Harold C. Hodge

Density and Refractive Index Studies of Dental Hard Tissues I. Methods for Separation and Determination of Purity

A rapid, quantitative method for the separation of the enamel, dentin, and cementum of a single tooth to obtain samples of known purity will permit the following investigations: 1) Normal values and ranges of variation in the composition of enamel and dentin. 2) Changes in composition associated with caries (5), pyorrhea or disturbances in nutrition, metabolism or endocrine balance. 3) Proportion of enamel to dentin in normal, hyperand hypoplastic teeth and changes due to attrition, erosion or caries. Methods for obtaining pure dentin or enamel by heating or grinding are unsatisfactory because of the time required and the incomplete recovery. The method described by Brekhus and Armstrong (3), based on the use of heavy liquids with density intermediate between dentin and enamel, offers a distinct improvement over previous methods, but leaves a few things to be desired. For instance, it would be advantageou§ to have (a) a more rapid method, (b) a check on the purity of the enamel and dentin fractions, and (c) an avoidance of filtration. According to the literature, a centrifugal separation method would seem to be desirable, especially when working with fine powders. Bernal and Crowfoot (2) found centrifugation to give a more accurate

Occupational fluoride exposure.

Effects of airborne fluoride on industrial health are discussed with regard to acute and chronic effects. Injuries to lungs and skin from acute exposures are described. Chronic effects are discussed with regard to industrial sources of fluoride and air concentrations vs. urinary concentrations of fluoride. An extensive literature review is presented in the form of a table showing responses in man exposed to industrial airborne fluorides. Osteosclerosis is discussed with regard to the fluoride air standard, bone fluoride, and air fluoride concentrations. Occupational exposures to fluoride are also discussed with regard to arthritis, shortness of breath, asthma, upper respiratory infections, chronic respiratory disease, effects on kidneys, effects on pregnancy, and indices of fluoride intoxication. A table is presented showing references to studies on responses in neighborhood residents exposed to fluoride emissions. (HLW)

Density and Refractive Index Studies of Dental Hard Tissues II. Density Distribution Curves 1,2

There is considerable variation in the values recorded in the literature for the density of the dental hard tissues. Hoppe (6), Karlstrom (4) and Thewlis (12) find the enamel density to be between 2.9 and 3.0 grams per cc. On the other hand, Morichini (9) reports a figure of 2.65; Pickerill (11) finds values between 2.72 and 2.85; Thurlow and Bunzell (13) set a figure of 2.49 while Brekhus and Armstrong (3) state the density to be between 2.6 and 2.7. For dentin there are fewer values and less disagreement. Black (2), in a study of a large series of wet dentin specimens found values between 2.06 and 2.11. Krause (7), Thewlis (12) and Brekhus and Armstrong (3) report the following values, respectively, 2.08, 2.10 and 2.24. Cementum was assumed by Brekhus and Armstrong to have a density of less than 2.04, since its removal was described by the use of a liquid of that density. No other experimental values have been reported. The differences in the quoted densities may be partly, but not wholly, explained on the basis of a variation in the density of the tissue itself, either occurring naturally or brought about by the differences in

Oral toxicity and metabolism of diuron (N-(3,4-dichlorophenyl)-N′,N′-dimethylurea) in rats and dogs

Abstract Diuron ( N -(3,4-dichlorophenyl)- N′,N′ -dimethylurea) has a relatively low order of acute oral toxicity in the rat. The LD 50 (14-day) for males was 3·4 g/kg. Ten daily doses of 1 g/kg were not lethal but growth depression was observed. In both studies, increased erythropoiesis was indicated histologically. Skin irritation and sensitization tests in guinea-pigs proved negative. 90-Day feeding studies in rats disclosed no growth depression at a dietary level of 400 ppm or less; slight in males at 2000 ppm; marked in both sexes at 2500 ppm and higher. Slight anaemia and enhanced erythropoiesis were observed at 250 ppm in females and in both sexes at 2500 ppm and above. An abnormal blood pigment, identified as sulphaemoglobin was detected at 2000 ppm and higher. Feeding studies on two dogs revealed no effect at 160 ppm for 1 month but slight growth retardation and a moderate anaemia were induced by 2-month feeding of increasing dietary levels commencing at 400 ppm and terminating at 2400 ppm. 2-Yr feeding studies were conducted on rats and dogs at dietary levels of 0, 25, 125, 250 and 2500 ppm. No effect was seen at the 25, 125 or 250 ppm levels in either species with the exception of a trace of abnormal blood pigment in some animals on 125 or 250 ppm diuron and of a trend towards reduced erythrocyte counts in dogs on 250 ppm. At the highest level of 2500 ppm the principal findings in both species were growth retardation, slight anaemia, presence of abnormal blood pigment, enlargement of spleen (occasionally in rats) and of liver (dogs) and increased erythropoiesis with splenic haemosiderosis. No histological changes were seen at any level and there was no evidence of carcinogenicity. In a three-generation reproduction study in rats maintained on 0 or 125 ppm diuron, no untoward findings were obtained. In metabolic studies in rats and dogs fed 25–2500 ppm diuron for 9 months–2 yr, tissue residue levels were proportional to the dietary intake of diuron but no tissue storage occurred. Excretion occurred in both faeces and urine. N -(3,4-Dichlorophenyl)urea was the predominant metabolite in the urine; small amounts of N -(3,4-dichlorophenyl)- N′ -methylurea, 3-4-dichloraniline, 3,4-dichlorophenol and unchanged diuron were also detected.

A five-year inhalation study with natural uranium dioxide (UO2) dust. II. Postexposure retention and biologic effects in the monkey, dog and rat.

Inhalation studies show that dogs, monkeys, and rats can breathe a natural uranium dioxide aerosol of approximately 1 mu m mass median particle diameter at a mean concentration of 5 mg U/m/sup 3/ (25 x Threshold Limit Value or 28 x Maximum Permissible Concentration in Air) for periods as long as 5 yr with little evidence of serious injury (L. J. Leach et al., Health Phys. 18: postexposure periods during which pulmonary neoplasia developed in a high percentage of the dogs examined 2 to 6 yr after exposure. Pulmonary and tracheobronchial lymph node fibrosis, consistent with radiation effects, apparently dose dependent, and more marked in monkeys than in dogs was also noted. No evidence of uranium toxicity was found in records of body weights, mortality, various hematologic parameters, or the histologic condition of the kidneys. (auth)

Toxicology and No-Effect levels of aldrin and dieldrin

Some of the critical values have been selected from the various criteria just reviewed and are listed below. Acute oral toxicity. Twenty to 70 mg/kg, aldrin or dieldrin, 12 species. The estimated lethal dose for man is approximately 5 g. Mortality on repeated doses. (a) Short-term: quail, dog, turkey, mouse, <25 ppm; cat and pheasant, <100 ppm; cow, sheep, and rabbit, <165 ppm; rat, <300 ppm. (b) Short-term or chronic: quail, 0.5 ppm of aldrin, 1 ppm of dieldrin; monkey, 5 ppm of dieldrin; mouse, 10 ppm of aldrin and dieldrin; dog, 10 ppm of aldrin, 25 ppm of dieldrin; turkey, 12.5 ppm of aldrin; rabbit, 80 ppm of aldrin, 20 ppm of dieldrin; rat, 100–150 ppm of aldrin or dieldrin. Body weight. No change at 2 ppm or less. Changes: monkey, 2.5 ppm of dieldrin; male turkey, 3 ppm of aldrin; sheep and cow, 7 ppm of aldrin in hay; dog (pup), 10–25 ppm of aldrin; rat, 300 ppm of aldrin or dieldrin. Food consumption, hematology, urine analyses. Not sensitive. Liver weight: body weight increase. Rat, 0.5, 2.5 ppm; dog, 3 ppm of aldrin, 1 ppm of dieldrin. Pathology. Rat, 2 ppm of aldrin, 0.5 ppm of dieldrin; dog, 3 ppm of aldrin, 8 ppm of dieldrin; mouse, 10 ppm of aldrin or dieldrin. Reproduction. Rat, fewer pregnancies, greater mortality of pups, 12.5 ppm of aldrin, 2.5 ppm of dieldrin; dog, greater mortality of pups, 8 ppm of aldrin, 25 ppm of dieldrin; sheep, greater mortality of lambs, 25 ppm of dieldrin; quail, some changes at 1–10 ppm of dieldrin; pheasant, 25 ppm of dieldrin. Human. Typical diets in England and in the United States are estimated to contain 0.001–0.002 ppm of dieldrin. Dieldrin concentrations in human fat probably average about 0.2 ppm. Blood concentrations exceeded 20 μg per 100 ml in exposed patients showing signs of intoxication.

A five-year inhalation study with natural uranium dioxide (UO2) dust-I. Retention and biologic effect in the monkey, dog and rat.

Monkeys, dogs and rats inhaled natural UO, dust of approximately 1 micron MMD, at a concentration of 5 mg U/m3, 6 hr per day, 5 days per week for periods up to 5 yr. Retention curves for U in the lungs and other tissues including bone were established in a program of serial sacrifice and animal replacement over the 5-yr exposure period for the dog and monkey and over a 1-yr period for the rat. The 2 major sites of U accumulation, the lungs and tracheobronchial lymph nodes (TLN), accounted for over 90% of the U found in the body. For the dog and monkey, a rapid build-up of U occurred in the lungs and TLN during the first year of exposure. After 1 yr the lungs contained approximately 2000 pg U/g in the dog and 3600 pg U/g in the monkey, near maximal values. Unlike lung, the U content of the TLN for both species continued to rise reaching maximal values of 50,000 to 70,000 pgU/g after 4 yr of exposure. In kidney, femur, spleen and liver, U concentrations were comparatively low; after 5 yr of exposure, monkey spleen showed the highest concentration (350 pg U/g), whereas dog spleen represented the lowest (0.9 pg U/g). Alpha radiation dosages, calculated from the organ burdens of U, indicate that dose rates to the lungs and the lymph nodes of each species surpassed 0.03 rad/wk during the first few months of exposure. At 5 yr, dose rates to dog lung and TLN and to monkey lung and TLN were 1.8,55,3.3 and 64 rads/wk, respectively. The integrated alpha radiation dose to dog and monkey lung, after 5 yr of exposure, was estimated to be 500 and 900 rads, respectively. At this time TLN values for both species were in the order of 10,000 rads. No evidence of U toxicity was found in body weights or mortality, in the NPN levels of the blood, or in the hematologic picture. Kidney injury did not occur at the exposure level of 5 mg U/m3 (20 x TLV or 28 x MPC,). Fibrotic changes suggestive of radiation injury, however, were seen occasionally in the TLN of dogs and monkeys and in monkey lungs after exposure periods longer than 3 yr in tissues with estimated alpha doses greater than 500 rads for lung and 7000 rads for TLW. The lung and lymph node data obtained in this study show that the animal body can accumulate sufficient U from prolonged exposures to insoluble U dust at 5 mg/ms to create potential radiologic hazards. The lung and TLN values were high enough, in fact, to anticipate radiation hazards in these tissues from exposures at or lower than the occupational TLV (250 pg U/ms) recommended by the ACGIH or the MPC, (6 x ,u Ci/cm3 M 180 ,ug U/ms) suggested by the ICRP. 599 * This paper is based on work performed under contract with the United States Atomic Energy Commission at the University of Rochester Atomic Energy Project, Rochester, New York and is Report NO. UR-491076. 7 Deceased 1964.

Hereditary Opalescent Dentin III. Histological, Chemical and Physical Studies'

Deceased 1969.

Chemical Analysis of Tooth Samples Composed of Enamel, Dentine, and Cementum

Hereditary opalescent dentin has been described under a variety of names but is probably less rare than the literature indicates (1). Clinically it presents a picture of excessive destruction of the teeth, together with a more or less noticeable violet color of the enamel and light to dark brown staining of exposed dentin. This anomaly is inherited as a dominant characteristic in which a severe disturbance in dentinal development appears to be the cause of the friability and peculiar color of the teeth (2). It is easily and specifically diagnosed by (a) its inherited nature, (b) the radiographic demonstration of the typical reduction in size or absence of pulp cavities and (c) the severe tooth destruction observed clinically.

Renal Clearance of Fluoride.

Introduction. Although many investigators have analyzed enamel, dentine, and cementum of teeth, separately, a smaller number have analyzed whole teeth in which enamel, dentine, and cementum occurred in unknown proportions. Results of recorded analyses on whole teeth are summarized in table 1, which includes indications of the materials analyzed. Most of the authors did not report results in terms of percentages of Ca (6), P (4), Mg (5), C02 (7), H20 (1), organic matter (2), and inorganic matter (3), but percentages in the table are recalculated from data for tooth composition as originally expressed, to make the values comparable. Whenever the basis of the original calculations was stated, i.e., percentage of ash-weight, percentage of dry-weight, etc., that basis is noted by a suffixed letter, as indicated in the footnote under the table. The reported data, though abundant, lead to conclusions that are in some cases self-contradictory, in others radically discordant, and never completely congruent; and have been used to support inclusive and sweeping theoretical inferences. Thorough consideration of the data is out of place here, but among the sources of contradictions are these: (a) materials not described, (b) precision of methods not ascertained, (c) insufficient number of analyses, (d) insufficient precision of analyses, (e) conclusions not checked by known statistical principles. Our own results are offered, not in the belief that they remove the contradictions, but to (a) increase