The decade of the 1990s is witnessing a resurgence of cholera on a global scale. Cholera entered Latin America after almost 100 years and for the first time in the 20th century in an explosive fashion beginning with concurrent outbreaks in several coastal cities in Peru in late January 1991. The origin of the strains of Vibrio cholerae responsible for the initial outbreaks in Peru remains an enigma. Across the globe, in October 1992 a series of outbreaks of cholera-like illness in Southern India was found to be caused by a non-O1 serogroup which was subsequently classified as Vibrio cholerae O139 Bengal. As with the Latin American epidemic, the O139 serogroup spread with amazing speed and in the matter of a year affected all the cholera endemic areas in India and several neighbouring countries in south-east Asia. Imported cases of O139 V. cholerae has now been reported from several countries across the globe. These two events have dominated the global cholera scenario in the 1990s and both these events are reviewed.

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It is actually not easy for research and development itself to judge which research results will actually lead us in the direction of truly benefiting society. Thus, it is essential for us to make efforts toward sound evaluation and unbiased judgment to ensure safety and to provide the most desirable products. Research activities that support this kind of effort can be regarded as"Regulatory Science, "which can be recognized as an important field of science having independent goals and measures not found in either the basic or applied sciences. From the viewpoint of research itself, the field can best be described as"evaluation science"and from the viewpoint of actual practice, the field might best be described as an"administrative science."Regulatory science must transcend the purely academic results of basic research. The knowledge that is required for this task must always be one step ahead of today's technology in order to evaluate tomorrow's products that are being developed with ever-advancing high technology. The research domain of regulatory science requires full utilization of available knowledge in order to make the final evaluation of the material itself and its impact on the environment. Therefore, the research that can help us to produce accurate estimates is actually of greater value than the discovery of new materials or mechanisms.

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Risk assessment is a scientific endeavour to evaluate and estimate the exposure to a substance and its consequent adverse health effects by the use of the available scientific information. The four phases of the risk assessment include hazard identification, exposure estimation, doseresponse assessment and risk characterization. Recently, risk management and risk communication have been added as its final components. At present, however, methods for identifying toxicants and exposed individuals and populations, models for inferring human health effects from animal studies, techniques for estimating risks and predicting health effects with few data are all in need of improvement or development. Fortunately, remarkable advances in biotoxicology and molecular biology have promoted new understandings in the mechanism of disease. Incorporation of these new data moved the evaluation closer to the goal of estimating actual human risks. Recently developed physiologically-based pharmacokinetic models for the estimation of active chemical levels at critical organs and their conjugation with biologically-based pharmacodynamic models of the process of carcinogenesis seem to be not only an essential part of a rational approach to quantitative cancer risk assessment, but also raise fundamental questions about the nature of the events leading to malignancy. These scientific progress will develop sound risk assessment, dissolve the wide divergency in regulatory decisions of agencies in different countries, and lead to better health protection.

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The specificity and mechanism of the Scott reaction for cocaine screening were studied. This reaction consists of three procedures : 1) addition of cobaltous thiocyanate/glycerol, 2) addition of hydrochloric acid, and then 3) mixing the solution with chloroform. Our experiment using 30 drugs showed that the precipitate-forming reaction of the first step above was not specific for cocaine. However, the color reaction using the three steps was highly specific for cocaine, at least in the test using low amounts (<1.0 mg) of drugs. Promazine, promethazine, chlorpromazine, imipramine, lidocaine and diltiazem showed positive reaction when 5 mg or more of these drugs were used. These findings indicated that the specificity of the Scott reaction is markedly affected by the amount of a drug used. The stoichiometric study indicated that cocaine binds to cobaltous thiocyanate at a molar ratio of 2 : 1. Based on this finding together with the specificity of the Scott reaction, we postulated a structure of cocaine-cobaltous thiocyanate.

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The difference in amounts of β-carotene adsorbed on attapulgite and sepiolite was discussed on the basis of adsorption isotherm from alkali-refined rape seed and soybean oils. The amounts adsorbed on attapulgites were larger than those on sepiolites. The difference in the amounts adsorbed on attapulgite and sepiolite could not be explained using their surface area, pore size distribution, acid strength, acidity or free fatty acids. It was concluded that triolein was competing with β-carotene for adsorption sites of attapulgite and sepiolite and that sepiolite was more accessible to triolein competition than attapulgite.

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The degree of carboxy hemoglobin in blood was determined by multivariate analysis for the purpose of correcting an error in the low degree region by multivariate analysis. The absorbance of blood was measured at eight points, from 530 nm to 580 nm, by a spectrophotometric method, and the data were corrected using two points within the eight measured points. These corrected values were used for multivariate analysis such as cluster analysis and principal component analysis. As a result, principal component scores were obtained, and the degree of carboxy hemoglobin in blood was determined using these scores.

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A simultaneous analytical procedure was devised for asulam as a carbamate herbicide, trichlorfon (DEP) as an organophosphorus pesticide and mecoprop (MCPP) as a phenoxy-acid herbicide in tap water and their source. Owing to the thermolability of DEP and the lower volatility of asulam and MCPP, detection in GC/MS is difficult. To raise the efficacy of GC/MS, the pesticide mixture was first methylated, followed by heptafluorobutylation. For asulam, the secondary amino and primary amino groups were methylated and heptafluorobutylated, respectively. Carboxyl group of MCPP was methylated, and hydroxyl group of DEP was heptafluorobutylated. Using Sep-pak PS-1 as the solid phase extraction tube, we carried out extraction of the pesticides from water samples and their condensation. A recovery test on surface water was performed to prove the method works even at a low level (2 μg/l) of the pesticides.

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The toxic effect of a trace amount of inhaled cadmium oxide (CdO) dust on bone collagen metabolism in workers who were employed in a Ni-Cd battery plant (Cd-workers) was investigated by measuring the urinary excretion levels of hydroxylysine glycosides (Hyl-Gs) and hydroxylysylpyridinoline (Pyr) as bone collagen metabolites. Urinary Cd levels in the Cd-workers were apparently higher than control levels, but urinary β₂-microglobulin levels were within control levels. There was no statistically significant difference between the urinary Hyl-Gs levels of the Cd-workers and those of age-adjusted controls who were not engaged in Ni-Cd battery making at the same plant. The urinary Pyr levels of the Cd-workers, however, were slightly higher than age-adjusted control levels, but statistical significance was not observed except for those in their forties. These results suggest that inhaled CdO dust is involved in osseous collagen metabolism in some way, especially in bone resorption.

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