Carcinogens inhalation exposure

No studies were located regarding carcinogenic effects in humans or animals after inhalation exposure to methyl parathion. 

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). 

Five recent studies investigated the potential toxic risk if CNTs reach the pleural cavity after inhalation exposure [6,88-91]. Three of these in vivo studies revealed that if CNTs are delivered to the abdominal cavity of mice or rats, they could induce a serious potential carcinogenic risk resembling that associated with exposure to certain asbestos fibers [6,88,89]. The other two studies described nontoxic responses [90,91]. 

Both isomers of dimethylhydrazine have been shown to be carcinogenic in rodents following chronic oral exposure and 6-mon inhalation exposure to 1,1-dimethylhydrazine. Increased tumor incidence was observed in mice, although these findings are compromised by the contaminant exposure to dimethylnitrosamine. An increased incidence of lung tumors and hepatocellular carcinomas was also seen in rats but not in similarly exposed hamsters. The U.S. Environmental Protection Agency (U.S. EPA) inhalation slope factors are currently unavailable for dimethylhydrazine. 

Studies in animals (shown in the lower half of Figure 2-3) have also focused on inhalation exposure, and most endpoints (except immunotoxicity) have been investigated. In contrast, the effects of oral exposure have received only limited attention, focusing mainly on the inflammatory and possible carcinogenic effects in the stomach. No information was located on dermal exposure of animals. 

No information is available from studies of humans on the carcinogenic effects of inhalation exposure to bromomethane, but chronic inhalation studies in mice and rats (Reuzel et al. 1987 ... 

Chronic inhalation exposure of rodents to 1,2-dibromoethane has been associated with neoplasms in the respiratory tract, as well as in other organ systems. Two studies have examined the carcinogenic potential of 1,2-dibromoethane in rodents after inhalation exposure (NTP 1982 Wong et al. 1982). There was also an A strain mouse assay (Adkins et al. 1986). 

Chemical carcinogen Oral exposure (mg/(kg day)) Inhalation exposure (pg/m3)-i... 

There are limited epidemiological data regarding carcinogenicity in humans following chronic inhalation exposure to kerosene. In one case-control study, there was no association between the use of kerosene stoves for cooking and bronchial cancer in nonsmoking women (Chan et al. 1979). In another case-control study, there was no association between renal cell cancer and occupational exposure to fuel oils. 

Limited epidemiological information exists for carcinogenicity in humans following inhalation exposure to kerosene (vapor) (Chan et al. 1979) and other fuel oils such as diesel fuel (vapor) (Partanen et al. 1991). These studies either test kerosene exposure by use of kerosene stoves, and so are limited for the same reasons as the respiratory studies described above, or measure fuel oil exposures according to occupation. In the latter case, confounding from exposure to other chemicals, such as gasoline, exists. Both studies are limited since the duration and level of fuel oil exposure were not identified. Other available data are also reported to be inadequate to assess the carcinogenic potential of fuel oils (lARC 1989 Lam and Du 1988). 

McKee R, Freeman J. 1993. Dermal carcinogenicity studies of petroleum-derived materials. In RGM Wang, JB Knaak, HI Maiback, eds.. Health Risk Assessment Dermal and Inhalation Exposure and Absorption of Toxicants CRC Press, Ann Arbor MI, 263-21 A. 

Aluminum does not appear to be a potential carcinogen. It has not been shown to be carcinogenic in human epidemiological studies or in animal studies after oral or inhalation exposure. 

Huff JE, Melnick RL, Solleveld HA, et al Multiple organ carcinogenicity of 1,3-butadiene in B6C3F1 mice after 60 weeks of inhalation exposure. Science 227 548-549, 1985... 

In a long-term inhalation study in male and female rats and female mice, there was no evidence of carcinogenicity after exposure at 75 or 500 ppm for 5 hours/day, 5 days/weekfor 76 weeks (rats) or 57 weeks (mice). Although there has been a report of five cases of blood dyscrasias, including leukemia, among individuals exposed to o- or p-dichlorobenzene, the lARC has concluded that the human data are inadequate to evaluate the carcinogenicity of dichlorobenzenes but the para-isomer is possibly carcinogenic to humans. ... 

Hydrazine or hydrazine salts are carcinogenic in mice after oral administration (pulmonary adenocarcinoma hepatocarcinoma) or intraperitoneal injection (pulmonary carcinoma) and in rats after oral administration (pulmonary adenocarcinoma). Hydrazine induced a significantly greater incidence of nasal tumors, primarily benign, in rats and in hamsters after 1 year of intermittent inhalation exposure at levels up to 5.0ppm. ... 

Morpholine has also been tested for carcinogenicity by inhalation exposure in rats. Exposure to 10, 50, or 150 ppm 6 hours/day, 5 days/week, for up to 104 weeks was associated with dose-related increases in inflammation of the cornea, inflammation and squamous metaplasia of the turbinate epithelium, and necrosis of the turbinate bones in the nasal cavity, but no significant increase in the incidence of tumors. ... 

As shown in Figure 2-4, there is a considerable body of data on the health effects of carbon tetrachloride in humans, especially following acute oral or inhalation exposures. Although many of the available reports lack quantitative information on exposure levels, the data are sufficient to derive approximate values for safe exposure levels. There is limited information on the effects of intermediate or chronic inhalation exposure in the workplace, but there are essentially no data on longer-term oral exposure of humans to carbon tetrachloride, most toxicity studies have focuses on the main systemic effects of obvious clinical significance (hepatotoxicity, renal toxicity, central nervous system depression). There are data on the effects of carbon tetrachloride on the immune system, but there are no reports that establish whether or not developmental, reproductive, genotoxic, or carcinogenic effects occur in humans exposed to carbon tetrachloride. 

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