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Increased serum levels of retinol and provitamin A carotenoids were clearly associated with a decreased prevalence of hearing impairment.

as (1-Cd-F excess /Cd-I excess ) ( Fig. 1), was 47.2% (range: -9.4-83.3%) in Group D1 and 36.6% (range: -9.2-73.5%) in Group D3, and the Cd balance rate, defined as (1-Cd-F output /Cd-I intake ), was 23.9% (range: -4.0-37.7%) in Group D1 and 23.7% (range: -8.2-56.9%) in Group D3. Conclusions-Cd-F and Cd-B are better biological monitoring parameters for assessing change in Cd-I than Cd-U. The Cd uptake and Cd balance rates appeared to be higher than those in previous papers when ingested Cd mainly originated in rice. (J Occup Health 2003; 45: 43-52) Key words: Cadmium, Volunteer experiment, Rice, Dietary intake, Absorption, Biological monitoring Toxicity due to cadmium (Cd) accumulation in the body is known to cause renal damage and resultant osteoporosis. Itai-Itai disease is one disastrous example of chronic Cd poisoning. Food is the main source of Cd intake for non-occupationally exposed people, and the average dietary Cd intake by the Japanese general population was recently calculated as 28 µg/d 1) , much higher than that in other countries; e.g., 9.9 in China 2) , 7.3 in Malaysia , 8.3 in Sweden 5) and 9 to 10 in Germany 6) . In Japan, rice and shellfish are the major sources of Cd intake, and other foods sold in Japanese markets contain a very wide range of Cd concentrations 7) . In order to determine a tolerable level of Cd intake from meals, we must establish a non-observed adverse effect level (NOAEL) based on the dose-response relationship between Cd in foods and adverse effects on the kidneys. At present, however, such data are not available, and in fact, a large-scale prospective study to establish the NOAEL is currently considered infeasible.On the other hand, the dose-response relationships

In Vitro Solubility and In Vivo Toxicity of Indium Phosphide: Isamu Kabe et al. Department of Preventive Medicine and Public Health, School of Medicine, Keio University—This study was designed to clarify the in vitro solubility and the in vivo basic toxicity of indium phosphide (InP). InP powder was clearly soluble in synthetic gastric fluid and quite insoluble in saline or synthetic lung fluid. Male ICR mice (SPF grade) were given InP at the doses of 0, 1,000, 3,000, and 5,000 mg/kg, intraperitoneally (i. p.) or orally (p. o.). During a 2‐week observation, no mice died. In i. p. treated mice, the serum indium concentration showed a dose‐dependent increase, and indium mainly accumulated in the lungs and liver. Dose‐dependent increases in lung and spleen weight were observed. Black granules of InP were deposited in the lymph nodes, spleen, lungs, and liver. Extramedullary granulopoiesis was observed. And eosinophilic exudates and mononuclear cells were seen in the pulmonary alveoli. Considering these findings, InP particles were presumably transferred to the spleen, liver, and lungs by way of lym‐ phokinetics, causing reticuloendothelial responses. Hematological examination showed increased proportions of stab cells and monocytes in 5000 mg/kg i.p. dosed mice. The p. o. administered mice showed no clear relationship between the dose and biological effects.

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