FLUORINE POISONING

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ANNOTATIONS

AN INTERNATIONAL ASSOCIATION OF THEMEDICAL PRESS

A MOVEMENT was projected from Milan last summerfor the organisation of an International Associationof the Medical Press and the preliminary statementwas to the effect that the first president would beDr. Hans Spatz, the editor ’of the Miinchener Medi-jSMUsce Wochenschrift ; the first treasurer Dr.Benno Schwabe; and the secretary-general SignorSanto Vanasia, giving his address as Casella

postale 3395, Milan. Among the council the nameswere printed, without any previous sanction, of theeditor of The Lancet and the editor of the Journalof the American Medical Association, together withthe editors of a dozen or fifteen other medical journals,who may or may not have given permission. Theeditor of The Lancet, not being satisfied that anythingpractical at the present stage of European politicscould develop from the movement, asked that hisname and that of The Lancet, placed on the circularwithout approval having been asked, should beremoved. Dr. Fishbein, editor of the Journal of theAmerican Medical Association, being communicatedwith, said that his name and that of his journalalso appeared on the circulars without any authority,and he enclosed to us a copy of a letter in which hehad protested against the treatment he had received.Dr. Fishbein was more fortunate than the editor ofThe Lancet, for he obtained a courteous statementfrom Signor Santo Vanasia, the source of all thecommunications, in the following words : "I was

merely showing the basis for my future work in caseof acceptance. According to your wishes I cancel

my previous indications although I have confidencethat your ideals agree with mine." The editor ofThe Lancet not only received no assurance that thereferences to the paper and to himself would becancelled, but finds that his name and that ofThe Lancet still remain on the circulars. In the lastcircular received, the name of Dr. Hans Spatz is

.still given as president of the projected Associationand that of Dr. Benno Schwabe as treasurer. Wehave now received a communication from Dr. HansSpatz that his name has been used without his

authority and that, in spite of repeated protests, ithas until now not been expunged from the lists.He adds also that false announcements of his appoint-ment as president have been made in the German

daily press. Further, Dr. Spatz has been informedby Dr. Benno Schwabe that the printed statementsof his position as treasurer to the movement have beenmade without his consent. Dr. Hans Spatz haspublished in the German press the withdrawal of hisname from the Association, with a criticism of theextraordinary procedures of the secretary-general.In publishing this repudiation by The Lancet of anyconnexion with the movement, we are asked byDr. Spatz to associate his name with our protest.

DEFICIENCIES IN ULCERATIVE COLITIS

ONE of the most interesting aspects of biologicalprocesses is the way in which a specific effect, howeverbrought about, always tends to set up the same trainof events. If a number of causes bring about thespecific effect, the resulting train of events may becommon to a number of conditions, although modifiedand supplemented in each of them by the particularexciting cause. The appreciation of these " syn-dromes," which are common to a number of disease s

is of enormous importance in theoretical medicine;although practical medicine-the slave of diagnosis-depends more upon the recognition of the particularresponse. The rise of body temperature (and itsinevitable sequelae) which accompanies many toxicprocesses is a good example of a general responsethat may be produced by many different stimuli.Another example is salt deficiency which is commonto Addison’s disease, pyloric stenosis, excessive

sweating, diarrhoea and vomiting, and (according toWelch, Adams, and Wakefield 1 of the Mayo Clinic)ulcerative colitis. A third example, less often recog-nised, is the response of the body to a forced andcontinuous loss of protein material. Such losses aremet with in, for example, pregnancy, lactation,chronic parenchymatous nephritis, and (as is alsodemonstrated by Welch and his colleagues) ulcerativecolitis. In all of these conditions the blood-ureatends to be low, indicating a small katabolism ofamino-acids and suggesting that all the availableones are being used for the synthesis of the proteinwhich is being " lost " ; the urea nitrogen in conse-quence forms very much less than the normal 70-80per cent. of the total nitrogen leaving the body.Where this happens it is clear that the treatmentshould include high protein feeding ; and whilethe success of a generous protein intake in chronicparenchymatous nephritis is well known and thevalue of protein in pregnancy and lactation is also

accepted, the Mayo Clinic workers do well to pointout the necessity for a liberal protein diet in ulcerativecolitis.

FLUORINE POISONING

MANY of our readers will recall the " fog disaster "which occurred in the valley of the Meuse aboveLiege early in December, 1930. Within a few daysseveral thousands persons suffered from an acutepulmonary affection, and 60 lost their lives. Acommission of inquiry was set up which came to theconclusion that the disaster was due to the accumula-tion of waste factory products, in the air of the narrowsteep river valley; a blanket of cold fog during wind-less weather acting like a closed roof to the valley.The commission suggested that sulphur dioxide(or its derivatives) was the chemical substanceresponsible. Those who were familiar with the

physiological effects of SO 2, and especially those whohave experienced considerable or prolonged exposureto this gas, were not impressed by the findings of thecommission on this head. Dr. Kaj Roholm of

Copenhagen now surveys 3 the whole problem inthe light of more recent knowledge about the toxicityof fluorine and its compounds, and makes out a strongcase for the belief that fluorine and not sulphur wasthe peccant agent. Here was a narrow deep valley,a dense pall of almost stationary fog, and in two placesin the valley (at Engis and in the Sclessin-Seraignarea) a number of factories (15 in all) throwingconsiderable quantities of fluorine into the air. It

may be unlikely that such a combination of circum-stances will arise in this country, but the possibilitythat chronic fluorine poisoning may be occurringcannot be so easily dismissed.

Fluorine poisoning may be produced as a result ofindustrial processes, from the ingestion of fluorine-

1 Welch, C. S., Adams, M., and Wakefield, E. C., J. clin.Invest., January, 1937, p. 161.

2 See Lancet, 1930, 2, 1305.3 A paper read before the Danish Society for Internal

Medicine, J. industr. Hyg. March, 1937, p. 126.

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contaminated soil or water, or occasionally (as inIceland) it may arise from the dust of volcaniceruptions after it has settled on the soil. A numberof industrial processes make use of raw materialscontaining fluorides: (1) Blast-furnaces, steel andmetal works; Dr. Roholm estimates the world’s

yearly output of calcium fluoride (fluorspar CaF 2)at 200,000-300,000 tons of which 80 per cent. isused in blast furnaces. During the smelting ofiron and steel, silicon tetrafluoride escapes into theair. (2) Glass and ceramic manufacture. (3) Zincsmelting: zinc ore usually contains fluorspar. (4)Superphosphate manufacture : phosphatite containsfluoride. (5) Chemical works. In the neighbourhoodof some of the factories in the Meuse valley, it wasobserved that glass rapidly lost some of its trans-parency. Plant life was damaged around some of thefactories. Animals fed upon contaminated herbagesuffered from dental and bone diseases or died withemaciation and cachexia.

In acute fluorine poisoning resulting from breathingcontaminated air, the symptoms and signs are those ofan acute pulmonary oedema, similar to that seenafter exposure to certain poison gases." In chronic

poisoning (whether the fluorine" is air- or water-

borne), the characteristic symptoms are mottling ofthe enamel of the teeth ; bony changes, (a) either adiffuse osteo-sclerosis with deposits in the ligamentousinsertions of the muscles, or (b) bony degenerationand softening (when the poisoning is more severe);general wasting; anaemia and cachexia. Now thatattention has been drawn to this matter, no

doubt a careful study of the possible risk in ourindustrial areas will be made. Dr. Roholm insiststhat factories giving off fluorine compounds shouldbe required to take measures for effective removalof the flusrine compounds from chimney smoke.

CAROTID SINUS FAINTING ATTACKS

IF medical problems often stimulate physiologicalresearch, physiological discoveries often point the

way to advances in medicine. The latter sequenceis exemplified by the story of the carotid sinus. Inthe last ten years the physiologists, led by Hering andHeymans, have elucidated the function of this curiousbulbous dilatation at the origin of the internal carotidartery, the walls of which, as well as the substanceof the adjacent highly vascular carotid body, are

furnished with numerous afferent nerve-endings.These endings are stimulated by the mechanicalstretching of the sinus walls due to the pressure ofits contained blood, and also (probably those in thecarotid body) by certain chemical changes in theblood, such as carbon dioxide excess, oxygen deficit,and the presence of sodium cyanide in minute amounts.Nerve impulses from the stimulated endings ascendin the vagus and glossopharyngeal nerves to themedulla and give rise to certain well-defined reflexeffects, notably slowing of the heart, splanchnicvasodilatation with fall in blood pressure, andincreased breathing. In respect of blood pressure,the carotid sinus mechanism clearly supplementsthe earlier known depressor reflex from the aorticwall in counteracting excessive rise in aortic pressureand thereby regulating the general blood pressureand the blood-supply to the brain. As to respiration,some of the effects formerly attributed to the actionon the respiratory centre of changes in the amountor composition of its blood-supply are now seen tobe brought about by the carotid sinus mechanism.Soma Weiss and his colleagues have lately looked

to the carotid sinus as an explanation of some varieties

of fainting attack in man, and they summarise theirobservations of the last few years in a recent paperyIf tlie patient’s fainting attack can be reproduced atwill by digital pressure over his carotid sinus in theneck, they argue that a hypersensitiveness of thereflex is the mechanism of the attack ; the conclusionis supported by other evidence as well. They haveinvestigated 57 patients showing this phenomenon,and they remark incidentally that many of themshowed local anatomical lesions, such as tuberculousadenitis of glands near the carotid bifurcation, or

athero-sclerotic lesions in the vessel itself. Theinduced fainting attacks fell into three groups. Inthe first a vagal effect predominated, with slowingor transient stoppage of the heart, which could beprevented by atropine. In the second, splanchnicdilatation and fall of blood pressure occurred, indi.cating a release of sympathetic vasoconstrictor toneas the chief reflex effect ; adrenaline counteractedthis, while small doses of nitrites accentuated it.In the third group carotid sinus stimulation appa.rently produced curious faints, with features suggest-ing amnesia, sleep, or cataplexy, which are more

difficult to explain physiologically, since bloodpressure and heart-rate were unaltered. The authorsnote that the patients subject to carotid sinus attacksoften show evidence of what they call vegetativeneuroses-" functional " symptoms such as constantfatigue, mental depression, palpitation, emotionalinstability. They could offer little evidence, however,that the carotid sinus was responsible for any symp-toms other than the fainting attacks and phenomena. directly associated with them. In 8 of 10 cases inwhich the carotid sinuses were surgically denervated,the syncopal attacks ceased but the other featuresremained unaltered. The authors conclude there-fore that they have displayed a reflex physiologicalmechanism for a symptom hitherto classed as "func-tional " and often " neurotic," and they wonder howmany more disorders of the same class, in the behaviourof the autonomic nervous system, may be amenableto similar explanation.

A SOUTH AFRICAN PROPRIETARY MEDICINESBILL

A Proprietary Medicines and Appliances Bill hasbeen introduced into the South African Parliamentwhich may have far-reaching results. It wouldmake it an offence to print, publish, or distribute anyadvertisement of a proprietary article which isindecent or improper, or fails to state the manii-facturer’s name and address, or refers to a testi-monial, or offers free treatment, or states that thearticle is a cure for any disease. The Bill goes further,indeed, than similar proposed legislation elsewhere,for it would penalise the use in advertisements of thewords " professor," " doctor," " physician," or"

surgeon." It forbids too any such advertisementwhich is "likely to conjure up in the mind of areasonable man the fear of serious consequences fromsome trivial complaint." Finally, the advertisermust not by name or implication refer to certaindiseases scheduled as incurable or requiring specialtreatment. There is an exception for appliancesfor deafness or rupture, but the list in the scheduleincludes alcoholism, appendicitis, blindness, cancer,deafness, diabetes, high blood pressure, infantileparalysis, malaria, pneumonia, sexual impotence,tuberculosis, and venereal diseases. If the Bill were

1 Ferris, E. B., Jr., Capps, R. B., and Weiss, S., Arch. Neur.Psych. February, 1937, p. 365.