Effects toxic

In acute poisoning with colchicine, there is hemorrhagic gastroenteritis, extensive vascular damage, nephrotoxicity, muscular depression, and an ascending paralysis of the central nervous system. 

Colchicine produces a temporary leukopenia that is soon replaced by a leukocytosis, sometimes because of a striking increase in the number of basophilic granulocytes. The site of action is apparently directly on the bone marrow. Myopathy and neuropathy also have been noted with colchicine treatment, especially in patients with decreased renal function. Long-term administration of colchicine entails some risk of agranulocytosis, aplastic anemia, myopathy, and alopecia azoospermia has also been described. 

Examples of teratogens include thalidomide, ethyl alcohol, and o-benzoic sulfim-ide (the artificial sweetener saccharin). Thalidomide is a drug that was used in the 1960s as a treatment for morning sickness in pregnant mothers. However, the toxic effects were discovered too late for 10,000 babies who were bom with various malformations. In Japan, where fish is a staple food, mothers ate fish contaminated with mercury compounds, causing children to be bom with cerebral palsy. 

Ethyl alcohol is found in alcoholic beverages and is a known teratogenic material, which is the reason doctors tell pregnant women not to drink alcohol. When a mother drinks, the unborn child drinks as well. Ethyl alcohol causes growth failure and impaired brain development. Unborn children exposed to alcohol may suffer the effects of Eetal Alcohol Syndrome when they are bom. Symptoms of Fetal Alcohol Syndrome include sleep disturbance, jitteriness, a higher incidence of impaired vision and hearing, lack of motor coordination, balance problems, abnormal thyroid function, and a decrease in immune system effectiveness. Additional teratogens include heavy metals, methyl mercury, mercury salts, lead, thallium, selenium, penicillin, tetracyclines, excess Vitamin A, and carbon dioxide. 

Class 6.2 infectious substances are the last type of toxic effect that will be presented here. Etiological toxins are among the most poisonous materials known. For example, the bacterium Clostridium botulinum, the cause of botulism, is a single cell that can release a toxin so potent that four-hundred thousandths of an ounce is enough to kill 1,000,000 laboratory guinea pigs. 

Infectious medical waste is a DOT Class 6.2 Infectious Substance. 

Response of an individual plant or animal species to a chemical is based on concentration length, type, and route of exposure and susceptible target organ. 

It was also found that the bio concentration potential is dependent on the age, sex, and species of the aquatic organisms. Many of these factors can be eliminated if the test is performed under identical conditions with the organisms of the same species, strain, sex, age, etc. or if the bio concentration factor is related to the lipid content of the organism (see Sect. 5.4). Some other important factors which may affect the bio concentration potential of chemicals in fish and other aquatic organisms are the toxic effects, bio availability, concentration of the chemicals in water, pH of the water, and especially the lipid content of the organisms. These factors will be discussed in more detail in the following sections. 

It was found that adverse effects, disease and mortality in both treated and control fish can influence the kinetics of the chemical in fish. Mortality, therefore, should normally be 10% at the end of the test. Geyer et al. [29] found that the elimination rate of a chemical in aquatic gill-breathing animals is greater, if toxic effects occur and especially if the lipid content is decreasing during the test. That means that the half-life (ti/2) and the bioconcentration factor of a chemical is smaller if the concentration in the water is so high that toxic effects occur. Therefore, the concentration of the test chemical in the water has to be so low that 

Biotic factors which can influence the lipid content of the organisms are numbers A. (1) to 

Extreme caution is necessary in the measurement of dosage inadvertent overdose may lead to an irreversible insulin shock. Serious consequences may result if insulin is not used under constant medical supervision if an overdose is untreated, hypoglycaemia may lead to convulsions and coma which should not be confused with hyperglycaemic coma. 

In acute, usually suicidal, overdoses of insulin, successful management has included excision of the injection site. 

Another concern is the fear that, since the vitamin is metabolised mainly via ethanedioic (oxalic acid), a high dose might lead to the formation of kidney stones. While there is no clear evidence that this occurs, and the phenomenon has been described as a myth, the commonsense advice is for those prone to recurrent stone formation or suffering from any renal impairment to avoid high doses which also exacerbate acidosis in chronic renal disease and renal tubular acidosis. Sustained hyperoxaluria has been found only rarely to accompany an excessive ingestion of vitamin C. 

In some cases megadoses in the range 1-2 g per day have produced mild ill effects of the intestinal tract including discomfort, pain, and osmosis diarrhoea. Realistically diarrhoea is almost certainly the only major side effect of over large doses for the otherwise healthy. 

Dietary levels in excess of600 mg per day were found to decrease the oxidase activity of human serum ceruloplasmin. It was suggested that this may be due to dissociation of the copper co-factor but no suggestion is made as to whether this may lead to illness like Wilson s disease in which ceruloplasmin levels are reduced and excess copper is deposited in the tissues. Very recent work has shown an enhanced uptake of copper from ceruloplasmin by human cells treated with both L-ascorbate and its D-isomer. 

Reference has already been made to the widespread practice of 

As has been remarked elsewhere, some higher authority ordered the deletion of the gene many millions of years ago which makes man a 

Endocrine toxins can be broadly categorized as those that exert a direct effect on the hormone-receptor mechanism or those that act via an indirect action. These include (Thomas 1994, 1995, 1998 Harvey 1996 Atterwill and Cockburn 1997 Capen 1997 Thomas and Colby 1997 Harvey, Rush, and Cockburn 1999 Rosol et al. 2001 Houck and Kavlock 2008). These include  

Age is an important factor in the assessment of toxic effects on endocrine organs. The developing endocrine system in immature animals appears to be generally more susceptible to toxic compounds than in mature animals— particularly the pituitary-gonadal axis. For some studies, it may be preferable to use male rather than female animals, thus avoiding the several metabolic effects of the estrus cycle. 

An endocrine disrupter is an exogenous xenobiotic or mixture absorbed into the body that disturbs the endocrine system by altering normal hormone levels, halting 

Compounds that are endocrine disrupters include natural animal hormones released into the environment, plant toxins or phytoestrogens, synthetic hormones present in sewage water and used for medical treatment (e.g., diethylstilbestrol), and several chemicals, including some pesticides and polychlorinated biphenols (PCBs). Endocrine disrupters enter the environment often as a by-product of many chemical and manufacturing processes and through waste disposal routes. Some evidence now suggests that effects of thyroid hormones and the immune system occur in addition to the disruptions of hormones that play a major part in the control of reproduction and development. 

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To acquire an overview of methods and examples of some pitfalls in modeling log P, log S, and the toxic effects of compounds... 

Table 3. Toxic Effects of Furfural and Main Derivatives ...

Registry of Toxic Effects of Chemical Substances (RTECS) On-Liae Database. National Library of Mediciae, Bethesda, Maryland. 

H. S. Christensen and T. Lugiubyl, eds., Registy of Toxic Effects of Chemical Substances, U.S. Dept, of Health, Education, Welfare, RockviUe, Md., 1975. 

SAN resins themselves appear to pose few health problems in that they have been approved by the EDA for beverage botde use (149). The main concern is that of toxic residuals, eg, acrylonitrile, styrene, or other polymerization components such as emulsifiers, stabilizers, or solvents. Each component must be treated individually for toxic effects and safe exposure level. 

The toxicity of these fluoroaluminates is mainly as inorganic fluorides. The ACGIH adopted (1992—1993) values for fluorides as F is TLV 2.5 mg/m. The oral toxicity in laboratory animal tests is reported to be LD q rat 2.15 mg/kg (41). Because of the fine nature of the products they can also be sources of chronic toxicity effects as dusts. 

D. V. Sweet, ed.. Registry of Toxic Effects of Chemical Substances-198511986 Edition, Vols. 1—5, DHHS (NIOSH) pubhcation no. 87-114, Washington, D.C., 1987. 

Oral appHcations of 1500 mg/kg/d for two weeks caused death of rats. Repeated oral appHcations (4 wks) of 30 p-L/kg to rats caused no toxic symptoms, 100 pL/kg resulted in minor toxic effects, and 300 pL/kg induced impairment of several organs andlethaHty. Repeated oral appHcations (26 x) of 0.1 mL/kg caused no toxic symptoms in cats or rabbits. Inhalation of 1500 ppm (2 wks) were without effects, whereas in a similar study with... 

RTECS National Institute for Occupational Safety and Health (NIOSH) registry of toxic effects of chemical substances contains toxicity data and references commercially important substances... 

The LC q (lowest possible lethal concentration) has been reported to be 23 ppm for a 30 min exposure time (mouse), 53 ppm for an exposure time of 100 min (rat, rabbit, and guinea pig), and 200 ppm for an exposure time of 10 min (monkey). No toxic effects were reported upon exposure to 1 ppm for 7 h/d over 55 days. The oral LD q (rat) of ketene is 1300 mg/kg, the low level of toxicity probably being due to the almost immediate formation of acetic acid and other acetates in the digestive tract. 

RTECS, Reght of Toxic Effects of Chemical Substances, VoL 2, NIOSH, Cincinnati, Ohio, 1981—1982, entry OA7700000, p. 595, and RQ8225000, p. 930 also available on CD-ROM through Canadian Centre for Occupational Health and Safety, Hamilton, Ontario, Canada, 1992. 

The alimentary symptoms may be overshadowed by neuromuscular dysfunction, accompanied by signs of motor weakness that may progress to paralysis of the exterior muscles or the wrist (wrist drop), and less often, of the ankles (foot drop). Encephalopathy, the most serious result of lead poisoning, frequendy occurs in children as a result of pica, ie, ingestion of inorganic lead compounds in paint chips this rarely occurs in adults. Nephropathy has also been associated with chronic lead poisoning (147). The toxic effects of lead may be most pronounced on the developing fetus. Consequendy, women must be particulady cautious of lead exposure (148). The U.S. Center for Disease Control recommends a blood level of less than 10 p.m per 100 mL for children. 

Lead is toxic to the kidney, cardiovascular system, developiag red blood cells, and the nervous system. The toxicity of lead to the kidney is manifested by chronic nephropathy and appears to result from long-term, relatively high dose exposure to lead. It appears that the toxicity of lead to the kidney results from effects on the cells lining the proximal tubules. Lead inhibits the metaboHc activation of vitamin D in these cells, and induces the formation of dense lead—protein complexes, causing a progressive destmction of the proximal tubules (13). Lead has been impHcated in causing hypertension as a result of a direct action on vascular smooth muscle as well as the toxic effects on the kidneys (12,13). 

Daylight fluorescent pigments (qv) are considered to be nontoxic. Since they are combinations of polymers and dyestuffs, the combined effect of the ingredients must be taken into account when considering the net toxic effect of these materials. Table 5 gives results of laboratory animal toxicity tests of standard modified melamine—formaldehyde-type pigments, the Day-Glo A Series, and the products recommended for plastic mol ding, Day-Glo Z-series. 

Safety. Magnesium oxide (fume) has a permissible exposure limit (PEL) (134) (8 hours, TWA), of 10 mg/m total dust and 5 mg/m respirable fraction. Tumorigenic data (intravenous in hamsters) show a TD q of 480 mg/kg after 30 weeks of intermittent dosing (135), and toxicity effects data show a TC q of 400 mg/m for inhalation in humans (136). Magnesium oxide is compatible with most chemicals exceptions are strong acids, bromine pentafluoride, chlorine trifluoride, interhalogens, strong oxidizers, and phosphorous pentachloride. 

The lowest dose reported to produce any toxic effect (toxic dose low). 

The toxic effects of mercury and mercury compounds as well as their medicinal properties have been known for many centuries. In the first century AD, Pliny indicated the use of mercuric sulfide (cinnabar or vermilion) in medicine and in cosmetics. This compound was probably known to the Greeks in the time of Aristotle (13). 

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