Asthma's Attack
A disease which literally steals the breath from its victims now has a stranglehold on health in the United States. Asthma rates have increased by 42% in the last decade, and 14 million Americans now suffering from the disease. Not only are there more people with asthma, there are more people dying from it; asthma mortality has increased by 58% since roughly 1982. The first Focus article examines the factors that may be contributing to these increases including allergens, air pollution, smoking, and genetics, as well as factors that may exacerbate asthma such as lower income, urban environments, and lack of access to health maintenance.
Cloud of Controversy
Although exposures of agricultural workers to pesticides have been widely explored, another environmental exposure may be putting farmworkers and their families at risk of serious health problems. Known by names such as farmer's lung disease, mushroom worker's lung, and grain fever, a variety of pulmonary diseases and conditions are the result of exposures to organic dusts including molds, pollens, bacteria, mites, microbial toxins, and insect fragments. In the second Focus article, researchers discuss the latest evidence for the exact cause-and-effect relationship between agricultural dusts and these syndromes.
No More Nitrates
The Innovations article illustrates a new solution to a growing problem: nitrates in drinking water. As the main component of fertilizers and pesticides, nitrates are increasingly finding their way into water systems through runoff from farms and as by-products of manufacturing. Several companies in Europe and the United States are developing systems that use bacterial bioreactors to reduce nitrates to environmentally harmless nitrogen oxide and water.
Ames versus Rodent Carcinogen Assays
Yoshikawa reviews the contradiction between nongenotoxic carcinogens and genotoxic noncarcinogens and suggests that the capacity for chemical carcinogens to induce cell proliferation may be more important for the development of tumors than genotoxicity. He presents data in support of the hypothesis that detection of cell proliferation is the most effective approach for predicting human and rodent carcinogenicity.
Chloroform in Tap Water
Weisel and Jo analyzed human breath concentrations of the common drinking water contaminants chloroform and trichloroethene after exposure via drinking, showering, and bathing. The ingestion doses were completely metabolized in the liver, while doses from the other two routes were dispersed throughout the body. Even though risk assessments for these toxicants traditionally consider only ingestion, data indicate that the dermal and inhalation routes contribute equally, suggesting that public health decisions should include all three routes of exposure.
Neutrophil Activation by PCBs
Polychlorinated biphenyls activate neutrophils, resulting in cell degranulation and production of toxic superoxide anions. Tithof et al. present data on chemical inducers or inhibitors of neutrophil activation and hypothesize that Aroclor 1242 causes toxicity associated with inflammatory diseases by a mechanism that involves a phospholipase A2-dependent release of arachidonic acid from affected cells. The authors used PCB congeners with low or high affinity for the Ah receptor to show that this signal transduction mechanism is a novel receptor-independent process.
Release of Bone Lead into Blood
Smith et al. used stable lead isotope methodology to distinguish contemporary lead exposure from skeletal lead accumulated decades earlier. Lead in blood and trabecular bone samples was measured in five patients who underwent hip or knee joint replacement. All subjects displayed low blood lead (1-6  g/dl) and low bone lead (0.6-7.0 g/g) concentrations. Isotopic differences revealed that the skeleton contributed 40-70% of the lead in their circulation, indicating that bone could contribute a significant endogenous source of lead exposure in previously exposed individuals.
Metallothionein and Cadmium Reproductive Toxicity
A transgenic mouse strain that over-expresses metallothionein metal binding protein was used by Dalton et al. to examine the reproductive toxicology of cadmium in both sexes of mice. Cadmium is spermatotoxic in males and delays embryo implantation in females. However, injection of 10 mol cadmium/kg caused pronounced testicular necrosis and rapid histological changes in both normal and transgenic mice. Similarly, in female mice, injection of 30-45 mol cadmium/kg caused maternal and embryonic toxicity that was unprotected by overexpression of metallothionein. The authors hypothesize that cadmium causes toxicity in the testes and uterus by vascular injury, and/or in cells that do not overexpress metallothionein, such as endothelial cells in the liver.
Metal Workers Exposed to Nitrosamines
A cohort of male workers in metal factories from Italy were examined for exposure to N-nitrosodiethanolamine (NDELA), a potentially carcinogenic contaminant found in cutting fluids. Monarca et al. report NDELA traces and thioether metabolites in the urine of workers in the high-exposure group compared to those from the low-exposure group or to unexposed controls, but no changes in mutagenic profiles between any of the groups. Smoking and coffee drinking displayed a variable influence on several of the biomarker responses.
Last Update: May 6, 1997
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