Effects of chronic chromium(vi) exposure on blood element homeostasis: an epidemiological study.

One hundred chromate production workers chronically exposed to low-level of hexavalent chromium [Cr(vi)] and eighty healthy individuals free from Cr exposure were recruited to the study. Personal sampling of airborne Cr was conducted and Cr content was quantified by Flame Atomic Absorption Spectrometry (FAAS). At the end of the sampling shift, blood samples were collected and element concentrations were measured by inductively coupled plasma mass spectrometry (ICP-MS) for Cr, Cd, Cu, Mo and Se and inductively coupled plasma atomic emission spectrometry (ICP-AES) for Ca, Fe, Mg and Zn. According to our results, 90% of the chromate production workers were exposed to airborne Cr in a concentration lower than 50 µg m(-3), which is the threshold limit value recommended by the American Conference of Governmental Industrial Hygienists and Chinese Ministry of Health. After Cr(vi) exposure, a significant increase in blood Cr, Cd, Fe, Mg, Mo, Se and Zn concentrations was observed, as well as a significant decrease in Ca concentration. A decrease in blood Cu was only observed among female workers. Blood Cr concentrations of the exposed workers (median = 15.68 ng mL(-1)) was four times higher than that of the controls (median = 3.03 ng mL(-1)), and significantly correlated with airborne Cr (r = 0.568, P<0.001). In addition, the inter-element correlations exhibited significant differences between the two groups. Our findings of the related health effects suggested that the underlying mechanisms of chronic Cr(vi) exposure on blood element homeostasis might be partly explained by oxidative stress in the body, dysfunction of Fe metabolism and renal injury.

Identification, characterization, and control of potential human carcinogens: a framework for Federal decision-making.

A two-stage process is proposed for a uniform framework for Federal agency decisions regarding the identification, characterization, and control of potential human carcinogens. Stage I would include the identification, through epidemiologic and/or laboratory studies, of chemicals that represent a potential carcinogenic risk and the characterization of that risk. Stage II would encompass the actual regulatory decision-making process regarding control of potential carcinogens. Stage I relies predominantly on scientific activity and judgment. Centralized management could enhance the efficiency and effectiveness of this process. The new National Toxicology Program may be able to perform this function. Stage II judgments are social and political. Centralization of stage II decision-making is not possible under current law.

Possible use of short-term tests for carcinogens in experimental epidemiology.

This brief overview pointed out the feasibility of applying the recently developed short-term bioassays for carcinogens/mutagens to the field of epidemiology. The simplicity and economy of these test systems permitted their adaptation for large-scale screening for intrinsic and extrinsic carcinogens with an eye to detecting subpopulations with elevated sensitivity to particular carcinogens.

The epidemiology of bladder cancer: a second look.

A case-control study among 574 male and 158 female bladder cancer patients and equal numbers of matched controls was conducted between 1969 and 1974 in 17 hospitals in six United States cities. We determined that cigarette smokers of both sexes were at higher relative risk than nonsmokers. Cigarette smoking was responsible for about one-half of male and one-third of female bladder cancer. There was an excess of bladder cancer patients with some previous occupational exposure, such as rubber, chemicals, and textiles. A weak association with coffee drinking, which appeared to be independent of smoking, was found for males. Users of artificial sweeteners were not over-represented among the cases. The authors conclude that the epidemiologic pattern of bladder cancer cannot be fully accounted for by cigarette smoking and occupational exposure and suggest a series of metabolic studies to assess the role of additional factors, such as nutrition.

Chemical carcinogenesis.

The field of chemical carcinogenesis is reviewed, with emphasis on three aspects: 1) environmental chemicals are a major cause of human cancer; 2) most chemical carcinogens require metabolic activation by mixed-function oxidases to electrophilic metabolites that form strong covalent chemical bonds with cellular macromolecules and thereby initiate the carcinogenic process; and 3) several systems are available in which normal cells can be transformed by chemical carcinogens into malignant cancer cells. Much has been learned about the cellular mechanisms of chemical carcinogenesis using these systems. They also have considerable potential to be used as prescreens for environmental carcinogens.