This paper offers a perspective on the health impacts of air pollution from incinerators by making a number of compari sons in terms of emissions, concentrations, damages and dam age costs. The latter are estimated by an impact pathway anal ysis, tracing the fate of a pollutant from source to receptors. Linearity is assumed for the increase of damages with incre mental exposure. The monetary valuation is based on a valu ation of mortality in terms of years of life lost, rather than sim ply the number of premature deaths. The method is applied to the incineration of municipal solid waste (MSW) with emissions equal to the regulations proposed by the European Commission in 1994 for typical per capita MSW production. Even if all MSW is incinerated (in accordance with these reg ulations), the total health damage costs are relatively minor. Also, the impacts of dioxins and carcinogenic metals are small compared to those of particles, NOx and SOx.
Carbon tetrachloride is a degreasing agent that was used at the Rocky Flats Plant (RFP) in Colorado to clean product components and equipment. The chemical is considered a volatile organic compound and a probable human carcinogen. During the time the plant operated (1953-1989), most of the carbon tetrachloride was released to the atmosphere through building exhaust ducts. A smaller amount was released to the air via evaporation from open-air burn pits and ground-surface discharge points. Airborne releases from the plant were conservatively estimated to be equivalent to the amount of carbon tetrachloride consumed annually by the plant, which was estimated to be between 3.6 and 180 Mg per year. This assumption was supported by calculations that showed that most of the carbon tetrachloride discharged to the ground surface would subsequently be released to the atmosphere. Atmospheric transport of carbon tetrachloride from the plant to the surrounding community was estimated using a Gaussian Puff dispersion model (RATCHET). Time-integrated concentrations were estimated for nine hypothetical but realistic exposure scenarios that considered variation in lifestyle, location, age, and gender. Uncertainty distributions were developed for cancer slope factors and atmospheric dispersion factors. These uncertainties were propagated through to the final risk estimate using Monte Carlo techniques. The geometric mean risk estimates varied from 5.2 x 10(-6) for a hypothetical rancher or laborer working near the RFP to 3.4 x 10(-9) for an infant scenario. The distribution of incremental lifetime cancer incidence risk for the hypothetical rancher was between 1.3 x 10(-6) (5% value) and 2.1 x 10(-5) (95% value). These estimates are similar to or exceed estimated cancer risks posed by releases of radionuclides from the site.
Previous studies in a rat model of asbestosis have demonstrated increased incorporation of tritiated thymidine by bronchiolar and alveolar epithelial cells 19 to 72 h after a single, 5-h exposure to chrysotile asbestos. This increase in thymidine labeling occurred at the first alveolar duct bifurcations, where terminal bronchioles end and where asbestos deposition is most concentrated. To determine whether airways more proximal than the terminal bronchioles exhibit a similar type of proliferative response to asbestos, incorporation of tritiated thymidine by airway epithelial cells was determined by light microscopic autoradiography. Incorporation by the epithelium in regions of the trachea, mainstem bronchi, and bronchioles was measured in lung tissue from sham-exposed and chrysotile asbestos-exposed rats, zero and 33 h after exposure. Sham-exposed animals and those studied immediately after exposure exhibited no increases in tritiated thymidine incorporation at any airway level. Tritiated thymidine incorporation by epithelial cells of bronchioles in peripheral regions of the lungs was significantly increased, as much as 20-fold, 33 h after chrysotile exposure. In the same asbestos-exposed animals, epithelial cells of the trachea, the bronchi, and the larger bronchioles did not exhibit increased cell labeling. The fact that asbestos was deposited throughout all airway levels, yet increased thymidine incorporation is observed primarily in the peripheral bronchiolar regions, raises interesting questions regarding the mechanisms of asbestos-induced cell proliferation.
In this paper we describe risk calculations performed to estimate inhalation of beryllium resulting from operational and accidental releases at the RFP. We evaluated soil and sediment monitoring data for beryllium and studied evidence of carcinogenicity and chronic beryllium disease. We also describe environmental transport modeling, provide estimates of uncertainty in the model predictions, and present distributions of carcinogenic risk resulting from the inhalation of beryllium for several generic receptor scenarios.
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