Report of the Director-General of Public Health, New South Wales.
- New South Wales. Department of Public Health
- Date:
- [1925]
Licence: Public Domain Mark
Credit: Report of the Director-General of Public Health, New South Wales. Source: Wellcome Collection.
98/244 page 66
![when there is any degree of anaemia or slight or severe symptoms or signs of] lead poisoning, when an examination of the blood is made while the worker is still engaged at his craft. In mild cases of lead poisoning the stippled cells disappear within a few days. In severe cases they will be found over a period of weeks or months after the last exposure to lead. They are not found in the blood of individuals not exposed to lead suffering from the sequelae of lead poisoning (nephritis, arterio-sclerosis, palsy) unless a mobilisation of the skeletal store of lead occurs. In small numbers from 1 to 300 per million, unassociatcd with other blood changes as reduced haemoglobin, polychromasia, changes in size and shape of the red cells, they have for the purpose of diagnosis in lead poisoning a better value than lead in the urine and the blue line, and must be construed along with the symptoms of the patient. But when associated with reduced haemoglobin, anisocytosis or poikilocvtosis or nucleated red cells, even in the absence of symptoms of lead poisoning they definitely establish a diagnosis of lead poisoning if there has been a definite lead intake and there is no reason to suspect a primary or secondary anaemia not resulting from lead. It will help to exclude other moderate anaemias if it is remembered that in no other condition is there found the same amount of stippling of the red cells with such slight changes in the blood picture generally. When a profound anaemia has resulted from lead poisoning and there are found gross changes in the red cells with nucleated reds including megaloblasts, there will in our experience always be found other signs and symptoms of lead poisoning which will enable one to know that the condition is not due to a pernicious or other primary anaemia. Pallor.—In a well-marked case of mild or severe chronic lead poisoning there is nearly always seen the pallor which is so characteristic a feature of plumbism. While this sign is often seen in subjects in whom the reduction of haemoglobin is marked, nevertheless it does not depend upon the presence of a definite anaemia. When a marked anaemia is present the face has an icteric colouring, due to the products formed by the destruction of red cells, while the pallor seen in other subjects is thought to depend upon the action of lead on the capillaries of the skin. It is generally remarked that while examining a patient with this pallor the face may become flushed and the appearance of the patient changed. Tremor.—A fine tremor of the fingers is frequently seen in subjects with lead poisoning, and is of importance when associated with more typical signs, but when occurring without them such a common sign of many diseases is of little diagnostic value. Muscular Paresis and. Palsy.—It is much more common to find a history of muscular weakness among lead workers than to find a definite palsy of the antibrachial, brachial, Aran-Duchenne or peroneal type- A subject affected by chronic lead poisoning will frequently complain cf difficulty in handling a trade tool owing to its apparently increasing weight, and will often refer to pain in the articulations associated with the muscles which are picked out by lead poisoning. Besides the muscles which are specially liable to bear the brunt of the poisoning, there may be a generalised weakness of all the muscles of the hands and arms. Sensory symptoms are rare, but there may occur “ a general lassitude accompanied by painful cramps or tremor of the muscles which are later involved. Sometimes formication, numbness or a dull ache, very rarely hyperaesthesia, develop in the injured region ” (2). Mental Disorders.—Mental disorders of a minor grade are often present in lead poisoning and in severe cases typical lead encephalopathy occurs rvith mania and epileptiform convulsions. Probably in all severe cases of poisoning there is a definite degree of mental change due to the cerebral irritation arising from the meningitis which is now described as the primary brain lesion of lead. “ In almost every case of plumbism there is a change in the mental attitude which may be so slight as to be overlooked entirely, or may consist in general sluggishness and dullness with poor memory inability to concentrate and a tendency towards restlessness and irritability.” On account of its similarity to other types of disease differential diagnosis of lead encephalopathy is very difficult. It may simulate tumors and syphilis of the central nervous system, cerebral haemorrhage, epilepsy, chronic alcoholism, uraemia, eclampsia, hysteria and even neurasthenic disturbances; and great care must therefore be employed in differentiation (2). Lead in Urine and Faeces.—During the years 1925-1926 we conducted a series of quantitative analyses for lead in the urine and faeces of individuals who were suspected to be suffering from lead poisoning. In many cases the industrial history of these subjects showed a remote or negligible exposure to lead, but we were glad to include them in our work, which we regard as a preliminary survey of the problem. Our industry has been rewarded by a considerable broadening of our view on the subject of lead excretion. In the meantime the American committee investigating the Tetraethyl problem in America has published a preliminary report, and we are able to compare our results with those they have published. It is still too early to express a definite opinion as to the amount of lead in urine which may be expected in the various stages of lead poisoning. It was our original intention to endeavour to determine the relation between the amount of lead in the urine and faeces to the various stages of lead poisoning and, in particular, to the mild or early chronic poisoning when the subject was but recently removed from his work. We cannot, however, go further than to say that an excretion of between 0’10 and 0-2 mgm. of lead per litre (or even more) may generally be expected in such cases, but where the anaemia is marked the amount excreted may be quite small. What effect morbid conditions of the kidneys have on the lead excretory function is unknown, and our only evidence suggests that probably acute nephritis inhibits excretion more definitely than chronic nephritis. Brown (19) in a recent account of lead poisoning among men engaged in ship-breaking reports the determination of the amount of lead in the urine of twenty-six men who were poisoned and of three who were not affected. The urine examined in each case was from a 24-48 hour specimen, and his results are given on a basis of 2,000 c.c. Reducing these results to one litre for comparison with our work, he found lead in amounts of from 0-25 to 1-25 mgm per litre, but the average was only 0-23 mgm. per litre. The unaffected workmen showed from 0-03 to 0-15 mgm. per litre. Of the men who were poisoned half the number showed an excretion above 0-2 mgm. per litre.](https://iiif.wellcomecollection.org/image/b31485169_0098.jp2/full/800%2C/0/default.jpg)
