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Toxicity human

Unreliability and lack of validity will attenuate test score differences between groups selected on the basis of a biological measure such as blood lead. An unreliable test introduces a large random element that reduces the proportion of total variance accounted for by exposure differences. And, if the test itself does not measure what it purports to measure (such as, intelligence ), it may reflect some possibly irrelevant qualities associated with a particular ethnic culture or social class. For this reason, some recent studies have more carefully investigated parental and class contributions. [Pg.6]

The report of a British government commission on lead expressed several reservations about Needleman et al., but misinterpreted two important aspects of that study. First, although the teacher s rating scale was criticized as not a standardized instrument, it was not used to classify children, only to prompt a response from the teacher. The striking dose-response functions, in fact, could be considered the validation of the inventory. Second, the report pays scant attention to a pervasive finding in toxicology, namely, the enormous variability in sensitivity within a population. [Pg.8]

The blood lead values in Yule et al. were based on bloods drawn 9-12 months before psychological testing. The authors remark as follows on the significance of that interval  [Pg.8]

If blood lead levels are so labile as some authorities believe, the finding of small, statistically significant relationships with attainment and intelligence are all the more surprising. [Pg.9]

This comment highlights issues that are not discussed often enough. [Pg.9]


Many studies have reported a link between consumption of sunburned potatoes, ie, those exposed to the sun and having an accumulation of chlorophyll and solanine under the skin, with incidences of teratogenic effects and even death (59—61). Because sunburned potatoes in the commercial marketplace are relatively rare, and because the long-term effects of consumption of potatoes at the maximum estabUshed limits of solanine concentration are uncertain, there is equal uncertainty of the tme incidence of human toxicity (62). [Pg.478]

Heavy metals are of importance in human toxicity because the body possesses only inactive mechanisms for their excretion thus chronic, low level intakes can accumulate to toxic proportions. Treatment has likewise been relatively unsuccessfiil, except for symptomatic reHef. No effective means has been discovered to increase excretion. [Pg.479]

Health, Safety, and Environmental Factors. Sulfur dioxide has only a moderate acute toxicity (183). The lowest pubHshed human lethal concentration is 1000 ppm for 10 months. The lowest pubHshed human toxic concentration by inhalation is 3 ppm for 5 days or 12 ppm for 1 hour. The lowest pubHshed human lethal concentration is 3000 ppm for 5 months. In solution (as sulfurous acid), the lowest pubHshed toxic dose is 500 flg/kg causing gastrointestinal disturbances. Considerable data is available by other modes of exposure and to other species NIOSH standards are a time-weighted average of 2 ppm and a short-term exposure limit of 5 ppm (183). [Pg.147]

Human toxicity, aquatic toxicity, and the environmental impact of engine coolants and deicing fluids ate typically measured on the fresh fluid only. Spent fluids contain varied contaminants that can drastically affect the toxicity and environmental impact of the fluid. Most pronounced is the impact of heavy-metal contaminants in spent antifreeze. Data on spent and recycled antifreeze, compiled by the ASTM Committee on Engine Coolants, show an average lead level 11 ppm, as weU as various other metal contaminants (iron, copper, zinc) (18). The presence of these contaminants in a used fluid may require special disposal techniques for the fluids. [Pg.192]

AH four butanols are thought to have a generaHy low order of human toxicity (32). However, large dosages of the butanols generaHy serve as central nervous system depressants and mucous membrane irritants. Animal toxicity and irritancy data (32) are given in Table 4. [Pg.358]

Toxicity Amelioration. Cancer researchers traditionally have not focused their attention on the question of toxicity amehoration. This is partiy attributed to the lack of predictive animal models for human toxicities. For example, the preclinical rat model, used as a predictor of myelosuppression, has failed to predict myelosuppression in humans in clinical trials. In addition, reduction of one toxicity may result in the emergence of another, more serious problem. Research efforts to address the problem of toxicity amelioration has progressed in several directions. The three most prominent areas are analogue synthesis, chemoprotection, and dmg targeting. [Pg.444]

Animal and Human Toxicity. The acute toxicity of lindane depends on the age, sex, and animal species, and on the route of adrninistration. The oral LD q in mice, rats, and guinea pigs is 86, 125—230, and 100—127 mg/kg, respectively. In contrast, most of the other isomers were considerably more toxic (94,95). Some of the other toxic responses caused by lindane in laboratory animals include hepato- and nephotoxicity, reproductive and embryotoxicity, mutagenicity in some short-term in vitro bioassays, and carcinogenicity (80). The mechanism of the lindane-induced response is not known. Only minimal data are available on the mammalian toxicides of hexachlorocyclopentadiene. [Pg.68]

A substance known to be so toxic to man as to afford a hazard to health during conveyance or which, in the absence of adequate data on human toxicity, is presumed to be toxic to man. [Pg.454]

Nitrogen tetroxide is one of the most insidious gases in terms of human toxicity. Inflammation of the lungs may cause only slight pain or pass unnoticed, but the resulting edema several days later may cause death. lOOppm is dangerous for even a short exposure, and 200 ppm may be fatal (Ref 25). Also see under Nitrous Fumes in this Vol... [Pg.315]

Dioxane is an impurity present in alcohol ethoxy sulfates formed during sulfation of the ethoxylated alcohol. 1,4-Dioxane is a carcinogen in rats and mice [312-314] and has been considered as a possible carcinogen to humans [315-317]. However, the no-effect dose in rats is equivalent to a daily intake of dioxane of 9.6-19.0 mg/kg/day, which corresponds to 0.672 g/day for humans. In other studies it has been determined that the threshold for onset of human toxicity of 1,4-dioxane lies above an intake of 76 mg/kg in adult males [318]. Although it seems to be demonstrated that amounts up to 1000 ppm of... [Pg.286]

Species The test species, whether animal or human, are identified in this column. Chapter 2, "Relevance to Public Health," covers the relevance of animal data to human toxicity and Section 3.4, "Toxicokinetics," contains any available information on comparative toxicokinetics. Although NOAELs and LOAELs are species specific, the levels are extrapolated to equivalent human doses to derive an MRL. [Pg.255]

The annelids include the bristle worms and blood worms in which toxicity is associated with bristle-like setae and/or biting jaws. In the order Polychaetae, toxicity is usually found in three genera (Chloeia, Eurythoe, Hemodice). The platyhelminthes are not associated with many cases of human toxicity. The only class of platyhelminthes in which toxicity can readily be found is in the Turbellaria. In the Rhynchocaela (ribbon worms), toxic species include Lineus sp. Some platyhelminthes (e.g., Planocera multitenta) have been found to contain tetrodotoxin 16). [Pg.319]

Human Toxicity Potential. As for aquatic toxicity, the database for human toxicity potential is still being established but is based on acceptable daily doses. The total potential is the sum of potentials released to different media. [Pg.43]

Human toxicity Acute effects Carcinogenicity Genotoxicity/mutagenicity Developmental Teratogenicity/mutagenicity Neurotoxicity Endocrine disruption... [Pg.28]

Actively try to include materials that are known to be environmentally benign. Estimate the risk of any proposed new material using computer-based models for eco-toxicity and human toxicity. [Pg.64]

The priority effects are carcinogenicity, mutagenicity, reproductive or developmental toxicity, endocrine disruption and neurotoxicity. Human toxicity is broader than priority effects, including acute toxicity, systemic toxicity (organ effects), immune system effects and skin/eye/respiratory damageaswellasthepriority effects. And toxicity as T includes both human toxicity and ecotoxicity. [Pg.293]


See other pages where Toxicity human is mentioned: [Pg.477]    [Pg.479]    [Pg.365]    [Pg.113]    [Pg.280]    [Pg.512]    [Pg.393]    [Pg.187]    [Pg.190]    [Pg.192]    [Pg.542]    [Pg.681]    [Pg.146]    [Pg.43]    [Pg.68]    [Pg.212]    [Pg.224]    [Pg.250]    [Pg.292]    [Pg.292]    [Pg.292]    [Pg.292]    [Pg.292]    [Pg.293]    [Pg.293]    [Pg.293]   
See also in sourсe #XX -- [ Pg.116 ]

See also in sourсe #XX -- [ Pg.38 ]




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Acute Human Toxicity

Alimentary toxic aleukia, human

Dermal toxicity Human skin, nature

Drug-Induced Pancreatic Exocrine Toxicity in Humans

Extrapolation of Toxicity Values from Animals to Humans

Gastrointestinal Toxicity Reasons for Poor Translation from Animal to Human

Health human toxicity

Hepatic Toxicity Reasons for Poor Translation from Animal to Human

Human Estimates of Nerve Agent Toxicity

Human and Environmental Toxicity

Human animal toxicity

Human body arsenic toxicity

Human body carbon monoxide toxicity

Human body lead toxicity

Human body mercury toxicity

Human epidemiology, animal toxicity

Human exposure to potentially toxic

Human exposure toxicity

Human impact, toxic

Human risk assessment toxic chemicals

Human studies drug toxicity

Human toxic data

Human toxicity data

Human toxicity delayed toxic effects

Human toxicity experience

Human toxicity potential

Human toxicity potential analysis

Human toxicity predictions

Human toxicity predictions development

Human toxicity pyrrolizidine alkaloids

Human toxicity, lead measurement techniques

Humanized antibodies selective toxicity

Humans, toxicity/potential risk

Insecticides human toxicity

Lead, human toxicity measurement

Manganese toxicity in humans

Mercury general human toxicity

Methanol fuel human toxicity

Ocular toxicity, humans

PBDEs human toxicity

Pyrethroids toxicity humans

Renal Toxicity Reasons for Poor Translation from Animal to Human

Reproductive and Developmental Toxicity of Lead in Human Populations

Respiratory Toxicity Reasons for Adequate Translation from Animal to Human

Toxic Effects of Smog and Its Constituents to Humans

Toxic Effects on Humans

Toxic chemicals entry Into human body

Toxic human studies

Toxic on human

Toxic potential human risk

Toxicity human experimentation

Toxicity of Lead in Human Populations

Toxicity on human

Toxicity testing potential human adverse effects predicted

Toxicity to Animals and Humans

Toxicity to humans

Toxicity xenobiotic-metabolizing human cell

Toxicity, evaluation human

Validation human toxicity data

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