Waste sites and smoking risks
The EPA estimated that nearly 4 million people live within 1 mile and more than 41 million live within 4 miles of the 1200 Super-fund sites, a national priority list of toxic waste dumps. Legator and Strawn (p. 8) suggest that management of risk to the most dangerous hazardous waste sites should be conducted swiftly and decisively, e.g., in a manner similar to the decisions reached to control risks from tobacco smoke. A response was solicited from Johnson and Lichtveld, who agree that prevention of exposure to toxic wastes is foremost in actions taken to preserve public health. They disagree that exposure scenarios between waste sites and tobacco are comparable, and comment further that there is a disparity between the large amount of scientific knowledge about to-bacco compared to the little known about waste sites. Johnson and Lichtveld conclude that further research on assessment of risks from hazardous waste sites is vital if we are to effectively protect human health.
Passive smoke and benzene
Concern about the sources of benzene pollution and health risks remains. An article by Wallace, published in
EHP
(82:165-169, 1989), is questioned by Rosebrook and Worm (p. 13). Data for higher concentrations of benzene indoors compared to outdoors, even in industrial locations, are presented. The protagonists debate the conclusion that tobacco smoke is a major source of benzene exposure in both passive and active smokers, thus accounting for the differences cited between indoor and outdoor exposure to benzene.
Dioxins and risk assessment
There is a large array of scientific knowledge about dioxin, including the characterization of a specific tissue receptor for this chemical, the complexity of the dose-response toxicity curve elicited by dioxin in a variety of systems, and the similarities between these biological responses and those involved in steroid hormone regulation. Human risk estimates for dioxin are currently being reevaluated by the U.S. EPA. Lucier et al. (p. 36) analyze the scientific foundation on which this reevaluation is based and discuss the biologically based dose-reponse mechanisms. One procedure being used to improve the estimates of risk for dioxin is mechanistic modeling, an iterative process that utilizes information derived from the whole organism, tissues, cells, and the biochemical and genetic level. Scientists recognize that dioxin perturbs the complex network that coordinates changes in gene expression and toxicity, but more information is needed before the exact relationship between this cascade of events and carcinogenesis is understood.
Arsenic from gold
The prevalence of arsenic in gold mining regions of Ghana is due to contamination that occurs during the roasting process for extraction of gold from arsenic and sulfur-containing ores. From 14 to 19 tons of airborne particles containing arsenic are released daily in the mining sector of Obuasi. Amonoo-Neizer and Amekor (p. 46) found that market crops grown on soils around the mines do not contain elevated levels of arsenic, although grasses and ferns downwind from the smelter contain as much as 70 mg arsenic/kg dry mass. Cooked food, local fish, and meat did not contain elevated levels of arsenic; however, the waters sampled contain from 3 to 10 ppm arsenic and are unfit for irrigation or consumption.
Mixed blessing
Retrospective examination of an NTP database of 379 chemicals identified significant correlations in site-specific carcinogenic response within species. Haseman and Lockhart (p. 50) have determined that changing the standard two-sex, two-species model to a male rat and female mouse test model would fail to detect only 15 of 162 chemicals causing site-specific tumors. Additionally, 12 chemicals causing tumors in 2 species would be reduced to 1-species carcinogens. Potential benefits of a reduced protocol are reduced costs that could translate into increased numbers of chemicals tested with faster data acquisition. The downside is a loss of sensitivity for detection of carcinogens and an inability to gain supporting information between sexes and/or species when borderline carcinogens are evaluated.
Control of lung repair
Young and Adamson (p. 56) used co-cultures of epithelial cells and fibroblasts to determine regulatory mechanisms for reparative processes after lung injury. Isolates of these pulmonary cells were obtained from lungs of bleomycin-treated rats at different stages of the injury-repair cycle. The authors hypothesize that during the initial stages of toxicity, fibroblasts secrete cell growth factors and promote epithelial cell proliferation, but during the ensuing repair phase, regenerating epithelial cells lose their ability to inhibit fibroblast proliferation, permitting progressive fibrosis of the lung.
Skin cancer
Cutaneous toxicity may take a variety of forms, including contact sensitization and skin carcinogenesis. In this issue Ashby and colleagues (p. 62) describe the relationship between chemical structure, bacterial mutagenicity, the potential to initiate contact sensitization, and the initiation of skin carcinogenicity. The results are based on observations made with 20 chemicals and have im-portant implications not only for understanding toxic processes within the skin, but also for the prospective identification of skin carcinogens and allergens.
Human
hprt
gene mutations
Small errors in copying and repairing genetic information occur continually in dividing cells of active tissues. Although most of this damage is repaired, there is a lower background rate of mutation that can be accurately measured. Exposure to toxicants such as those in cigarette smoke can increase the frequency of errors. Burkhart-Schultz et al. (p. 68) analyze the genetic code in human white blood cells and report that many types of mutations occur at the
hprt
gene locus (encoding sequence for a specific enzyme). The study indicates that certain locations in the
hprt
gene are mutated more often than others, and hence may be more susceptible to copying errors or misrepair of damage. As the spectrum of changes in the gene caused by toxicants is defined, comparison with the background mutations will reveal changes induced by exposure.
Residential EMF and cancer risk
An early study in Denver showed that there was a direct relationship between measured electromagnetic fields (EMF) and electrical wiring in residential homes and an association between EMF and the incidence of childhood leukemia. Savitz and Kaune (p. 76) reanalyze the data by simplifying the original Wert-heimer-Leeper wiring code, reducing variation and improving precision, and suggest that EMF is associated with enhanced risk for leukemia, as well as for total cancers and brain cancer.
Last Update: August 30, 1997
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