ppb by mass has. 3 g of the solute for every billion grams (1000 t) of the solution. The World Health Organization has set the acceptable standard for lead in drinking water at... 

Toxicokinetics Relating to the fate of toxic chemicals within living organisms— that is, questions of uptake, distribution, metabolism, storage, and excretion factors that determine how much of a toxic form reaches the site of action. 

Cronin MTD, Netzeva TI, Dearden JC, Edwards R, Worgan ADR Assessment and modeling of the toxicity of organic chemicals to Chlorella vulgaris development of a novel database. Chem Res Toxicol 2004 17 545-54. 

The complex outer layers beyond the peptidoglycan in the Gram-negative species, the outer membrane, protect the organism to a certain extent from the action of toxic chemicals (see Chapter 13). Thus, disinfectants are often effective only at concentrations higher than those affecting Gram-positive cells and these layers provide unique protection to the cells from the action of benzylpenicillin and lysozyme. 

For some toxins it is possible to demonstrate an apparent improvement in functional response at levels of exposure which are below a threshold. This effect, which has been termed hormesis , is most effectively demonstrated in the consistently improved longevity of animals whose caloric intake is restricted rather than allowing them to feed ad lib (Tannenbaum, 1942). Clearly in this instance, the observed effects are the result of exposure to a complex mixture of chemicals whose metabolism determines the total amount of energy available to the organism. But it is also possible to show similar effects when single chemicals such as alcohol (Maclure, 1993), or caffeic acid (Lutz et al., 1997) are administered, as well as for more toxic chemicals such as arsenic (Pisciotto and Graziano, 1980) or even tetrachloro-p-dibenzodioxin (TCDD) ( Huff et al., 1994) when administered at very low doses. It is possible that there are toxins that effect a modest, reversible disruption in homeostasis which results in an over-compensation, and that this is the mechanism of the beneficial effect observed. These effects would not be observed in the animal bioassays since to show them it would be necessary to have at least three dose groups below the NOAEL. In addition, the strain of animal used would have to have a very low incidence of disease to show any effect. 

Measurement of exposure can be made by determining levels of toxic chemicals in human serum or tissue if the chemicals of concern persist in tissue or if the exposure is recent. For most situations, neither of these conditions is met. As a result, most assessments of exposure depend primarily on chemical measurements in environmental media coupled with semi-quantitative assessments of environmental pathways. However, when measurements in human tissue are possible, valuable exposure information can be obtained, subject to the same limitations cited above for environmental measurement methodology. Interpretation of tissue concentration data is dependent on knowledge of the absorption, excretion, metabolism, and tissue specificity characteristics for the chemical under study. The toxic hazard posed by a particular chemical will depend critically upon the concentration achieved at particular target organ sites. This, in turn, depends upon rates of absorption, transport, and metabolic alteration. Metabolic alterations can involve either partial inactivation of toxic material or conversion to chemicals with increased or differing toxic properties. 

A variety of chemicals may be leached from the aerial portions of plants by rainwater or by fog-drip (16) including organic acids, sugars, amino acids, pectic substances, gibberellic acids, terpenoids, alkaloids, and phenolic compounds. Colton and Einhellig (17) suggested that leaf leachates of velvetleaf (Abutilon theophrasti) may be inhibitory to soybean (Glycine maxT We have recently discovered specialized hairs on the stems of velvetleaf plants which exude toxic chemicals. 

Minimization of agricultural losses from soil toxins Toxins from soils appear to be responsible for inhibition of nitrogen fixation, metabolism and nodulation in legumes. Removal of toxins could be achieved by proper adsorption techniques and also by growing companion plants that contribute organic matter to microoranisms which help to destroy or degrade toxic chemicals. 

If we assume that those peculiarities of the toxin which cause their distribution are localized in a special group of the toxin molecules and the power of the organs and tissues to react with the toxin are localized in a special group of the protoplasm, we arrive at the basis of my side chain theory. The distributive groups of the toxin I call the haptophore group and the corresponding chemical organs of the protoplasm the receptor. . .. Toxic actions can only occur when receptors fitted to anchor the toxins are present. 

Working groups were organized with specific responsibility to assess the utility and limits of four different methods (or tools) currently used by EPA and industry for evaluating hazards posed by toxic chemicals (1) laboratory toxicity data, (2) microcosm test data, (3) site-specific data, and (4) chemical fate and exposure model results. The Exposure Modeling Committee (3.) report presented an assessment of the current extent of field model testing and recommendations for future testing efforts. 

Rosen JF, Chesney RW, Hamstra AJ, et al. 1981. Reduction in 1,25-dihydroxyvitamin D in children with increased lead absorption. In Brown SS, Davis DS, eds. Organ-directed toxicity Chemical indices and mechanisms. New York, NY Pergamon Press, 91-95. 

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