Cancer risk exposure

In additional EPA studies, subchronic inhalation was evaluated ia the rat for 4 and 13 weeks, respectively, and no adverse effects other than nasal irritation were noted. In the above-mentioned NTP chronic toxicity study ia mice, no chronic toxic effects other than those resulting from bronchial irritation were noted. There was no treatment-related increase ia tumors ia male mice, but female mice had a slight increase in bronchial tumors. Neither species had an increase in cancer. Naphthalene showed no biological activity in other chemical carcinogen tests, indicating Htde cancer risk (44). No incidents of chronic effects have been reported as a result of industrial exposure to naphthalene (28,41). 

Colorectal Cancer. Colorectal cancer occurs frequently in the UK population but is historically rare in Asia. Rates in Japan have, however, increased rapidly in recent years.Interestingly, there appears to be an association between oestrogen exposure and colon cancer risk has been shown to increase in women with increasing age of first live birth, and to decrease with increasing parity (number of children). In addition, many colon tumours express sex hormone receptors, and this is thought to play a part in development of the tumours. "... 

The odor perception threshold for benzene in water is 2 ing/L. The benzene drinking water unit risk is 8.3 x lO L/pg. Calculate the potential benzene intake rate (mg benzene/kg-d) and the cumulative cancer risk from drinking water with benzene concentrations at half of its odor threshold for a 30 year exposure duration. 

The cancer risk equation described below estimates tlie incremental individual lifetime cancer risk for simultaneous exposure to several carcinogens and is based on EPA s risk assessment guidelines. Tliis equation represents an approximation of the precise equation for combining risks wliich accounts for tlie joint probabilities of tlie same individual developing cancer as a consequence of exposure to two or more carcinogens. The difference between tlie precise equation and tlie approximation described is negligible for total cancer risks less tlian 0.1. Thus, tlie simple additive equation is appropriate for most risk assessments. The cancer risk equation for multiple substances is given by ... 

The reader should note that tlie introductory comments in tine similarly titled subsections of the previous section applies to carcinogens as well. The calculation proceeds as follows. First, smn tlie cancer risks for each exposure patliway contributing to exposure of the same individual or subpopulation. For Superfimd risk assessments, cancer risks from various exposure patliways are assumed to be additive, as long as tlie risks are for tlie same individuals and time period (i.e., less-tlian-lifetime e.xposures have all been converted to equivalent lifetime exposures). Tliis smnmation procedure is described below ... 

Total E.xposure Cancer Risk = Risk (exposure pathwayi) +... 

Accidental release, toxics Short duration exposure yields low cancer risk non-cancer health effects of much greater concern. 

Environmental tobacco smoke mid gasoline vapors both contain mixtures of trace luiiounts of many of the individual compounds regulated as Air Toxics under Title 111, section 112 of the 1990 Clean Air Act Amendnmts. Much of the general public is more likely to be exposed to these mixtures during the course of their lives tlian to specific compounds on the air toxics list. Hence, estimation of the cancer risk resulting from exposure to these mixtures is a useful and relevant exercise. 

Toxicity and cancer dose-response data for tire constituents of the gasoline Estimated additional cancer risk for dwelling s occupants when exposure data me combined with cancer dose-response data... 

Tables (3-1, 3-2, and 3-3) and figures (3-1 and 3-2) are used to summarize health effects and illustrate graphically levels of exposure associated with those effects. These levels cover health effects observed at increasing dose concentrations and durations, differences in response by species, minimal risk levels (MRLs) to humans for noncancer end points, and EPA s estimated range associated with an upper- bound individual lifetime cancer risk of 1 in 10,000 to 1 in 10,000,000. Use the LSE tables and figures for a quick review of the health effects and to locate data for a specific exposure scenario. The LSE tables and figures should always be used in conjunction with the text. All entries in these tables and figures represent studies that provide reliable, quantitative estimates of No-Observed-Adverse-Effect Levels (NOAELs), Lowest-Observed-Adverse-Effect Levels (LOAELs), or Cancer Effect Levels (CELs).

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. 

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). 

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). 

Vartiainen T, Pukkala E, Rienoja T, et al. 1993. Population exposure to tri- and tetrachloroethylene and cancer risk Two cases of drinking water pollution. Chemosphere 27 1171-1181. 

Qi — The upper-bound estimate of the low-dose slope of the dose-response curve as determined by the multistage procedure. The q, can be used to calculate an estimate of carcinogenic potency, the incremental excess cancer risk per unit of exposure (usually pg/L for water, mg/kg/day for food, and pg/m for air). 

The EPA classifies all radionuclides, including americium, as Group A (known human) carcinogens (EPA 1997b). Lifetime excess total cancer risk per unit intake or exposure for ingestion, inhalation, and external exposure to 241 Am and 243Am are included in Table 8-1. The EPA has not derived reference concentrations (RfCs) or reference doses (RfDs) for americium (IRIS 2001). 

The exposure pathways of concern identified during the baseline risk assessment include direct contact, with the possible ingestion of contaminated soil (1 x 10 3 4 associated excess cancer risk), and potential ingestion of contaminated groundwater in the future through existing or newly installed offsite wells (2 x 11 0 2 associated excess cancer risk). 

The risk assessment has also concluded that a level of 200 mg/kg for lead in the soil will be a protective level for expected site exposures along with an excess cancer risk level for TCE-contaminated soil (56 pg/L). Based on investigations of activities at the site, the TCE-contaminated soil has not been determined to be a listed RCRA hazardous waste, as the cleaning solution records indicate the solution contained less than 10% TCE. However, the lead-contaminated soil is an RCRA hazardous waste by characteristic in this instance due to extraction procedure (EP) toxicity. None of the waste is believed to have been disposed at the site after November 19, 1980 (the effective date for most of the RCRA treatment, storage, and disposal requirements). 

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. 

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