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Increased Cancer Risk

Several retrospective cohort studies of workers exposed to unquantified levels of trichloroethylene have been conducted. All of these studies have limitations that restrict their usefulness for evaluating the carcinogenicity of trichloroethylene. None has shown clear, unequivocal, evidence that trichloroethylene exposure is linked to increased cancer risk. [Pg.58]

The information available regarding the association of occupational exposure to lead with increased cancer risk is generally limited in its usefulness because the actual compound(s) of lead, the route(s) of exposure, and level(s) of lead to which the workers were exposed were often not reported. Furthermore, potential for exposure to other chemicals including arsenic, cadmium, and antimony occurred, particularly in lead smelters, and smoking was a possible confounder (Cooper 1976 IARC 1987). These studies, therefore, are not sufficient to determine the carcinogenicity of lead in humans, and the following discussion is restricted to the most comprehensive of these studies. [Pg.128]

For maximum protection of human health from the potential carcinogenic effects of exposure to arsenic through drinking water or contaminated aquatic organisms, the ambient water concentration should be zero, based on the nonthreshold assumption for arsenic. But a zero level may not be attainable. Accordingly, the levels established are those that are estimated to increase cancer risk over a lifetime to only one additional case per 100,000 population. These values are estimated at 0.022 pg As/L for drinking water and 0.175 pg As/L for water containing edible aquatic resources (USEPA 1980 Table 28.7). [Pg.1529]

Lipid modifying drugs (statins) have shown secondary cardio-vascular preventive effects (myocardial infarction) in a very large number of patients. Only one study (Shepherd et al. 2002) has been conducted in the elderly and showed similar results. However there was a significant increased cancer risk (25%). [Pg.31]

Methylene chloride does not increase cancer risk in humans under any conditions (in which case actual risk will be zero). [Pg.245]

A mortality study of 165 workers who had been exposed to low concentrations of dioxane (since 1954) did not show any increased cancer risk. ... [Pg.282]

There is no conclusive evidence from epidemiological studies that mercury increases cancer risk in humans. In the few studies in which increases have been reported, concomitant exposure to other known carcinogens has confounded the results. The lARC has determined that there is inadequate evidence in humans for the carcinogenicity of mercury and mercury compounds. In animals there is inadequate evidence for carcinogenicity of metallic mercury and limited evidence for the carcinogenicity of mercuric chloride. [Pg.438]

This causes two problems in cancer-risk policy. First, because the public (and, hence, policymakers) worries about small levels of increased cancer risk resulting from chemical exposures, the number of subjects required to differentiate small risks from zero risk is enormous, which makes the studies prohibitively expensive. Second,... [Pg.9]

Fascination with the hypothetical risks from pesticides may increase cancer risks. Fruits and vegetables are of major importance for reducing cancer if they become more expensive because of reduced use of synthetic pesticides then consumption is likely to decline and cancer to increase. The effects of such policies will be most notable on people with low incomes who must spend a higher percentage of their income on food, and who already eat fewer fruits and vegetables. [Pg.144]

No measurement of exposure to diethyl sulfate was available for the industrial processes investigated in the epidemiological studies. It is therefore difficult to assess the contribution of diethyl sulfate to the increased cancer risks. Furthennore, exposure to mists and vapours from strong inorganic acids, primarily sulfuric acid (see lARC, 1992b), may play a role in increasing these risks.]... [Pg.1406]

Nitrous acid, formed from organic precursors such as nitrosamines and from nitrite and nitrate salts, is a potent accelerator of the deamination of bases. Bisulfite has similar effects. Both agents are used as preservatives in processed foods to prevent the growth of toxic bacteria. They do not appear to increase cancer risks... [Pg.294]

Cancer slope factors are upper bounds, approximating a 95% confidence limit, on the increased cancer risk posed by a lifetime exposure to a carcinogen (EPA 2006). [Pg.45]

A wide variety of effects have been observed in adults exposed to 2,3,7,8-TCDD at work or following an accidental release of 2,3,7,8-TCDD into the environment. The primary targets appear to be the skin, liver, thyroid, and cardiovascular, endocrine, and immune systems an increased cancer risk has also been observed. In the absence of data to the contrary, it is likely that these organs/systems will also be sensitive targets in children. [Pg.337]

In 2005, a study appeared in Cancer Letters that would have evoked widespread media coverage if it had been about an illegal drug, rather than about a pharmaceutical company product (El-Zein, 2005). Researchers from the University of Texas examined 12 children treated with therapeutic effects of Ritalin to determine whether this central nervous system stimulant produces cytogenetic abnormalities in pediatric patients at therapeutic doses. Using peripheral blood lymphocytes taken from the children, they found a 2.4-fold increase in chromosome aberrations and similar defects. They concluded, These findings warrant further investigations of the possible health effects of methylphenidate in humans, especially in view of the well-documented relationship between elevated frequencies of chromosome aberrations and increased cancer risk. ... [Pg.313]

Implementation of emergency-response procedures based on theoretical excess risk values of 10 to 10 may be problematical. For example, if such values were used, they would be based on an anticipated increased cancer risk of 10 to 10 a policy consistent with EPA s acceptable cancer risk for lifetime exposures to known or suspect human carcinogens. However, the public health and safety risks associated with evacuation and other response measures might pose greater risks of injury or perhaps death. Thus, setting AEGL values based on uncertain theoretical cancer risk estimates might lead to response measures that increase actual or total risk for the exposed population. [Pg.139]


See other pages where Increased Cancer Risk is mentioned: [Pg.555]    [Pg.350]    [Pg.926]    [Pg.189]    [Pg.10]    [Pg.1506]    [Pg.376]    [Pg.1150]    [Pg.136]    [Pg.164]    [Pg.169]    [Pg.216]    [Pg.384]    [Pg.157]    [Pg.710]    [Pg.1506]    [Pg.6]    [Pg.1218]    [Pg.555]    [Pg.1190]    [Pg.480]    [Pg.394]    [Pg.233]    [Pg.83]    [Pg.397]    [Pg.147]    [Pg.31]    [Pg.32]    [Pg.926]    [Pg.350]    [Pg.16]   


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Cancer risk

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