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Carcinogenicity non-carcinogens

PFNA Non-carcinogen Non-carcinogen Non-carcinogen Non-carcinogen Non-carcinogen Non-carcinogen... [Pg.189]

M. p. 168-169 C. This reagent has superseded benzidine for blood detection, showing same sensitivity and specificity but it is non-carcinogenic in doses at which benzidine produces a high incidence of neoplasms. [Pg.391]

There are numerous methods available to identify the potential for chemicals to cause both healtli conditions and adverse effects on tlie eiiviroiiment. These can include, but are not limited to, toxicology, epidemiology, molecular and atomic structural analysis, MSDS sheets, engineering approaches to problem solving, fate of chemicals, and carcinogenic versus non-carcinogenic healtli hazards... [Pg.299]

Section 10.7 Fate of Chemical Health Hazards Section 10.8 Carcinogens versus Non-carcinogens... [Pg.300]

Section 13.2 Qualitative Risk Scenarios Section 13.3 Quantitative Risk Non-carcinogens Section 13.4 Quantitative Risk Carcinogens Section 13.5 Risk Uncertainties/Liinitations Section 13.6 Risk-Based Decision Making Section 13.7 Public Perception of Risk... [Pg.396]

The measure used to describe the potential for noncarcinogenic toxicity to occur in an individual is not expressed as tlie probability of an individual suffering an adverse effect. The EPA does not at tlie present time use a probabilistic approach to estimate tlie potential for noncarcinogenic healtli effects. Instead, tlie potential for non carcinogenic effects is evaluated by comparing an exposure level over a specified time period (e.g., lifetime) witli a reference dose derived for a similar exposure period. Tliis ratio of exposure to toxicity is called a liazard quotient and is described below. (The reader is referred to Chapter 11 for additional details on tlie material tliat follows). The noncancer liazard quotient assumes tliat tliere is a level of exposure (i.e., RfD) below which it is unlikely for even sensitive populations to experience adverse healtli effects. [Pg.398]

To assess die overall potential for non carcinogenic effects posed by several exposure pathways, the total haziird index for each exposure duration (i.e., chronic, subchronic, and shorter-term) should be calculated separately. This equation is described below ... [Pg.402]

In health risk assessments, non carcinogenic risks are estimated via Hazard Indices . A general equation for a liazard index (HI) is as follows ... [Pg.414]

If tlie pollutant causes iui acute non carcinogenic risk, tlie inaximuin one hour concentration is used for C, and tlie acute reference exposure limit is used for tlie REL. Likewise, if tlie pollutant causes a clironic non carcinogenic risk, tlie one year average concentration is used, as is tlie clironic reference exposure limit. In tliis procedure, a Iiazard index is calculated for each pollutant separately, and tlien tlie indices are summed for each toxicological endpoint (i.e., tlie respiratory system, tlie central nervous system, etc.). Finally, tlie total hazard index is tlien compared to a value wliich is considered significant. [Pg.415]

Eye, nose, and throat irritation headaches, nausea. Some VOCs are suspected or known carcinogens or causes of adverse reproductive effects. Some VOCs also have unpleasant odors or are irritants. VOCs are thought to be a cause of non-specific health symptoms. [Pg.57]

Nitrosomethylurethane1 has been reported to be a potent carcinogen by Druckrey and Preussmann.2 These investigators suggest that nitrosomethylurethane be handled with greatest care or, preferably, be replaced whenever possible with />-tolyl-sulfonylmethylnitrosamide,3 which was shown to be practically non-toxic and non-carcinogenic under conditions for which the urethane was toxic and/or carcinogenic. [Pg.86]

M. Joona, Non-carcinogenic tire extender oils providing good dynamic performance. Rubber World, 235(4), 15, 2007. [Pg.1040]

Purchase, l.P.H. (1994). Current knowledge of mechanisms of carcinogenicity genotoxic vs. non-genotoxic. Human and Experimental Toxicology 13, 17-28. [Pg.365]

Toxicological Chronic toxicity Carcinogenicity Fertility study (multi-generation) Embryotoxicity (non-rodent) Acute/subacute toxicity in 2nd species Toxicokinetics... [Pg.321]

Nie AY, McMillian MK, Leone AM, Parker JB, Piechta L-A, Bryant S, et al. A gene signature for non-genotoxic carcinogens. Society of Toxicology, 2005. [Pg.160]

An update of a previous study (Axelson et al. 1978), Axelson (1986) evaluated an expanded cohort of 1,424 men (levels of trichloroethylene exposure inferred from measured urinary metabolite concentrations) and found a significant increase in incidences of bladder cancer and lymphomas, and a lower than expected incidence of total cancer mortality. A further update of this work (Axelson et al. 1994) expanded the cohort to include 249 women, tracking cancer morbidity over 30 years, and found no correlation between exposure concentration or exposure time and cancer incidence at any site. The highest standardized incidence ratio noted in this study was 1.56 (95% Cl of 0.51-3.64) for 5 cases of non-Hodgkin s lymphoma observed in men. Although four of these cases occurred in persons exposed for at least 2 years, and 3 cases had a latency of 10 years or more, urinary levels of TCA showed that 4 of the 5 cases were exposed to the lowest levels of trichloroethylene (urinary levels of TCA 0-49 mg/L). The study authors mentioned that a urinary TCA level below 50 mg/L corresponds to a trichloroethylene exposure concentration of about 20 ppm. The study authors concluded that "this study provides no evidence that trichloroethylene is a human carcinogen, i.e., when the exposure is as low as for this study population."... [Pg.59]

This study, like that of Fisher and Allen (1993), incorporated a linear multistage model. However, the mechanism of trichloroethylene carcinogenicity appears to be non-genotoxic, and a non-linear model (as opposed to the linearized multistage model) has been proposed for use along with PBPK modeling for cancer risk assessment. The use of this non-linear model has resulted in a 100-fold increase in the virtually safe lifetime exposure estimates (Clewell et al. 1995). [Pg.130]

Safe" secondary amines resulting in non-carcinogenic N-nitroso compounds after nitrosation (German Patent Application No P 3029 318 6)... [Pg.226]

Roman-Franco, A.A. (1982). Non-enzymic extramicrosomal activation of chemical carcinogens by phagocytes a proposed new pathway. J. Theor. Biol. 97, 543-555. [Pg.260]


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See also in sourсe #XX -- [ Pg.171 ]




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