With intense dusting all the dusts used produced much the same effects, both immediate and remote.

With moderate exposures some dusts are much more readily eliminated than others. While coal dust and shale dust enter the lung with great readiness they do not produce, under these conditions, permanent lesions; and the lung might pass for normal after a twelvemonth.

Flue dust and crystalline silica are not eliminated with such readiness.

Two methods are available for distinguishing the dusts—perhaps three.

1. Coal and shale are taken up by cells which are quickly shed and consequently do not set up processes which block lymphatics. These cells frequently break down, and masses of dust are to be seen on the surface of the alveolar walls.

Flue dust and the crystalline silica are taken up by cells which tend to remain in situ and form plaques, which appear early and persist. They are the only site of fibrosis made out in this investigation.

Dusts which form plaques are not readily eliminated.

2. Rate of elimination is more important than rate of invasion. Dusts which are not readily eliminated after moderate exposures are to be avoided.

3. There are two ways out of the lung: direct via the bronchi in the form of plugs of mucin, dust cells and dust; and indirectly via the lymphatics. These ultimately bring some of the dust to the large bronchi at the root of the lung, and the dust can be traced through the connective tissue, muscular, and mucous coats into the epithelium, whence it is excreted. Colourless dusts become pigmented, and to judge from the data as yet available, the more marked the pigmentation the readier the elimination. It is possible that pigment plays a part in this bronchial excretory process, on the analogy of the lipochromes and the deposit of particles in the skin. The different rates at which dusts reach the mucous coats of large bronchi illustrates their relation to lymphatic drainage.

It is of importance to make out whether dusts observe an “all or none rule” or whether they exhibit gradation.

Flue dust for instance in all these experiments produced permanent lesions; but a great deal entered the lung and a great deal was eliminated. Specimens taken from animals immediately after exposure to flue dust, Transvaal quartz, and flint, show more flue dust than crystalline silica; but in cases taken later, owing to flue dust elimination being more rapid, the dust remaining is nearly the same in quantity in all three.

Experiments were carried out (series 10) to determine whether these three dusts can be eliminated like coal and shale if the amount of dust in the air be slight and the invasion of the lung moderate. It is worth making great efforts to diminish the dust cloud if there are reasonable grounds for thinking that under these circumstances rate of elimination might approach rate of invasion. If, on the other hand, a considerable proportion of any dust that enters remains, then other methods must be sought.

The result of these experiments was not very encouraging although it was fairly clear that dosage was an important factor. While it is certainly not the case that concentration of dust in the air × duration of exposure is a constant; still with flue and silica the dose must be very small if accumulation is to be avoided.

More encouraging results were obtained by adding coal. The vigorous catarrhal reaction produced results in the relatively inert dust being carried out in the plugs along with the coal; and these experiments have certainly left the impression that under the conditions described the lungs would practically free themselves from flue or crystalline silica dust if these dusts enter in small quantities only and with coal. The fact that crystalline silica—even when present in considerable quantities—does not always tend to produce grave pulmonary disease, may perhaps be accounted for by assuming that when silica is relatively benevolent there is inhaled together with it some substance that provokes a reaction in the lung with shedding of epithelium and expectoration of débris. If flue dust has been used for stone dusting with impunity it may be due to the presence of coal, since, experimentally, it behaves like the silica group when used pure.

Under the conditions of these experiments:

Dusts that make mischief are dusts that accumulate.

Dusts that are eliminated are dusts that produce a marked initial reaction with much shedding of epithelium.

Dusts that accumulate do not produce so marked an initial reaction, there being much less shedding of epithelium.

Dusts that produce an initial reaction tend to carry out with them the more inert.

An outbreak of food poisoning which occurred at Brighton in November, 1917, showed several features of unusual interest which makes its publication of value. While the epidemiological inquires and pathological investigations were carried out separately a coherent narrative is best obtained by combined presentation. The pathological investigations were carried out for, and at the request of, the Local Government Board.

The outbreak occurred in the Royal Sussex County Hospital which at the time contained 369 residents, 227 being patients and 142 staff. Twenty-eight persons suffered from food poisoning, 24 of whom were patients and 4 members of the staff. Two deaths occurred but both were patients already suffering from severe diseases.

(1) There were nineteen cases and eight deaths at the depot during the epidemic.

One doubtful case during this period recovered, and a sporadic case in June due to Type I also recovered; these are not included in the above, nor is one man who went on leave to Blackpool, and developed the disease (Type II) on arrival.

(2) So far the reserve battalions have had three cases only, with two deaths, although a high carrier-rate wave has been detected in two.

(3) All the cases (except the June case) at the depot occurred during exceptionally cold weather. In the chart the cases appear to lie in thetrough of a great depression of the curve of mean weekly temperature (broken line). They also follow immediately upon exceptional crowding (black line).

(4) There was a well-marked premonitory rise in the carrier-rate in December 1916, before the first case occurred, and an enormous rise before the epidemic was really established.The carrier-rate, which was 19·25% on December 23rd, reache dwhat is usually considered the danger point of 20% (see War OfficeMemorandum on Cerebro-spinal Fever, page 2) just six days before the first case occurred.

It would appear that estimations of the carrier-rate by means of large sample swabbings afford a reliable warning of the imminence or danger of an epidemic.

(5) The cases in the epidemic were nearly all due to the meningococcus of Type II, the organism present in the outbreak of 1916.

The rise in the carrier-rate was also chiefly due to the increase ofcarriers of this type. Freshly joined recruits showed few carriers at all and very few Type II carriers when swabbed before having slept in the barracks.

(6) During the epidemic, the carrier-rate among non-contacts was substantially the same as amongst the actual contacts of cases, averaging34% for the period, in each case.

(7) The proportion of agglutinable strains to inagglutinable strains of organisms morphologically indistinguishable from the meningococcus increased very markedly during the epidemic period.

(8) The treatment of the whole population by the steam zinc sulphate solution spray (which was carried out daily for two seven-day periods with an interval of a fortnight), was followed by a satisfactory drop in the carrier-rate, and by a temporary cessation of cases on each occasion.

(9) 60% of the actual patients suffering from the disease were in their first month of service.

40% of the patients had either been inoculated or vaccinated within seven days of onset (three on the same day); 60% within afortnight.

(10) Previous and concurrent epidemics of German measles, influenza and bronchitis had helped (by causing coughing and sneezing and by lowering vitality) to produce the great rise in the carrier-rate, which culminated in the case epidemic.

(1) Killed agglutinable broth cultures of the various dysentery bacilli may be prepared by the formalin and cold storage process and may be standardized by the method elaborated by Prof. Dreyer for the typhoid and paratyphoid bacilli.

(2) Since formalin (0·1 %) usually causes a gradual loss of sensitiveness to agglutination during the early life of the emulsion, a certain period (two months) must be allowed to elapse before the emulsion can be used as standard.

(3) After such a period the sensitiveness of the emulsions remains unaltered for at least ten months, and probably much longer.

(4) By none of the other methods of preparation investigated could satisfactory standard agglutinable cultures be made.