Carcinogen risk and

The human and environmental protection goals in EUSES are human populations (workers, consumers, and man exposed via the environment) and ecological systems (micro-organisms in sewage treatment systems, aquatic ecosystems, terrestrial ecosystems, sediment ecosystems, and predators). Repeated dose toxicity, fertility toxicity, maternal toxicity, developmental toxicity, carcinogenic risk, and lifetime cancer risk can be calculated for the cases that literature data is available. 

Danthron is available as a standardised preparation in combination with the faecal softeners poloxamer 188 (co-danthramer) and docusate sodium (as co-danthrusate). It acts in 6-12 h. Evidence from rodent studies indicates a possible carcinogenic risk and long-term exposure to danthron should be avoided. 

The EGA considers fossil fuel consumption, global warming potential, summer smog potential, acidification, eutrophication, carcinogenic risk, and human toxicity. The EGA did not consider waste generation or water consumption. To provide a more complete EGA, the waste generation and water consumption were calculated for each plastic based on reference sources. 

Slezakova, K., Pires, J.C.M., Castro, D., Alvim-Ferraz, M.C.M., Delerue-Matos, C., Morais, S. Pereira, M.C. 2013b. PAH air pollution at a Portuguese urban area Carcinogenic risks and sources identification. Environmental Science and Pollution Research 20 3932-3945. 

Acroleiu, iu lARC Monographs on the Evaluation of Carcinogenic Risk of Chemicals to Humans. Some Monomers, Plastics and Synthetic Elastomers andMcrolein, Vol. 19, International Agency for Research on Cancer, Lyon, France, 1979, pp. 479—494. 

Vanillin has a low potential for acute and chronic toxicity, with a reported oral LD q in rats of 1580—3300 mg/kg. Dietary doses up to 20,000 ppm adrninistered to rats for two years resulted in no adverse toxicologic or carcinogenic effects. Vanillin is classified as a GRAS substance by EEMA. Consequently, at levels normally found in the human diet, vanillin would present no significant health or carcinogenic risk to humans. 

The Evaluation of Carcinogenic Risks to Humans Dy Cleaning, Some Chlorinated Solvents and Otherindustrial Chemicals, L4RC Monographs, 63 (Feb. 1995). 

UK Ministry of Agriculture Fisheries and Food and Flealth and Safety Executive, Annual Report of the Working Party on Pesticide Residues in Food (1997), MAFF Publications, London, 1997. lARC, Monographs on the Evabiation of the Carcinogenic Risk of Chemicals to Hnmans Volume 56 Some Naturally Occurring Substances Food Items and Constituents, Heterocyclic Aromatic Amines and Mycotoxins, WFIO, Geneva, 1979, p. 397. 

International Agency for Research on Cancer (1996) "Printing processes and printing inks, carbon black and some nitro compounds". lARC monographs on the evaluation of carcinogenic risks ro humans, Vol. 6.5, pp. 67-70. Internarional Agency for RKsearch on Cancer, Lyon, France. 

This section describes how the tj pes of to.xicity inforniation arc considered in the to.xicity assessment for carcinogenic effects. A slope factor and the accompanying weight of evidence determination are the toxicity data most commonly used to evaluate potential human carcinogenic risks. The methods the USEPA uses to derive these values arc outlined below. 

Because the slope factor is often an upper 95 percentile confidence limit of the probability of response based on experimental animal data used in tlie multistage model, tlie carcinogenic risk estimate will generally be an upper-bound estimate. Tliis means tliat tlie EPA is reasonably confident tliat tlie true risk will not exceed the risk estimate derived tlirough use of tliis model and is likely to be less than tliat predicted. 

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. 

From the detailed studies performed either using individual alcohol sulfates and alcohol ether sulfates or formulated products by oral administration and skin contact, no evidence of carcinogen risk was found. Similar conclusions were obtained when these sulfates or formulated products were tested for mutagenic and teratogenic properties. 

Monte Carlo simulation, an iterative technique which derives a range of risk estimates, was incorporated into a trichloroethylene risk assessment using the PBPK model developed by Fisher and Allen (1993). The results of this study (Cronin et al. 1995), which used the kinetics of TCA production and trichloroethylene elimination as the dose metrics relevant to carcinogenic risk, indicated that concentrations of 0.09-1.0 pg/L (men) and 0.29-5.3 pg/L (women) in drinking water correspond to a cancer risk in humans of 1 in 1 million. For inhalation exposure, a similar risk was obtained from intermittent exposure to 0.07-13.3 ppb (men) and 0.16-6.3 ppb (women), or continuous exposure to 0.01-2.6 ppb (men) and 0.03-6.3 ppb (women) (Cronin et al. 1995). 

ARC. 1995. Monographs on the evaluation of carcinogenic risks to humans. Vol63. Drycleaning, some chlorinated solvents, and other industrial chemicals. World Health Organization, Lyon, France. 

If linear (dose) models without thresholds are to be used for carcinogen (or other) risk assessment, estimation of exposure at specified levels becomes irrelevant to risk assessment or, at least, its use is nonintuitive. For example, a carcinogen risk analysis may be based on a linear, nonthreshold health effects model. The total health risk would thus be proportional to the long-term exposure summed for all affected people for the identified period, and exposure of many people at low concentrations would be equivalent to exposure of a few to high concentrations. The atmospheric dispersion that reduces concentrations would also lead to exposure of more people therefore, increments... 

As a rule, the level of precision of a risk estimate cannot exceed the precision of the exposure and effects data from which it is obtained. In the following we will focus upon carcinogenic risk estimation, for which it will often be possible to achieve at least interval estimates of risk. 

In order to extrapolate laboratory animal results to humans, an interspecies dose conversion must be performed. Animals such as rodents have different physical dimensions, rates of intake (ingestion or inhalation), and lifespans from humans, and therefore are expected to respond differently to a specified dose level of any chemical. Estimation of equivalent human doses is usually performed by scaling laboratory doses according to observable species differences. Unfortunately, detailed quantitative data on the comparative pharmacokinetics of animals and humans are nonexistent, so that scaling methods remain approximate. In carcinogenic risk extrapolation, it is commonly assumed that the rate of response for mammals is proportional to internal surface area... 

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