This study was undertaken to determine whether or not biological levels of mercury correlate better to values of exposure to mercury estimated by personal monitoring methods than to those obtained by conventional environmental monitoring methods. Mercury was collected for personal monitoring by amalgamating mercury vapor with gold wire in a glass tube attached to a worker's collar, and for environmental monitoring by placing bubblers containing a scrubbing solution of acidic permanganate in the work area. Individual levels of exposure to mercury were based on an 8-hour time weighted average (TWA).
Six workers from a thermometer manufacturing plant and from the same workshop were divided into two job groups for study. One, the indirect contact group consisted of 3 packers who did not handle metallic mercury and two, the direct contact group, of 3 machine operators who came into direct contact with the chemical.
1. For the indirect contact group, the TWA exposure levels for environmental monitoring and personal monitoring were equal. For the direct contact group, TWA exposure levels obtained by personal monitoring were 70% higher than those by environmental monitoring.
2. The TWA exposure (μg/cu m)/Urine (μg/dl) ratio in the direct contact group, when estimated by environmental monitoring, approximated 2.9 (2.2-3.5) and when estimated by personal monitoring, approximated 4.8 (4.2-5.9). The ratio obtained by personal monitoring was about 1.7 times higher than that by environmental monitoring. In contrast, the TWA exposure/Urine ratio in the indirect contact group approximated 5.1 (4.4-5.9) when monitored by environmental methods and 5.7 (5.3-6.2) by personal methods. The ratios obtained by the two different methods were in close agreement in this case.
3. The TWA exposure (μg/cu m)/Blood (μg/l) ratio in the direct contact group, when estimated by environmental monitoring, approximated 0.7 (0.6-0.9) and when estimated by personal monitoring, approximated 1.2 (1.0-1.4). However the TWA/Blood ratios estimated by environmental monitoring and by personal monitoring were 1.3 (1.2-1.4) and 1.4 (1.3-1.5) respectively for the indirect contact group.
From the above results, it is clear that the levels of individual exposure indicated by environmental monitoring, were lower than what was, in fact, the actual exposure. Therefore, it is recommended that personal monitoring be used to estimate worker exposure to mercury vapor when there is potential contact with metallic mercury and when air mercury levels fluctuate.
4. Since mercury vapor emanating from contaminated clothing may be a significant source of additional exposure for workers, such concentrations of mercury vapor from workers' clothing were also measured. Vapor which emanated from clothing over an 8-hour period were at levels of 19-218μg Hg for the indirect contact group and 200-897μg Hg for the direct contact group. If one assumes that floor space per individual is 10m³, and that workers usually wear the same contaminated clothing for an entire 8-hour day, the extrapolated mercury levels for workers exposed to mercury from clothing would be 20-90μg Hg/cu m. In the National Institute for Occupational Safety and Health criteria for mercury, “exposure” is defined as exposure to levels above 20μg Hg/cu m of air. Therefore, it is evident that the levels of mercury emanating from clothing can not be ignored when sources of exposure to mercury are being considered.

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In view of the fact that there are only a few studies on the effects of cadmium (Cd) on teeth, experiments were carried out on the distribution of Cd in teeth. Also the effects of Cd on another essential (Zn), non essential element (Pb), which is a member of the same family as Cd in the periodic table and indispensable to teeth, were investigated.
Dogs were chosen for this experiment because canine teeth are similar to human teeth and, in addition, because a pure strain could be bred easily.
Dogs subjected to our experiments were litter mates of a first hybrid generation and were bred under fixed conditions. Cd was administered in the form of CdCl₂ in a dose of 2mg Cd/kg i.p. once a week, starting when the animals reached six weeks of age. The dogs were divided into a short term group and a long term group to the former Cd was administered 4 times and to the latter 20 times. Each group was paired with a control group that received water when Cd was given to the experimental groups. The amounts of Cd in various viscera (soft tissues) and teeth (hard tissue) as well as an essential element, zinc (Zn), and a nonessential element, lead (Pb), were measured and compared with those obtained for the controls.
1) The Cd administered accumulated markedly in the liver and in the renal cortex in both the short and long term groups. The amount in the liver of the latter was about 3 times as large as that of the former, and in the renal cortex about 3.5 times as great.
2) Zinc in the liver and the renal cortex increased markedly due to Cd accumulation, and there was some increase in Zn in the blood, pulp, renal medulla, lung and adrenal gland.
In the pancreas, stomach, ovary and brain, however, there was no increase in Zn level despite the Cd accumulation.
3) Lead actually decreased in the viscera in the long term group as compared to the short term group, implying that Pb shows nonparallel behavior with respect to Cd.
4) Cd accumulated in large amounts in the dental germ of the permanent teeth in the short term group and in the pulp of the permanent teeth in the long term group, both of which are soft tissues. On the other hand, there was only little Cd accumulation in hard tissues such as deciduous teeth and the crowns and the roots of permanent teeth.
5) Zn markedly increased in the pulp of the permanent teeth where there were large Cd accumulations, but it also increased in the crowns and roots of the teeth where Cd was not markedly accumulated.
6) There was a tendency for increasing amounts of Pb in the crowns and the roots of the teeth. In deciduous teeth and the dental germ of the permanent teeth, Pb did not show any increase.
7) The accumulation of metal elements in teeth was more marked for the mandible than for the maxilla in the short term group, and vice versa in the long term group.
8) The hard dental tissue, different from the hard osseous tissue and the soft visceral tissue, is said to have scarcely any metabolism. However, an increase in the Zn amount in teeth suggests the possibility of considerably high metabolism in the hard dental tissues and of a strong selectivity factor in absorbing substances.

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It is impossible to calculate the age-adjusted death rate of a disease in a group without the age distribution of the population in that group. Instead, the crude relative frequency of the disease per number of total deaths can be used, but, the age-adjusted relative frequency is considered to be a better indicater than crude relative frequency.
A model has been constructed in which the death rate of an observed group is different from that of a standard group only for an objective disease and where death rates of other diseases are equal between the two groups. Direct age-adjusted relative frequency of the objective disease is not affected by the age distribution of the population of the observed group, but indirect age-adjusted relative frequency is affected slightly by the age distribution of the model. In the case where the death rate of the objective disease of the observed group is greater than that of the standard group, age-adjusted relative frequency of the observed group is less than the value calculated for the mortality rates of the two groups, but in the reverse case the relative frequency is greater.
Relative frequency of a disease for a group is affected by variations in the death rates of other diseases in that group, while the death rate from a disease is not affected by death rates from other diseases.
A skewed value is obtained for age-adjusted relative frequency if the age distribution of deaths of an observed group is greatly different from that of a standard group.

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Female Wistar rats with an average body weight of 100g were divided into 8 groups according to three levels of vitamin D₂ added to their diets (0, 1 and 5IU/100g of food), two levels of cadmium (0 and 10mg/100g of food) and the method-oral or subcutaneous-for administration of cadmium.
Rats were exposed to cadmium for 500 days.
There was a significant decrease of the iron content in the liver, kidney and femur in rats which had ingested cadmium and in vitamin D-deficient control rats. However in the rats which had been injected cadmium there was no decrease in iron in the liver, and only a slight decrease in iron in the femur and kidney was observed.
Significant reductions of hematocrit and hemoglobin were found only in those rats which had received cadmium both orally and subcutaneously, although there was no significant difference for iron concentrations in organs between rats having ingested cadmium and rats receiving it both orally and subcutaneously.
These results indicate that cadmium-induced anemia can not explained merely as an iron deficiency caused by the oral exposure to cadmium.

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Accumulations of and excretions of arsenic in rats where the arsenic is administered continuously over long periods of time has as yet been left for study. This is because methods to measure trace amounts of arsenic in biological sample have not been well established. This author has reported on an accurate and highly sensitive new method to determine arsenic levels in biological samples which involves flameless atomic absorption spectrometry using a carbon tube atomizer. In order to measure arsenic accumulations and excretions in rats organs, the above method was applied to appropriate biological specimens. As a result, arsenic levels were measured.
Procedure: One hundred and five male Wister rats weighing 80±1g were divided into four groups, five rats to a cage. Arsenic was in all cases administered as a single daily dose per os with catheter, and three groups (75 rats) were administered solutions of sodium arsenite amounting to either 10μgAs, 50μgAs or 100μgAs/day continuously for 100 days. The fourth group (30 rats) served as the control. For the determination of arsenic concentrations in rats organs, five rats from each group were sacrified at days 0 (control group only), 20, 40, 60, 80 and 100. And the amounts of arsenic excreted in the feces and urine were checked between every third and fourth day.
Result: 1. The amounts of arsenic excreted in the urine of control rats showed a constant level of about 30% of ingested total arsenic (contained naturally in a standard diet). The group administered 10μgAs/day arsenic excreted 13% of the administered arsenic which increased to 25% as the duration of administrations increased. The groups administered 50μgAs/day and 100μgAs/day excreted from 5 to 15% of the administered arsenic.
2. The amount of arsenic excreted in feces of control rats was almost equal to that in urine (approximately 30%). At early stage, rats administered arsenic excreted lesser amounts of arsenic (approximately 17∼22%) than the controls (approximately 30%). However, arsenic excretion ratios increased to about 30% as the period extended. These results are shown in Table 4.
3. The average arsenic level in the whole blood of the controls at day 0 was 1.8ppm, increasing to 7.8ppm after 100 days. Most of the arsenic in blood is absorbed by erythrocytes. After arsenic was administered, it accumulated in blood at high levels. The concentrations of arsenic in blood was higher for subjects than for controls (Table 5).
4. Arsenic accumulations in rats organs were obsereved for both subject and control groups rats except in the case of the skull of the 10μgAs/day and control groups. High concentrations of arsenic in the lungs, heart, kidneys, spleen, liver, testes, brain, muscles, skull and the hair from the experimental group were found when compared to those of control. The spleen, liver, kidneys and the lungs showed the highest concentrations of arsenic of all examined viscera.
5. There were high correlations between arsenic concentrations in body hair and in viscera. Therefore, viscera arsenic concentrations may be hypothesized by examining the levels found in body hair alone (Table 11).

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