Radioactive “mixed” waste contains radionuclides and varying quantities of semivolatile and/or volatile organics, some or all of which may be named specifically by the RCRA. They are presently stored above-ground at great cost to the user. Analytical procedures which can identify the presence, or at least confirm the absence, of RCRA organics in radioactive waste are necessary for deciding the proper approaches for disposal. Our general analytical strategy removes organic species in “mixed” wastes in such a way that transfer of activity is minimized. Analytical equipment and procedures listed in EPA-approved methods are used wherever possible; however, alternative procedures such as solid-phase extraction (for semivolatiles) have been evaluated as reasonable alternatives. Final quantitations are performed on the nonradioactive concentrated extract in conventional organic analytical laboratories using EPA-approved analytical methods.

A newly developed automatic smoke exposure machine (SEM II) was used to generate [14C]dotriacontane-labeled University of Kentucky reference 2A1 or 2R1 cigarette smoke. The SEM II is a large-capacity (480 mice) dynamic smoke exposure system in which smoke is routed through the animal containment system as a continuously flowing stream. Mice are restrained about the neck in stock-like holders for "nose-only" exposure. Using standard smoke exposure conditions, the deposition and internal distribution of the total particulate matter (TPM) from cigarette smoke was determined in BC3Fl/Cum male and female mice. Results show: (a) smoke exposure conditions can be varied so that deposition from 30 to 200 μg TPM/lung can be obtained, (b) 80–90% of the TPM deposition was found in the respiratory tissues, (c) the mouse-to-mouse variation for TPM deposition in pulmonary tissue was ∼20%, (d) similar deposition and distribution of TPM was observed in male and female mice, and (e) deposition and distribution of TPM was not altered in mice exposed to smoke on a daily basis over a 6-month period of time.

Specific-pathogen-free female F344 rats were exposed by inhalation to what was considered a maximal tolerated dose of cigarette smoke. Total pulmonary deposition of smoke particulates from a single cigarette was 0.25 mg in young rats. Rats were exposed to smoke from 7 cigarettes/day for as long as 2.5 years, at which time 30% of the rats remained alive. Mortality of smoke-exposed animals was not different from that of untreated or sham-exposed controls. Hyperplastic and metaplastic areas in the epithelium of the nasal turbinates, larynges, and tracheae of exposed animals were observed at death. The lungs of exposed rats contained areas of focal alveolitis consisting of accumulated pigmented macrophages, epithelial hyperplasia, fibrosis, and disrupted alveolar structure. Smoke exposure did not change the total number of tumor-bearing animals relative to controls; however, exposed rats had significantly fewer tumors in the hypophyses, hematopoietic-lymphoid systems, uteri, and ovaries but an increased number of tumors in the respiratory tracts and dermes. Only 1 of 93 (1%) control rats had a tumor (an alveologenic carcinoma) in the respiratory tract as opposed to 7 of 80 (9%) exposed animals (nasal tumors: 1 adenocarcinoma and 1 squamous cell carcinoma; pulmonary tumors: 5 adenomas, 2 alveologenic carcinomas, and 1 squamous carcinoma).

Heterotopically transplanted rat tracheas were continuously exposed to measured amounts of benzo(a)pyrene over a period of 1 to 6 months. The cumulative doses ranged from 10 to 2490 microng. The morphological response of the tracheal epithelium was characterized by hyperplasis during the first 2 weeks, followed by atrophy. Squamous metaplasias did not appear until after 4 months of exposure; at 4 and 6 months numerous dysplastic lesions and noninvasive carcinomas resembling those seen in the airways of humans were found in the higher carcinogen dose groups. The first invasive carcinomas developed at 4 months in the groups given 1250 microng or more benzo(a)pyrene. The lowest dose tested that produced a carcinoma within the observation period of 22 months was 300 microng benzo(a)pyrene. The majority of the neoplasms were squamous cell carcinomas, although several adenocarcinomas and sarcomas also developed. Since a variety of metaplastic and dyplastic lesions can be induced by carcinogenic polycyclic hydrocarbons in the transplanted rat tracheas, this experimental model appears to be well suited for the study of the sequential epithelial changes that lead to respiratory tract neoplasia.

A method was developed for continuously exposing tracheal epithelium to measured amounts of carcinogen. Beeswax was the vehicle for sustained release of carcinogen, and tracheas transplanted to s.c. sites were target tissues. In the experiment reported here, transplanted rat tracheas were exposed to a potent carcinogen, 7,12-di-methyl benz(a)anthracene (DMBA). The rate of release of DMBA from the beeswax carrier within the tracheal lumen approached first order when the initial concentration of carcinogen was high (3200 to 325 microng in a 24.45-mg pellet). With lower concentrations, where the carcinogen was dissolved in the beeswax, initial release was rapid, and most of the carcinogen was delivered within 4 weeks. At high DMBA dose levels, the entire tracheal epithelium was uniformly replaced by keratinizing squamous metaplasia after 1 week of exposure, and after 2 months, when from 280 to 910 microng DMBA had been delivered, all transplants had developed invasive squamous carcinomas. Sarcomas also developed in 19% of the transplants. At lower dose levels the epithelial reactions were more varied, and tumor development was more protracted. The lowest DMBA dose presently known to diduce carcinomas in this experimental model is 40 microng, which is in the dose range used for tumor initiation in skin carcinogenesis studies in mice.