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Highlights: [•] Oxidative decomposition of formaldehyde on Pt/TiO2 occurs at room temperature. [•] Fluoride poisoning phenomenon of Pt/TiO2 nanosheets is explained. [•] This poisoning is due to F-blocking of Pt catalytic active sites. [•] Pt/TiO2 nanosheet-type catalysts can be easily regenerated by washing with NaOH solution. [Copyright &y& Elsevier]

The 1783–1784 Laki eruption was one of the most severe natural catastrophes to occur in Iceland since settlement (around 870 CE). Vegetation damage by sulphate aerosol and fluorine poisoning caused a massive decimation of livestock which brought famine and excess deaths of 1.6 of the population. 18th Century Iceland was a Danish dependency and, despite the abundance of fish in the surrounding waters, a subsistence farming community and thus highly dependent on livestock. During the famine, the Danish government was in principle willing to provide relief. However, local authorities in Iceland were slow to ask for help, and did not dare to exploit the means at their disposal (e.g. the right to ban the export of Icelandic foodstuff) without consent from Copenhagen. The Danish officials in turn were unwilling to act decisively upon incomplete information. These two factors prevented timely measures. While 4.4 × 105 kg of grain were provided for famine relief in summer 1784, the merchants exported 1.2 × 106 kg of fish, which greatly aggravated the hunger in the second winter. The effects of this 'natural' catastrophe could therefore have been significantly reduced by efficient government measures. • The 1783 Laki eruption caused severe famine in Iceland • Danish authorities attempted relief but were ineffective • Main obstacles were transport and communication issues, unclear responsibilities and conflict of interest [ABSTRACT FROM AUTHOR]

The article covers results of health state monitoring in patients with fluorosis stages I and II, who remain or continue contact with fluor and its compounds. The author evaluated treatment efficiency for fluorosis patients and risk group members, demonstrated efficiency of therapy designed with consideration of biologic rhythms in various body systems, clinical manifestations and the disease pathogenesis.

The studies covered hemostasis changes in workers with occupational fluorosis. The disorders diagnosed could be a risk factor for IHD in aluminium production workers

Four endemic fluorosis regions in China and their environmental epidemiological characteristics were summarized in this paper. It shows that the epidemiology of endemic fluorosis is closely related to geochemical parameters of local environment. The food-web and dose-effect relationship of fluoride from environment to human body in different types of endemic fluorosis regions were studied. And the safety threshold of fluoride in different regions was determined. The results have provided a scientific basis for environmental risk assessment of fluoride in China.

Several drugs can induce bone disorders. Steroid-induced osteoporosis is the best known of all drug-induced bone disorders. However, bone disorders have also been described in association with newer drugs (LH-RH analogs, retinoids, cyclosporine, etc.). The purpose of this revue is to familiarize radiologists with drug-induced bone disorders in order to achieve earlier diagnosis, hence, improve treatment.

The effect of transfer fluorine compounds through placenta is a possibility their influence on fetus. There are known many examples of unprofitable activity fluorine compounds during pregnancy. There is mentioned among others increase percentage of preterm labours, stillbirths, congenital abnormalities and also deaths of newborns just after delivery. The mechanisms of toxic influence fluorine compounds on fetus have probably character of direct influence on embryo's cells or disturb the punction of placental tissue with following consequences. The real teratogenic fluorine compounds activity was not completely proved.

Skeletal fluorosis continues to be endemic in many parts of India. Osteosclerosis and interosseous membrane calcification have long been regarded as hallmarks of this disease. Our study showed in addition a wide variety of radiological patterns: coarse trabecular pattern, axial osteosclerosis with distal osteopenia and diffuse osteopenia. Subjects with osteopenic changes had a significantly lower dietary intake of calcium than those groups having normal radiological findings, predominant osteosclerosis or coarse trabecular pattern (p < 0.001, p < 0.01, and p < 0.01 respectively). This suggests the role of calcium intake in determining the skeletal changes in endemic fluorosis.

Feeding broiler chicks on graded levels of fluorine (0, 25, 125, 625 and 3125 ppm F) from NaF for 4 weeks (4-7 weeks of age) resulted in various alterations which depended on the level of contamination. The main changes included poor growth and feed conversion, high mortality rate, disorders of bone formation, decreased relative weights of pituitary, adrenal, heart, liver, spleen, lungs, kidneys and gizzard and changes in intestinal dimensions. Also, the biochemical tests revealed other kinds of physiological disfunction mainly in the form of anaemia (low haematocrit, haemoglobin, total protein, albumin and globulin fractions), intoxication (increased methaemoglobin), nephrotic (raised phosphorus and magnesium) and hepatic (elevated lipoproteins and lowering enzymatic activity) disfunctions. The general observations and postmortem examination confirmed also the biochemical findings which revealed the harmful effect of feedborne-fluorine intoxication in broiler chicks.

Two new cases of osteofluorosis are presented. They are attested by the existence of a bone X-ray densification, by histological lesions of hyperosteoidosis and a large increase in the fluorine content. One is a 61 year-old man who consumed 2.5 l a day of Vichy St-Yorre (a mineral water containing 8 mg of fluorine ions per litre) during 11 years; the other, an 86 year-old man who during 20 years took 500 mg of niflumic acid a day, a non-steroidal anti-inflammatory drug containing 3 fluorine atoms per molecule (i.e., 50 mg fluorine per 250 mg gellule). Both these hypertensive patients had severe renal insufficiency. These two observations serve as a reminder of the indispensable precautions to be observed when prescribing fluorine salts in the treatment of post-menopausal osteoporosis: at least the plasma creatinine level should be available in order to calculate the endogenous creatinine clearance and any possible supplementary intake of fluorine salts should be checked.

The results of surveys carried out between 1976 and 1985 in the fluorosis-endemic area of the Ethiopian Rift Valley is summarised, with emphasis on the neurological complications resulting from the crippling osteofluorosis. The neurological manifestations in the forms of myelopathy with and without radiculopathy (respectively 72% and 28%) occurred after exposure to high fluoride (greater than 4 ppm) for longer than 10 years. These deficits were clearly found to be a consequence of fluoride deposition in bones, resulting in generalised sclerosis and osteophytosis, with reduction in the diameter of the intervertebral foramina and of the spinal conal. Advanced osteosclerosis commonly causes severe spastic quadriparesis in flexion, accompanied by distressing spasms and urinary incontinence. The dilemma of these medical problems in relation to the agro-industrial economic developments of the Ethiopian Rift Valley is discussed.

A 20-30 years' occupational and/or environmental exposure to fluorine may cause osteosclerosis, especially of the spine and pelvic bones, and calcification of spinal ligaments. The radiological picture may mimic many other diseases, especially ankylosing spondylitis, diffuse idiopathic hyperostosis, and rare bone diseases, such as Albers-Schönberg disease. As clinical findings are often not characteristic, early diagnosis is based on the history of occupational exposure, examination of urinary fluoride excretion (over 8 mg F-/litre in 24 hours) and radiological signs. It is also useful to monitor the concentration of atmospheric fluoride.

The bones of two patients, one with a moderate and one with a severe chronic industrial fluorosis (stage I-II and stage III), and the bones of three control persons were examined. The following parameters were determined: the fracture load, the fracture load/unit area (resistance to pressure) of the body of the first lumbar vertebra, the bending strength of the neck of the femur and of the lower third of the femur, the fracture load/unit area and the modulus of elasticity of femoral slices 2 cm thick and of precisely defined cylinders from the femoral cortex. The microhardness according to Vickers on the cross section of the femur was also determined. The results obtained are discussed with regard to fluoride therapy of osteoporosis.

Rabbit subacute fluoride intoxication effects (21,4 mg a day for 10 months) are researched on fluor, calcium and phosphorus metabolism and on skeletal radiology. Fluoremy increase (p less than 0.05) and there is a strong fluor retention (p less than 0.01), due to fluor digestive utilization coefficient increase (p less than 0.05), in spite of relative hyperfluorury (p less than 0.05). Calcemy decreases (p less than 0.01), but phosphatemy and alkaline phosphatasemy do not vary but a little. Calcium and phosphorus balances become negative (p less than 0.05), due to calcium digestive utilization coefficient inversion (p less than 0.05) and phosphorus digestive utilization coefficient decrease (p less than 0.05) and hypercalciury (p less than 0.05) and hyperphosphatury (p less than 0.05) with phosphorus renal reabsorption coefficient decrease (p less than 0.05). Some skeletal radiological abnormalities appear on rachis and limbs.

Fluor, which is a natural substance contained in rice, vegetables, marine products and some seasonings, is assimilated into the body through ingestion. Approximately 60% of the total amount of this fluor intake would be based on rice. A histological study of cervical spine, knee ligaments, Achilles tendon and viscera of rabbits (approx. 12-16 weeks old) was made after injection with sodium fluoride in this study. The rabbits were divided into three groups: Group A (administered NaF 86.2 mg/kg, 5.7 mg/ml, 7 rabbits); Group B (administered NaF 31.5 mg/kg, 2.85 mg/ml, 6 rabbits) and a Control Group of 3 rabbits. Five rabbits in Group A (71.4%) and all six rabbits in Group B (100%) developed ossification of the posterior longitudinal ligament. Ossification of the yellow ligament was also found in two rabbits in Group A and one in Group B. No ossification was found in the Control Group. Both enchondral and intramembranous ossification were found in ossification of posterior longitudinal ossification in the rabbits.

A patient with chronic fluorine intoxication from mineral water demonstrated an abnormal intense uptake of Tc-99m MDP in the whole spine, the bone metaphyseal regions, and the sternum ("tie sternum"). Results of a bone biopsy revealed an intense osteomalacia and a high fluorine concentration. Bone imaging performed one year after the patient stopped drinking mineral water was normal.

Following several series of tests, it was shown that the administration of 500 mg/day of niflumic acid, at a dose of 250 mg morning and evening, causes in subjects with a weight between 65 and 75 kilos a moderate but permanent and relatively stable rise in the levels of plasma ionised fluorine. This constant concentration of ionised fluorine in the plasma contrasted with the marked and rapid variations which follow the ingestion of sodium fluoride, which is usually prescribed in the treatment of osteoporosis. This may explain why the fluoride ion is more active on osteogenesis when it is liberated in the organism from niflumic acid by way of metabolic processes. The dosage of 500 mg daily is much less than that which produces fluorosis after prolonged treatment; it suggests a trial of niflumic acid in the treatment of osteoporosis, respecting naturally the contra-indications, and supervising the digestive tract as always with anti-inflammatory drugs.

Skeletal fluorosis was reported as a disease endemic to an area in the Madras Presidency of Indian in 1937 and prior to this, it was known as an occasional disease. There are two endemic areas in India, one in Punjab and the other in Andhra Pradesh State. This disease is also endemic in some parts of China and Africa. The manual labourers are more frequently affected as they consume huge quantities of water with high fluoride levels. The cervical spine is often affected, manifesting as cord compression. Forty cases of fluorotic cervical cord compression, who underwent surgery are studied regarding their clinical features, radiological aspects and outcome following surgery. In selected cases of cervical fluorotic myelopathy, surgical decompression appears to be necessary and also rewarding.

Nine transiliac bone biopsies from 7 patients with skeletal fluorosis due to prolonged ingestion of often high quantities of Vichy Saint-Yorre water were analyzed. Four of these patients also suffered from a chronic renal failure. A histomorphometric study was possible in 8 out of the 9 biopsies. The measurement of bone fluoride content, and a microradiographic examination, were performed on all bone samples. The radiologically evident osteosclerosis observed in each patient was confirmed by the significant increase of trabecular bone volume. Furthermore, the osteoid surfaces were very extended but the thickness of osteoid seams was normal in 6 out of 8 cases. Two biopsies demonstrated a morphological evidence of osteomalacia with abnormally thick osteoid seams. Calcification rate, measured in one of these 2 cases after tetracycline double labeling, was extremely low (less than 0.20 micron/d). The bone fluoride content was significantly high in each specimen (greater than 0.40 bone ash%) and correlated with relative osteoid volume (r' = 0.91) and thickness index of osteoid seams (r' = 0.83). Histologically, bone tissue showed modifications classically reported in the various types of skeletal fluorosis (formation defects, mottled bone with mottled periosteocytic lacunae). In conclusion, the prolonged administration of Vichy Saint-Yorre water containing 8.5 mg of fluoride ion per liter, provokes a skeletal fluorosis. This intoxication appeared very quickly if the patient suffered from an even mild renal failure. Once again, it is shown that a disturbed renal function predisposes to an excessive retention of fluoride.