Download the full version of the testbank or solution manual at

https://testbankdeal.com

Investment Banking Valuation Leveraged

Buyouts and Mergers and Acquisitions 2nd
Edition Rosenbaum Test Bank

https://testbankdeal.com/product/investment-
banking-valuation-leveraged-buyouts-and-mergers-
and-acquisitions-2nd-edition-rosenbaum-test-bank/

Explore and download more testbank or solution manual

at https://testbankdeal.com
 Recommended digital products (PDF, EPUB, MOBI) that
you can download immediately if you are interested.

Mergers Acquisitions and Other Restructuring Activities

7th Edition DePamphilis Test Bank

https://testbankdeal.com/product/mergers-acquisitions-and-other-
restructuring-activities-7th-edition-depamphilis-test-bank/

testbankdeal.com

Mergers Acquisitions and Other Restructuring Activities

8th Edition DePamphilis Test Bank

https://testbankdeal.com/product/mergers-acquisitions-and-other-
restructuring-activities-8th-edition-depamphilis-test-bank/

testbankdeal.com

Mergers Acquisitions and Other Restructuring Activities

8th Edition DePamphilis Solutions Manual

https://testbankdeal.com/product/mergers-acquisitions-and-other-
restructuring-activities-8th-edition-depamphilis-solutions-manual/

testbankdeal.com

THiNK 3rd Edition Boss Test Bank

https://testbankdeal.com/product/think-3rd-edition-boss-test-bank/

testbankdeal.com
Ethics for the Legal Professional 8th Edition Orlik Test
Bank

https://testbankdeal.com/product/ethics-for-the-legal-
professional-8th-edition-orlik-test-bank/

testbankdeal.com

Canadian Organizational Behaviour 7th Edition McShane Test

Bank

https://testbankdeal.com/product/canadian-organizational-
behaviour-7th-edition-mcshane-test-bank/

testbankdeal.com

Financial Accounting Tools for Business Decision-Making

Canadian 7th Edition Kimmel Solutions Manual

https://testbankdeal.com/product/financial-accounting-tools-for-
business-decision-making-canadian-7th-edition-kimmel-solutions-manual/

testbankdeal.com

Essentials of Entrepreneurship and Small Business

Management 6th Edition Scarborough Test Bank

https://testbankdeal.com/product/essentials-of-entrepreneurship-and-
small-business-management-6th-edition-scarborough-test-bank/

testbankdeal.com

Fundamentals of Anatomy and Physiology 11th Edition

Martini Test Bank

https://testbankdeal.com/product/fundamentals-of-anatomy-and-
physiology-11th-edition-martini-test-bank/

testbankdeal.com
Family Business 4th Edition Poza Solutions Manual

https://testbankdeal.com/product/family-business-4th-edition-poza-
solutions-manual/

testbankdeal.com
Exploring the Variety of Random
Documents with Different Content
have definite relation to the hardness or softness of the body. The higher the
proportion of silicic acid in the glaze the harder the firing it will stand; the more the
flux materials are in excess the lower will the melting point be.
The most important flux materials are, arranged in order of decreasing fusibility,
lead oxide, baryta, potash, soda, zinc oxide, chalk, magnesia, and clay.
The glaze is made by first mixing the ingredients dry, and then either fritting them
by fluxing in a reverberatory furnace and finally grinding them very finely in water or
using the raw material direct. In the fritting process in the case of the lead glazes
the soluble lead compounds become converted into less soluble lead silicates and
double silicates.
The glaze is applied in different ways—dipping, pouring, dusting, blowing, and
volatilising. Air-dried and biscuited objects are dipped; pouring the glaze on is
practised in coarse ware, roofing-tiles, &c.; dusting (with dry finely ground glaze,
litharge, or red lead) also in common ware; glaze-blowing (aerographing) and glaze
dusting on porcelain. In these processes machines can be used. Bricks are only
occasionally glazed with glazes of felspar, kaolin, and quartz, to which lead oxide is
often added in very large quantity. Lead poisoning in brick works in view of the
infrequent use of lead is not common, but when lead is used cases are frequent.
Kaup quotes several cases from the factory inspectors’ reports: thus in three roof-
tiling works examination by the district physician showed that almost all the workers
were affected.
Coarse ware pottery is made of pervious non-transparent clay with earthy fracture
—only a portion of this class of ware (stoneware) is made of raw materials which fire
white. Such ware generally receives a colourless glaze. The clay is shaped on the
potter’s wheel, and is then fired once or, in the better qualities, twice.
Grinding the ingredients of the glaze is still often done in primitive fashion in
mortars. The glaze is usually composed of lead oxide and sand, often with addition
of other lead compounds as, for example, in quite common ware, of equal parts of
litharge, clay, and coarse sand. Sometimes, instead of litharge, galena (lead
sulphide) or, with better qualities of ware, red lead or ‘lead ashes’ are used.
The grinding of the glazes in open mills or even in mortars constitutes a great
danger which can be prevented almost entirely by grinding in ball mills. The glaze
material is next mixed with water, and the articles are either dipped into the creamy
mass or this is poured over them. In doing this the hands, clothes, and floors are
splashed. The more dangerous dusting-on of glaze is rarely practised. Occasionally
mechanical appliances take the place of hand dipping. Placing the ware in the glost
oven is done without placing it first in saggars.
In the better qualities of pottery cooking utensils, which are fired twice, a less
fusible fritted lead glaze is generally used. Coloured glaze contains, besides the
colouring metallic oxides, 30-40 per cent. of litharge or red lead.
 As Kaup shows, Continental factory inspectors’ reports make only isolated
references to occurrence of lead poisoning in potteries. Insight into the conditions in
small potteries is obtained only from the Bavarian reports. In Upper Bavaria ninety-
three potteries employ 157 persons who come into contact with lead glaze. Eleven
cases were known to have occurred in the last four years. Teleky found thirty-six
cases of lead poisoning (mostly among glostplacers) in the records of the Potters’
Sick Insurance Society of Vienna.
Chyzer has described the striking conditions in Hungary. There there are about
4000 potters, of whom 500 come into contact with lead glaze. Chronic lead
poisoning is rife among those carrying on the occupation as a home industry.
Members of the family contract the disease from the dust in the living rooms. This
dust was found to contain from 0·5 to 8·7 per cent. of lead.
In the china and earthenware factories in Great Britain, in the ten years 1900-9,
1065 cases with fifty-seven deaths were reported.
Manufacture of stove tiles.—The application of glaze to stove tiles is done in
different ways. The two most important kinds are (1) fired tiles and (2) slipped tiles.
In the production of fired tiles a lead-tin alloy consisting of 100 parts lead and 30-36
parts tin—so-called ‘calcine’—are melted together in fireclay reverberatory or muffle
furnaces and raked about when at a dull red heat so as to effect complete oxidation.
The material when cool is mixed with the same quantity of sand and some salt,
melted in the frit kiln, subsequently crushed, ground, mixed with water, and applied
to the previously fired tiles. In this process risk is considerable. Presence of lead in
the air has been demonstrated even in well-appointed ‘calcine’ rooms. In unsuitably
arranged rooms it was estimated that in a twelve-hour day a worker would inhale
0·6 gramme of lead oxide and that 3-8 grammes would collect on the clothes.
Slipped tiles are made in Meissen, Silesia, Bavaria, and Austria by first applying to
them a mixture of clay and china clay. The glaze applied is very rich in lead,
containing 50-60 parts of red lead or litharge. Generally the glaze is applied direct to
the unfired tiles and fired once. Figures as to occurrence of poisoning in Germany
are quoted by Kaup from the towns of Velten and Meissen. Among from 1748 to
2500 persons employed thirty-four cases were reported in the five years 1901-5.
Thirteen cases were reported as occurring in the three largest factories in Meissen in
1906.
From other districts similar occurrence of poisoning is reported. In Bohemia in a
single factory in 1906 there were fourteen cases with one death, in another in 1907
there were fourteen, and in 1908 twelve cases; eight further cases occurred among
majolica painters in 1908.
Stoneware and porcelain.—Hard stoneware on a base of clay, limestone, and
felspar has usually a transparent lead glaze of double earth silicates of lead and
alkalis, with generally boric acid to lower the fusing-point; the lead is nearly always
added in the form of red lead or litharge. The portion of the glaze soluble in water is
fritted, and forms, when mixed with the insoluble portion, the glaze ready for use.
The frit according to Kaup contains from 16 to 18 per cent. of red lead, and the
added material (the mill mixing) 8-26 parts of white lead; the glaze contains from 13
to 28 parts of lead oxide. The ware is dipped or the glaze is sometimes aerographed
on. Ware-cleaning by hand (smoothing or levelling the surface with brushes, knives,
&c.) is very dangerous work unless carried out under an efficient exhaust. Colouring
the body itself is done with coloured metal oxides or by applying clay (slipping) or by
the direct application of colours either under or over the glaze. Some of the under-
glaze colours (by addition of chrome yellow or nitrate of lead or red lead) contain
lead and are applied with the brush or aerograph or in the form of transfers.
Plain earthenware is either not glazed or salt glazed; only when decorated does it
sometimes receive an acid lead glaze.
Porcelain receives a leadless glaze of difficultly fusible silicate (quartz sand, china
clay, felspar). Risk is here confined to painting with lead fluxes (enamel colours)
containing lead. These fluxes are readily fusible glasses made of silicic acid, boric
acid, lead oxide, and alkalis, and contain much lead (60-80 per cent. of red lead).
In the glass industry lead poisoning may occur from use of red lead as one of the
essential ingredients. In Great Britain, in the years 1900-9, forty-eight cases were
reported in glass polishing from use of putty powder.

LETTERPRESS PRINTING, ETC.

Type metal consists of about 67 per cent. lead, 27 per cent. antimony, and 6 per
cent. tin, but sometimes of 75 per cent. lead, 23 per cent. antimony, and 2 per cent.
tin.
The actual printer comes least of all in contact with lead. Use of lead colours
(white lead, chromate of lead, &c.) may be a source of danger, especially in the
preparation of printing inks from them and in cleaning the printing rolls. A further, if
slight, danger arises from the use of bronze powder consisting of copper, zinc, and
tin. The two last-named metals contain from 0·1 to 0·5 per cent. of lead, and in the
application and brushing off of the bronze there is a slight risk.
The compositor is exposed to constant danger from handling the type and
disturbing the dust in the cases. This dust may contain from 15 to 38 per cent. of
lead. Blowing the dust out of the cases with bellows is especially dangerous, and
want of cleanliness (eating and smoking in the workroom) contributes to the risk.
Type founders and persons engaged in rubbing and preparing the type suffer.
Introduction of type-casting machines (linotype, monotype) has lessened the danger
considerably.
No lead fumes are developed, as a temperature sufficiently high to produce them
is never reached. In all the processes, therefore, it is lead dust which has to be
considered.
The following figures of the Imperial Statistical Office as to occurrence of lead
poisoning among printers in Vienna indicate the relative danger:

Average No. of Average No. of Percentage of

Occupation. Members, 1901- Cases, 1901- Cases, 1901-
1906. 1906. 1906.
Compositors 3182 90·3 2·8
Printers 809 20·3 2·4
Casters and Stereotypers 241 15·8 6·6
Females employed in casting 74 8·17 10·8

In Bohemia there is reference to thirty-eight cases in letterpress printing in 1907

and twenty-seven in 1908.
Among 5693 persons treated for lead poisoning between the years 1898 and 1901
in hospitals in Prussia, 222 were letterpress printers.
Between 1900 and 1909 in Great Britain 200 cases of lead poisoning were
reported.

VARIOUS BRANCHES OF INDUSTRY

The number of industries using lead is very large. Layet as long ago as 1876
enumerated 111. We, however, limit ourselves to those in which the risk is
considerable.
Use of lead beds in file-cutting has given rise to many cases. Further, to harden
the file it is dipped into a bath of molten lead. From 3 to 6 per cent. of lead has
been found in the dust in rooms where hardening is done.
Of 7000 persons employed in file-cutting in the German Empire in the years 1901-
5 on an average 30·5 or 0·43 per cent. were affected yearly. In Great Britain 211
cases were reported in the years 1900-9.
In polishing precious stones formerly many cases of lead poisoning occurred, the
reason being that the polishers come into contact with particles of lead and fix the
diamonds to be polished in a vice composed of an alloy of lead and tin. Danger is
increased when the stones are actually polished on revolving leaden discs. In
Bohemia granite polishing used to be done in this way, but is now replaced in many
factories by carborundum (silicon carbide).
Musical instrument making in Bohemia in the years 1906-8 was found regularly to
give rise to cases of lead poisoning from use of molten lead in filling them with a
view to shaping and bending. In lead pipe and organ pipe works, lead burning,
plumbing, &c., considerable risk is run.
 Often the causes of lead poisoning are difficult to discover, and, when found,
surprising. Thus shoemakers have suffered from holding leaden nails in the mouth.
Again, cases in women have been reported from cutting out artificial flowers or
paper articles with aid of lead patterns, or counting stamps printed in lead colours.8

MERCURY

As metallic mercury gives off vapour even at ordinary temperatures, poisoning can
occur not only in the recovery of the metal from the ore, but also in all processes in
which it is used.
Chronic industrial poisoning occurs principally in the preparation and use of
mercury salts, in recovery of the metal itself and of other metals with use of an
amalgam, in water gilding, from use of nitrate of mercury in the preparation of
rabbit fur for felt hat making, from use of mercury pumps in producing the vacuum
in electric filament lamps, and in making barometers and thermometers.
Preparation.—Mercury is obtained by roasting cinnabar (sulphide of mercury).
When cinnabar is heated with access of air the sulphide burns to sulphur dioxide and
the mercury volatilises and is subsequently condensed. Formerly the process was
carried on in open hearths; now it is done usually in blast furnaces. The mercury is
condensed in Idria in large chambers cooled with water, while at Almaden in Spain it
is collected in a series of small earthenware receptacles (aludels), from small
openings in which the mercury flows in gutters and collects. The mercury so
recovered is usually redistilled.
On the walls of the condensers a deposit of sulphide and oxide of mercury
collects, removal of which is one of the operations most attended with risk.
Recovery of silver or gold by amalgamation with mercury is carried on only in
America. The metallic silver or gold is taken up by the mercury, from which it is
recovered by distillation.
The conditions in the quicksilver mines of Idria in Austria have improved of late
years. Thus in the five years prior to 1886 of 500 cases of illness more than 11 per
cent. were due to chronic mercurial poisoning. In 1906, 209 persons were employed,
of whom only one-third were permanent hands. Among these the sickness rate was
very high (95-104 per cent.). Of 741 cases of illness among the miners there were
six of mercury poisoning, and of 179 among persons employed in recovery of the
metal, twelve cases.1
The conditions of employment in the cinnabar mines of Monte Amiata in Italy have
recently been described in detail.2 Here, although the recovery of the metal is
carried out in modern furnaces, thus greatly reducing the danger, nevertheless
nearly all the furnace workers suffer from chronic poisoning.
 In silvering of mirrors the leaf of tinfoil was spread out on an inclined table;
mercury was poured over it and the sheet of glass laid on the top with weights. The
superfluous mercury was squeezed out and ran away owing to the sloping position
of the table. Now this process, even in Fürth, is almost entirely replaced by the
nitrate of silver and ammonia process. Years ago the number of cases of poisoning
was very serious in places where, as in Fürth, the work was carried on as a home
industry.
In the production of incandescent electric bulbs danger arises from breaking of the
glass pipes of the pumps and scattering of mercury on the floor of the workrooms.
Since there is a growing tendency to replace mercury pumps by air pumps such
cases ought to become rare.
In water gilding—a process little employed now—the metal objects (military
buttons, &c.) to be gilded, after treatment with a flux, are brushed over with the
mercury amalgam, and subsequently fired to drive off the mercury. Unless careful
provision is made to carry away the vapour chronic poisoning cannot fail to occur.
Even sweeps have been affected after cleaning the chimneys of water gilders’
workshops. In Great Britain, between 1899 and 1905, six cases were reported
among water gilders.
In the manufacture of barometers and thermometers mercury poisoning is not
infrequent. Between 1899 and 1905 sixteen such cases were reported in England;
during the same period there were seventeen cases among those putting together
electrical meters.
Risk of mercurial poisoning is constantly present in hatters’ furriers’ processes and
in subsequent processes in felt hat factories. The risk from use of nitrate of mercury
is considerable to those brushing the rabbit skins with the solution (carotting), and
subsequently drying, brushing, cutting, locking, and packing them. According to
Hencke in 100 kilos of the carotting liquid there are 20 kilos of mercury. In England,
in the years 1899-1905, thirteen cases of mercurial poisoning were reported in
hatters’ furriers’ processes. Among eighty-one persons so employed the medical
inspector found twenty-seven with very defective teeth as the result of the
employment, and seventeen with marked tremor.
In the manufacture of mercurial salts poisoning occurs chiefly when they are made
by sublimation, as in the manufacture of vermilion, of corrosive sublimate (when
mercurous sulphate is sublimed with salt), and in the preparation of calomel (when
sublimate ground with mercury or mercurous sulphate mixed with mercury and salt
is sublimed). Between 1899 and 1905 in England seven cases were reported from
chemical works. As to occurrence of mercury poisoning from fulminate of mercury,
see the chapter on Explosives.

ARSENIC
 Chronic industrial arsenical poisoning, both as to origin and course, is markedly
different from the acute form.
The chronic form arises mainly from inhalation of minute quantities of metallic
arsenic or its compounds in recovery from the ore, or from the use of arsenic
compounds in the manufacture of colours, in tanyards, and in glass making. Acute
industrial arseniuretted hydrogen poisoning is especially likely to occur where metals
and acids react on one another and either the metal or the acid contains arsenic in
appreciable amount. Further, arseniuretted hydrogen may be contained in gases
given off in smelting operations and in chemical processes.
Recovery of Arsenic and White Arsenic.—Pure arsenic is obtained from native cobalt
and arsenical pyrites by volatilisation on roasting the ore in the absence of air. After
the furnace has been charged sheet iron condensing tubes are affixed to the mouths
of the retorts, which project out of the furnace, and to these again iron or
earthenware prolongs. Arsenic condenses on the sides of the sheet metal tubes and
amorphous arsenic, oxides, and sulphides in the prolongs. After sublimation has
been completed the contents of the prolongs are removed and used for production
of other arsenic compounds; the (generally) argentiferous residues in the retorts are
removed and further treated in silver smelting works; finally, the crusts of crystalline
arsenic (artificial fly powder) are knocked out from the carefully unrolled sheet iron
tubes.
As can be readily understood from the description opportunity of poisoning from
volatilisation of arsenic and of arsenic compounds is considerable. Metallic arsenic is
used for making hard shot, and for increasing the brilliancy and hardness of metal
alloys (type metal, &c.).
White arsenic (arsenic trioxide) is obtained by roasting with access of air in
reverberatory furnaces arsenical ores and smelting residues. The vapours of white
arsenic sublime and are condensed as a powder in long walled channels or in
chambers, and are resublimed in iron cylinders. White arsenic is used in making
colours, in glass (for decolourising purposes), as an insecticide in the stuffing of
animals, &c.
Industrial Arsenic Poisoning.—In the extraction of arsenic and preparation of
arsenious acid danger is present. But reliable accounts in literature of poisoning
among those engaged in arsenic works are wanting.
Those engaged in roasting operations and packing suffer much from skin
affections. Similar poisoning is reported in the smelting of other arsenical ores—
nickel, cobalt, lead, copper, iron, and silver, from arsenic compounds present in the
fumes. This is especially the case in the smelting of tin, which generally contains
arsenical pyrites.
Danger is present also in unhairing (i.e. removing the wool from sheep skins),
since the skins imported from Buenos Aires and Monte Video are treated with a
preservative which, in addition to sodium nitrate, soda, and potash, contains
generally arsenious acid.
In tanneries a mixture of arsenic sulphide (realgar) and lime is used for unhairing.
Arsenic is used also for preserving and stuffing animal furs; but although affections
of the skin are described I cannot find reference to arsenical poisoning.
The inspector for East London in 1905 refers to severe eczematous eruptions on
face, neck, and hands, affecting workers in a sheep dip works—mainly in the
packing of the light powder in packets.
Formerly the use of arsenic in the manufacture of colours was great, especially of
emerald (Schweinfurter) green. This is made by dissolving arsenious acid in potash
with addition of acetate of copper. Drying and grinding the material constitute the
main danger. Scheele’s green is another arsenical colour.
Use of arsenic colours is becoming less and less. But in colour printing of paper
and colouring of chalk they are still employed. They are used, too, as mordants in
dyeing, but cases of poisoning from these sources in recent years are not to be
found.
The dust in many glass works contains, it is stated, as much as 1·5 per cent of
white arsenic.
Despite the numerous opportunities for arsenical poisoning in industries it is rare
or, at any rate, is only rarely reported.
Arseniuretted Hydrogen Poisoning.—Industrial poisoning from arseniuretted
hydrogen is caused mostly by inhalation of the gases developed by the action on
one another of acids and metals which contain arsenic. Hydrogen gas as usually
prepared for filling balloons gives occasion for poisoning.
In Breslau in 1902 five workmen became affected, of whom three died from
inhalation of arseniuretted hydrogen gas in filling toy balloons.1
Further, use of hydrogen in lead burning may expose to risk, and also preparation
of zinc chloride flux.
Of thirty-nine recorded cases of arseniuretted hydrogen poisoning twelve were
chemists, eleven workers filling toy balloons, seven aniline workers, five lead
smelters, three balloonists, and in one the origin could not be traced. Nineteen of
these proved fatal within from three to twenty-four days.2
Cases are recorded (1) in the reduction of nitroso-methylaniline with zinc and
hydrochloric acid; (2) in the preparation of zinc chloride from zinc ashes and
hydrochloric acid; (3) from manufacture of zinc sulphate from crude sulphuric acid
and zinc dust; (4) in spelter works in the refining of silver from the zinc crust with
impure hydrochloric acid; and (5) in the formation room of accumulator factories.
 The English factory inspectors’ report describes in 1906 occurrence of three cases
in an electrolytic process for the recovery of copper in which the copper dissolved in
sulphuric acid was deposited at the cathode, and hydrogen at the lead anode. In the
1907 report mention is made of two cases, one affecting a chemist separating
bismuth from a solution of bismuth chloride in hydrochloric acid, and the other
(which proved fatal) a man who had cleaned a vitriol tank.
The poisoning resulting from ferro-silicon is in part referable to development of
arseniuretted hydrogen gas.

ANTIMONY

It seems doubtful if industrial poisoning can really be traced to antimony or its

compounds; generally the arsenic present with the antimony is at fault. Erben1
considers that industrial antimony poisoning occurs among workmen employed in
smelting antimony alloys in making tartar emetic through inhalation of fumes of
oxide of antimony.
A case is cited of a workman in Hamburg engaged in pulverising pure antimony
who was attacked with vomiting which lasted for several days, and the inspector of
factories noted epistaxis (nose bleeding) and vomiting as following on the crushing
of antimony ore.
Compositors in addition to chronic lead poisoning may suffer, it is alleged, from
chronic antimony poisoning, showing itself in diminution in the number of white
blood corpuscles and marked eosinophilia. These changes in the blood could be
brought about experimentally in rabbits. Antimony was found by the Marsh test in
the stools of those affected.

IRON

Pig iron is obtained by smelting iron ores in blast furnaces (fig. 29), through the
upper opening of which charges of ore, limestone or similar material to act as a flux,
and coke are fed in succession. The furnaces are worked continuously, using a blast
of heated air; carbon monoxide is produced and effects the reduction of the ore to
molten iron. The latter accumulates in the hearth and is covered with molten slag;
this flows constantly away through an opening and is collected in slag bogies for
removal, or is sometimes cooled in water.
The crude iron is tapped from time to time, and is led in a fluid condition into
moulds called ‘pigs,’ in which it solidifies. Cast iron is occasionally used direct from
the blast furnace for the purpose of making rough castings, but generally it is further
refined before being used in a foundry by remelting with cast iron scrap in a cupola
furnace.
 Fig. 29.

a Hearth; b Bosh; c Shaft; d Gas

uptake; e Down-comer; f Tuyères
with water cooling arrangement;
g Blast pipes; h Tapping hole; k
Supporting columns; l Furnace
bottom; m Charging hopper; n
Bell with raising and lowering
arrangement.

Wrought iron is made by treating pig iron in refinery and puddling furnaces; in
these much of the carbon is removed as carbon monoxide, and from the puddling
furnace the iron is obtained as a pasty mass which can be worked into bars, rods, or
plates.
Steel is made in various ways. The Acid Bessemer process consists in forcing
compressed air in numerous small streams through molten cast iron, in iron vessels
(converters) which are lined with ganister, a silicious sandstone. These can be
rotated on trunnions. Basic Bessemer steel is made in similar converters by the
Thomas-Gilchrist or basic process, which can be applied to pig irons containing
phosphorus. The latter is removed by giving the converter a basic lining of calcined
magnesium limestone mixed with tar.
In the Martin process steel is obtained by melting together pig iron with steel
scrap, wrought iron scrap, &c., on the hearth of a Siemens regenerative furnace with
a silicious lining.
In iron smelting the most important danger is from blast furnace gas rich in
carbonic oxide. Sulphur dioxide, hydrocyanic acid, and arseniuretted hydrogen gas
may possibly be present.
When work was carried out in blast furnaces with open tops the workers engaged
in charging ran considerable risk. But as the blast furnace gas is rich in carbonic
oxide and has high heating capacity these gases are now always led off and utilised;
the charging point is closed by a cup (Parry’s cup and cone charger) and only
opened from time to time mechanically, when the workers retire so far from the
opening as to be unaffected by the escaping gas. The gas is led away (fig. 29)
through a side opening into special gas mains, is subjected to a purifying process in
order to rid it of flue dust, and then used to heat the blast, fire the boilers, or drive
gas engines.
Severe blast furnace gas poisoning, however, does occur in entering the mains for
cleaning purposes. Numerous cases of the kind are quoted in the section on
Carbonic oxide poisoning.
The gases evolved on tapping and slag running can also act injuriously, and
unpleasant emanations be given off in granulating the slag (by receiving the fluid
slag in water).
In the puddling process much carbonic oxide is present. Other processes,
however, can scarcely give rise to poisoning.
The basic slag produced in the Thomas-Gilchrist process is a valuable manure on
account of the phosphorus it contains; it is ground in edge runners, and then
reduced to a very fine dust in mills and disintegrators. This dust has a corrosive
action already referred to in the chapter on Phosphorus and Artificial Manures.
The poisoning caused by ferro-silicon is of interest. Iron with high proportion of
silicon has been made in recent years on a large scale for production of steel. Some
4000 tons of ferro-silicon are annually exported to Great Britain from France and
Germany. It is made by melting together iron ore, quartz, coke, and lime (as flux) at
very high temperature in electrical furnaces. The coke reduces the quartz and ore to
silicon and metal with the production of ferro-silicon. Certain grades, namely those
with about 50 per cent. silicon, have the property of decomposing or disintegrating
into powder on exposure for any length of time to the air, with production of very
poisonous gases containing phosphoretted and arseniuretted hydrogen. The iron and
quartz often contain phosphates, which in presence of carbon and at the high
temperature of the electrical furnace would no doubt be converted into phosphides
combining with the lime to form calcium phosphide; similarly any arsenic present
would yield calcium arsenide. These would be decomposed in presence of water and
evolve phosphoretted and arseniuretted hydrogen gas. In addition to its poisonous
properties it has also given rise to explosions.
 [In January 1905 fifty steerage passengers were made seriously ill and eleven of
them died. In 1907 five passengers died on a Swedish steamer as the result of
poisonous gases given off from ferro-silicon, and more recently five lives were lost
on the steamer Aston carrying the material from Antwerp to Grimsby.[C] This
accident led to full investigation of the subject by Dr. Copeman, F.R.S., one of the
Medical Inspectors of the Local Government Board, Mr. S. R. Bennett, one of H.M.
Inspectors of Factories, and Dr. Wilson Hake, Ph.D., F.I.C., in which the conclusions
arrived at are summarised as follows:

1. Numerous accidents, fatal and otherwise, have been caused

within the last few years by the escape of poisonous and explosive
gases from consignments of ferro-silicon, which, in every instance,
have been found to consist of so-called high-grade ferro-silicon,
produced in the electric furnace.
2. These accidents, for the most part, have occurred during
transport of the ferro-silicon by water, whether in sea-going vessels
or in barges and canal-boats plying on inland waters.
3. These accidents have occurred in various countries and on
vessels of different nationalities, while the ferro-silicon carried has,
in almost every instance, been the product of a different
manufactory.
4. Ferro-silicon, especially of grades containing from 40 per cent.
to 60 per cent. of silicon, is invariably found to evolve considerable
quantities of phosphoretted hydrogen gas, and, in less amount, of
arseniuretted hydrogen, both of which are of a highly poisonous
nature. A certain amount of the gas evolved is present, as such, in
the alloy, being ‘occluded’ in minute spaces with which its
substance is often permeated.
5. As the result of careful investigation, it has been shown that
certain grades of ferro-silicon—notably such as contain about 33
per cent., 50 per cent., and 60 per cent. of silicon—even when
manufactured from fairly pure constituents, are both brittle and
liable to disintegrate spontaneously, this latter characteristic being
apt to be specially marked in the case of the 50 per cent. grade.
All these grades are commonly employed at the present time.
6. In the event of disintegration occurring, the amount of surface
exposed will, obviously, be greater than if the mass were solid.
7. Evolution of poisonous gases is greatly increased by the action
of moisture, or of moist air, under the influence of which
phosphoretted hydrogen is generated from calcium phosphide,
which, in turn, is formed, in large part, at any rate, from the
calcium phosphate present in anthracite and quartz, at the high
temperature of the electric furnace. If spontaneous disintegration of
the alloy also occurs, much larger quantities of gas would be given
off from such friable and unstable material, other conditions being
equal. The greater or less tendency of a given sample to evolve
poisonous gases, and even a rough estimate of their probable
amount may be arrived at by the use of test-papers prepared with
silver nitrate.
8. There is no evidence that low-grade ferro-silicon (10 to 15 per
cent.), produced in the blast-furnace, has ever given rise to
accidents of similar character to those known to have been caused
by the high-grade electrically produced alloy. Blast-furnace ferro-
silicon does not evolve poisonous gases even in presence of
moisture.
9. As regards ferro-silicon produced in the electric furnace, the
evidence available goes to show that certain percentage grades are
practically quite innocuous. This statement applies to grades of
alloy of a silicon content up to and including 30 per cent., and
probably also, though in considerably less degree, to those of 70
per cent. and over.
10. In view of the fact that the use of ferro-silicon of grades
ranging between 30 per cent. and 70 per cent. apparently is not
essential in metallurgical operations, with the possible exception of
basic steel manufacture, it will be advisable that the production of
this alloy of grades ranging between these percentages should be
discontinued in the future.
11. The proprietors of iron and steel works making use of ferro-
silicon will assist in the protection of their workpeople, and at the
same time act for the public benefit by restricting their orders to
grades of this material, either not exceeding 30 per cent., or of 70
per cent. and upwards, according to the special nature of their
requirements.
12. But as, pending international agreement on the question,
intermediate percentages of ferro-silicon will doubtless continue to
be manufactured and sold, the issue, by the Board of Trade, of
special regulations will be necessary in order to obviate, so far as
may be possible, chance of further accidents during the transport of
this substance.
Inter alia, these regulations should require a declaration of the
nature, percentage, date of manufacture, and place of origin of any
 such consignment.

The suggested regulations are printed on p. 291.]

ZINC

Industrial poisoning from zinc is unknown. The chronic zinc poisoning among
spelter workers described by Schlockow with nervous symptoms is undoubtedly to
be attributed to lead.

COPPER: BRASS

Occurrence of brass-founder’s ague.—Opinion is divided as to whether pure

copper is poisonous or not. Lehmann has at any rate shown experimentally that as
an industrial poison it is without importance.
Occurrence, however, of brass-founder’s ague is undoubtedly frequent. Although
neither pure zinc nor pure copper give rise to poisoning, yet the pouring of brass (an
alloy of zinc and copper) sets up a peculiar train of symptoms. As the symptoms are
transient, and medical attendance is only very rarely sought after, knowledge of its
frequency is difficult to obtain.
Sigel,1 who has experimented on himself, believes that the symptoms result from
inhalation of superheated zinc fumes. In large well-appointed brass casting shops
(as in those of Zeiss in Jena) incidence is rare.
Lehmann2 very recently has expressed his decided opinion that brass-founder’s
ague is a zinc poisoning due to inhalation of zinc oxide and not zinc fumes. This
conclusion he came to as the result of experiments on a workman predisposed to
attacks of brass-founder’s ague. Lehmann’s surmise is that the symptoms are due to
an auto-intoxication from absorption of dead epithelial cells lining the respiratory
tract, the cells having been destroyed by inhalation of the zinc oxide. He found that
he could produce typical symptoms in a worker by inhalation of the fumes given off
in burning pure zinc.
Metal pickling.—The object of metal dipping is to give metal objects, especially of
brass (buckles, lamps, electric fittings, candlesticks, &c.), a clean or mat surface and
is effected by dipping in baths of nitric, hydrochloric, or sulphuric acid. Generally
after dipping in the dilute bath the articles go for one or two minutes into strong
acid, from which injurious fumes, especially nitrous fumes, develop with occasionally
fatal effect (see the chapter on Nitric Acid). Unfortunately, there are no references in
the literature of the subject as to the frequency of such attacks.
Recovery of gold and silver has been already referred to in the chapters on
Mercury, Lead, and Cyanogen.
 Mention must be made of argyria. This is not poisoning in the proper sense of the
word, as injury to health is hardly caused. Argyria results from absorption of small
doses of silver salts which, excreted in the form of reduced metallic silver, give the
skin a shiny black colour. Cases are most frequently seen in silverers of glass pearls
who do the work by suction. Local argyria has been described by Lewin in silvering
of mirrors and in photographers.

III. OCCURRENCE OF INDUSTRIAL POISONING IN

VARIOUS INDUSTRIES
The most important facts have now been stated as to the occurrence of poisoning
in industry, and there remain only a few gaps to fill in and to survey briefly the risks
in certain important groups of industry.

TREATMENT OF STONE AND EARTHS

Lime Burning: Glass Industry

Lead poisoning in the ceramic industry (earthenware, porcelain, glass, polishing of

precious stones, &c.) has been dealt with in detail in the chapter on Lead. There is
further the possibility of chrome-ulceration, of arsenic poisoning, and conceivably
also of manganese. Further, poisoning by carbonic oxide and carbon dioxide may
occur from the escape of furnace gases where hygienic conditions are bad. In
charging lime kilns poisoning by carbonic oxide has occurred. The report of the
Union of Chemical Industry in 1906 describes the case of a workman who was
assisting in filling the kiln with limestone. As the furnace door was opened for the
purpose gas escaped in such amount as to render him unconscious. He was picked
up thirty minutes later, but efforts at resuscitation failed.
Carbonic oxide poisoning, again, may arise from the use of Siemens regenerative
furnaces, especially glass furnaces: details are given in the chapter on Illuminating
Gas.
Hydrofluoric acid is present as an industrial poison in glass etching (see Fluorine
Compounds). Persons employed in this process suffer from inflammation of the
respiratory tract and ulceration of the skin of the hands. I could not find any precise
statement as to the frequency of the occurrence of such injuries. Use of sand-
blasting to roughen the surface of glass has to some extent taken the place of
etching by hydrofluoric acid.

TREATMENT OF ANIMAL PRODUCTS

In tanning use of arsenic compounds for detaching the wool from skins and of gas
lime for getting rid of hair may cause injury to health. With the latter there is
possibility of the action of cyanogen compounds (see the chapters on Arsenic and
Cyanogen).

PREPARATION OF VEGETABLE FOOD STUFFS AND THE LIKE

In fermentation processes as in breweries and the sugar industry accumulations of

carbonic acid gas occur, and suffocation from this source has been repeatedly
described. Mention in this connection should be made of the use of salufer
containing some 2 per cent. of silicofluoric acid as a preservative and antiseptic in
beer brewing. In the sulphuring of hops, wine, &c., the workers may run risk from
the injurious action of sulphur dioxide. Arsenic in the sulphuric acid used for the
production of dextrine may set up industrial poisoning. Poisoning from ammonia gas
can occur in cold storage premises. Industrial poisoning from tobacco is not proved,
but the injurious effect of the aroma and dust of tobacco—especially in women—in
badly arranged tobacco factories is probable.

WOOD WORKING

Injurious woods.—In recent literature there are several interesting references to

injury to health from certain poisonous kinds of wood—skin affections in workers
manipulating satinwood, and affections of the heart and general health in workers
making shuttles of African boxwood. Details of these forms of poisoning are reported
from England and Bavaria. The wood used for making the shuttles was West African
boxwood (Gonioma Kamassi). It appears that the wood contains an alkaloidal poison
which affects the heart’s action. The workers suffered from headache, feeling of
sleepiness, lachrymation, coryza, difficulty of breathing, nausea, and weakness. Four
workers had to give up the work because of the difficulty in breathing. Inquiry was
made by Dr. John Hay of Liverpool in 1908 and by the medical inspector of factories
in 1905. The following table shows the symptoms found:

Persons Examined.
Symptoms. 1905. 1907-1908.
(1) Number. Per cent. Number. Per Cent.
(2) (3) (4) (5)
Headache 27 24·1 18 22·8
Feeling of somnolence 10 9·0 17 21·5
Running of eyes 13 11·6 9 11·3
Running of nose 28 25·0 20 28·0
Breathing affected 34 30·4 13 16·4
Nausea or sickness 13 11·6 3 3·8
Faintness or weakness 11 9·6 1 1·2
 The later inquiry shows considerable diminution in the amount of complaint as to
respiratory trouble. This may have been due to the improved conditions of working,
freely acknowledged by the men. Men were examined who had complained of the
effects of the wood in 1905, and had continued uninterruptedly at the same kind of
work during the interval without any obvious further injury to their health, although
they preferred working on other woods.
East Indian boxwood had to be discarded in the shuttle trade owing to its irritant
action on the eyes. Sabicu wood from Cuba was stated to give off ‘a snuffy dust
under the machine and hand planes, the effect of which upon the worker is to cause
a running at the eyes and nose, and a general feeling of cold in the head. The
symptoms pass off in an hour or so after discontinuance of work.’ Reference was
made in the report for 1906 to eczematous eruptions produced by so-called Borneo
rosewood, a wood used owing to its brilliant colour and exquisite grain in fret-saw
work. The Director of the Imperial Institute experimented with this wood, but failed
to discover injurious properties in it. At the same time experiments with the wood
and sawdust of East and West Indian satinwood were undertaken, but also without
result.
From inquiries subsequently made it appeared that much confusion existed as to
the designation ‘satinwood,’ as under this name were classed both East and West
Indian satinwood and also satin walnut. The evidence was clear that East Indian
satinwood was more irritating than West Indian. Satin walnut wood is apparently
harmless. In the shipbuilding yards of East London, Glasgow, and Bristol affections
of the skin were recognised, but susceptibility to the wood varied. One man asserted
that merely laying a shaving on the back of his hand would produce a sore place.
The injurious effects here seem to disappear quickly. Exhaust ventilation is applied,
but there is a tendency to give up the use of the wood.
Isolated cases of illness have been ascribed to working teak and olive wood. In
Sheffield the following are held to be irritating: ebony, magenta rosewood, West
Indian boxwood, cocos wood. Some kinds of mahogany are said to affect the eyes
and nose.
Use of methylated spirit in polishing furniture is said to lead to injury to health
although not to set up actual poisoning. Lead poisoning can occur from the sand-
papering of coats of paint applied to wood.
In impregnating wood with creosote and tar the effects on the skin noted in the
chapter on Tar are observed.

TEXTILE INDUSTRY

In getting rid of the grease from animal wool carbon bisulphide or benzine may be
used.
 The process of carbonising in the production of shoddy may give rise to injury to
health from acid fumes. Lead poisoning used to be caused by the knocking together
of the leaden weights attached to the Jacquard looms. This is a thing of the past, as
now iron weights are universal.
Opportunity for lead poisoning is given in the weighting of yarn—especially of silk
with lead compounds.
In bleaching use of chlorine and sulphur dioxide has to be borne in mind.
In chemical cleaning poisoning by benzine may occur.
In dyeing and printing use of poisonous colours is lessening, as they have been
supplanted by aniline colours. On occurrence of aniline poisoning in aniline black
dyeing see the section on Aniline. Use of lead colours and of chromate of lead are
dealt with in special sections.
 PART II
THE SYMPTOMS AND TREATMENT OF INDUSTRIAL
POISONING

In this section the most important diseases and symptoms of industrial poisoning
will be described. In doing this—considering the mainly practical purpose of this
book—theoretical toxicological details and any full discussion of disputed scientific
points will be omitted.

I. INTRODUCTORY
Hitherto in this book we have intentionally followed the inductive method, from
the particular to the general: we began by citing a number of important instances of
industrial poisoning, but only now will endeavour be made to give a definition of the
terms ‘poison’ and ‘poisoning.’
Attempts at such definitions are numerous; every old and new text-book of
toxicology contains them. A few only hold good for our purpose. It is characteristic
that Lewin, after attempting a definition of the conception ‘poisoning,’ himself rejects
it and declares that he can see no practical disadvantage in the impossibility of
defining this notion, because deductions based upon the knowledge of undoubted
cases can never be dispensed with, even if a definition were possible: one
justification the more for our inductive method.
But we will not quite dispense with a definition.
Poisons are certain substances which are able chemically to act on an organism in
such a way as to effect a permanent or transient injury to its organs and functions;
an injury consequently to the health and well-being of the person affected; this
injury we call poisoning.
In the present book we have refrained from including industrial infections among
industrial poisonings, and the subject has been limited to poisoning in the restricted
and current sense of the word.
An industrial poison is a poison employed, produced, or somehow occasioned in
industrial occupation, which is brought about inadvertently, and consequently
against the will of the person poisoned.
From a simple survey of the action of industrial poisons in general we may group
them as follows:
 1. Poisons which act superficially, i.e. which cause in the organs
which they touch gross anatomical lesions (irritation, corrosion, &c.)
—so-called contact-effect. To this class belong especially irritant
and corrosive poisons.
2. Blood poisons, i.e. poisons which are absorbed by the blood
and change it; this change can affect either the blood colouring-
matter, with which certain poisons form chemical compounds, or
the blood corpuscles themselves can be altered or destroyed (for
instance, poisons having a hæmolytic action).
3. Poisons with definite internal action, so-called remote or
specific effect. To this class belong the poisons which, after being
absorbed into the system, act upon definite organs or tissues in a
specific manner (nerve poisons, heart poisons, &c.).

It is indeed possible for one and the same poison to display two or all three of
these modes of action.
The effect of poison depends upon an interaction of the poison and the organism,
or its single organs. Selection as regards quality and quantity is a property of the
organism as well as of the poison: the nature and amount of the poison taken in are
determining factors on the one side, and on the other the constitution, size, and
weight of the affected organism. The chemical constitution of the poisonous
substance determines the qualitative property of the poison.
Further, certain physical properties of the poison determine its action, especially its
form, solubility in water, and its power of dissolving fat. These affect its susceptibility
to absorption, to which point we shall return shortly; the hygroscopic capacity of a
poison produces a highly irritant and corrosive action.
Industrial poisons can be absorbed (1) as solid substances, (2) as liquids, and (3)
as gases. Since industrial poisoning, as defined above, is of course neither desired
nor intended by the sufferer, who unsuspectingly takes into his system poison used
or developed in the factory, solid substances in finely divided condition—in the form
of dust—can be considered as industrial poisons. Accordingly, industrial poisons can
be classed as due to dust, gases, and liquids.
The poison may be introduced into the body through the functional activity of the
organism by the lungs or alimentary tract, or it may penetrate the uninjured or
injured surface of the skin.
Industrial poisons which contaminate the air of the factory are inhaled—these are
consequently either poisonous dusts or gases and vapours.
As a rule, only industrial poisons in a liquid form enter through the skin, which
may be either intact or wounded; gaseous poisons seldom do; poisons in the form of
fat or dust can only pass through the skin after they have been first dissolved by the
secretions of the skin or of a wound, so that they come to be absorbed in solution.
Most frequently those liquid poisons which are capable of dissolving the fat of the
skin are thus absorbed, and next, such liquids as have a corrosive effect, breaking
down the resistance of the skin covering and producing an inflamed raw surface. But
such poisons much more easily enter through the mucous membrane, as this
naturally offers a much weaker resistance than the skin.
From a quantitative point of view it is especially the amount of poison actively
assimilated which determines the effect. Every poison is without effect if assimilated
in correspondingly small quantities. There is consequently a minimum poisonous
dose, after which the poison begins to act; but this minimum dose can only be
ascertained and specified when the qualitative properties and the weight of the
organism are also taken into consideration; it has therefore a relative value. The
strongest effect which a poison is able to produce is the destruction of the life
functions of the organism, the fatal effect. This fatal dose, however, can only be
determined relatively to the qualities of the organism in question.
Not only is the absolute quality of the poison of decisive significance, but the
degree of concentration often influences its action, that is to say, the greater or less
amount of effective poison contained in the substance conveying it into the
organism; concentration plays an important part in many industrial poisons,
especially, as is obvious, in corrosive poisons.
A further important point is the time which it takes to absorb the poison. The
action of the poison—the whole expression of the symptoms of poisoning—is
essentially influenced by this fact.
Usually gradual and repeated absorption of small quantities produces slow onset
of symptoms, while sudden absorption of larger quantities of poison brings about
rapid onset of illness. In the former case the poisoning is called chronic, in the latter,
acute. Acute industrial poisoning is sometimes so sudden that the affected person
cannot withdraw himself in time from the influence of the poison, nor prevent its
entrance in considerable quantities into his system; this is often caused by the fact
that the effect of the poison is so rapid that he is often suddenly deprived of power
to move or of consciousness, and remains then exposed to the action of the poison
until help comes. Such accidents are mostly caused by poisonous gases.
Occasionally also considerable quantities of poison enter quite unnoticed into the
body, such as odourless poisonous gases in breathing, or poisonous liquids through
the skin. In chronic industrial poisoning unsuspected accumulation of poison takes
place, until symptoms of illness ultimately reveal themselves; as the first stages of
poisoning are not recognised in time by the person affected, he continues exposed
to the influence of the poison for weeks, months, even years, until the chronic effect
has reached its full development and becomes obvious. Such insidious industrial
poisoning arises through the continual absorption into the lungs or stomach of small
quantities of poisonous dust, gases, and vapours, during constant or frequent work
in an atmosphere containing such gases; poisonous liquids also, by soiling hands
and food, or by penetrating the skin, can produce slow industrial poisoning.
Industrial poisoning which in respect of its duration stands midway between acute
and chronic is called sub-acute poisoning. This usually means that more frequent
absorption of greater quantities of poison has taken place, though not in doses large
enough to produce an immediately acute effect. This is important legally because
industrial poisonings caused through the sudden absorption of poison in sufficient
quantity to act immediately or to bring about subsequent symptoms of poisoning,
are reckoned as accidents. Thus acute and many sub-acute industrial poisonings are
accounted accidents. Chronic industrial poisonings, acquired gradually, count as
illnesses. But as in certain cases it cannot be decided whether sudden or gradual
absorption of the industrial poison is in question, this distinction is an unnatural one.
It is also unnatural in the legal sense, for there is often no material reason for
regarding as legally distinct cases of chronic and acute industrial poisoning. To this
we shall refer later in discussing the question of insurance against industrial
poisoning.
We have from the outset assumed that the effect of the poison depends not only
on the nature of the poison itself, but also on that of the organism, considered both
quantitatively and qualitatively.
Significant in a quantitative respect is the body weight of the organism, and the
fatal dose of the poison must be ascertained and stated in connection with the body
weight, calculated as a rule per kilo of the live weight.
The qualitative point of view must reckon with the differing susceptibility of
organisms for poison. This varying susceptibility to the action of poison, the causes
of which are very obscure, is called disposition.
Different species (of animals and men) exhibit often very different degrees of
susceptibility towards one and the same poison; the differences in this respect are
often very considerable, and one cannot simply transfer the experience
experimentally gained from one species of animal to man or another species of
animal, without further experiment. Besides disposition, sex, and still more age,
often determine within the same species marked difference of susceptibility to a
poison. Further, there is an individual disposition due to qualities peculiar to the
individual, which makes some persons more than usually immune and others
specially susceptible. Individuals weakened by illness are particularly susceptible to
poisoning. Two diseases, in especial, favour the operation of poison, influencing
disastrously the capacity for assimilating food, and reducing the general resisting
power of the body; of these tuberculosis stands first.
Individual disposition plays in industrial poisoning a part which must not be under-
estimated; it determines the possibility of acclimatisation to a poison; some
individuals capable of resistance habituate themselves—often comparatively easily—
to a poison, and become, up to a certain limit, immune against it, that is, they can
tolerate a quantity which would be injurious to others not so accustomed. With other
individuals, however, the opposite effect is apparent. Repeated exposure to the
action of the poison leads to an increased susceptibility, so that acclimatisation is not
possible. Innate hyper-sensitiveness of the individual towards a poison is called
idiosyncrasy. Frequently, for example, this quality shows itself as hyper-sensitiveness
of the skin towards the harmful action of certain poisons. A marked lowering in the
sensitiveness, innate or acquired, of the organism towards a poison is called
immunity.
The possibility of the absorption and action of a poison presupposes—speaking
generally—its solubility, and indeed its solubility in the body juices.
In general, poison can be absorbed at very different points of the body; so far as
industrial poisons are concerned, these are the mucous membrane of the respiratory
passages, the mucous membrane of the digestive tract, and the skin, intact or
broken. The rapidity of absorption depends on the nature of the poison, of the
individual, and the channel of absorption. Of industrial poisons gases are relatively
the most quickly absorbed; sometimes indeed so swiftly that the effect follows
almost immediately.
Elimination of industrial poisons is effected principally by the kidneys, the intestinal
canal, the respiratory organs, and, more rarely, the skin. Rapidity of elimination also
depends on the nature of the poison and of the person poisoned.
If elimination is insufficient, or absorption takes place more quickly than excretion,
the poison accumulates in the body, and has a cumulative effect which in chronic
industrial poisonings plays a very important rôle. Under certain circumstances
poisons are not thrown off, but stored up—fixed—in the body.
The poison absorbed in the body can act unchanged from the place where it is
stored. A number of poisons, however, undergo in the organism chemical change
through which the action of the poison is partly lessened, rarely increased. Among
such changes and weakening of the poison are: oxidation, as, for example, of
organic poisons into their final products (carbonic acid, water, &c.), oxidation of
benzene into phenol, oxidation of sulphur dioxide into sulphuric acid, &c.; reduction
in the case of metals, peroxides, &c.; neutralisation of acids by alkaline juices;
chemical union (for instance, of aromatic compounds with sulphuric acid). The
splitting up of albuminous bodies is not of importance in regard to industrial poisons.

GENERAL REMARKS ON THE TREATMENT OF INDUSTRIAL POISONINGS

Although in industrial poisoning the importance of treatment is small in

comparison with that of preventive measures, in discussing particular forms of
poisoning, full weight must be given to it; and in order to avoid repetition, certain
points will be brought forward here.
 Of the treatment of chronic industrial poisonings not much in general can be said;
unfortunately, special treatment has often little chance. It will usually be of
advantage to maintain the activity of the excretory organs. So far as there is
question of poisons affecting metabolism and injuriously influencing the general
state of nutrition, treatment aiming at improving the general health and strength
offers hope of success. For nervous symptoms, especially paralysis, disturbance in
sensation, &c., treatment generally suitable to nervous diseases can be tried
(electro-therapeutics, baths, &c.). In treatment of acute industrial poisonings, which
often demand the prompt intervention of laymen, ‘first aid’ is more hopeful.
The most important general rules of treatment arise in reference to irritant poisons
which produce ulceration of the skin, and further in regard to those poisons which
cause unconsciousness, especially blood poisons.
When an irritant poison is acting on the skin, the first object to be aimed at is
naturally the immediate removal of the cause of corrosion by water, or, better still,
neutralisation by an alkaline solution (for example, soda solution) in the case of
corrosive acids, and weak acids (organic acids, acetic acid, citric acid) in the case of
caustic action by alkalis. Such remedies must be at hand in factories as part of the
equipment for first aid, where irritant poisonings can occur.
In those industrial poisonings which result in loss of consciousness, arrest of
respiration and suffocation, attempts at resuscitation should at once be made. In
these attempts at resuscitation, artificial respiration is of the greatest importance; of
course the sufferer must first be withdrawn from the influence of the poison, i.e. be
brought into fresh air. Great care must be taken, especially where it is necessary to
enter places filled with a poisonous atmosphere, to prevent the rescuers, as is often
the case, themselves falling victims to the influence of the poison. They should be
provided with suitable smoke helmets or breathing apparatus.
We will not describe the methods of resuscitation and artificial respiration
universally enjoined; they can be found in every first-aid handbook.
Emphasis is laid on the great importance of treatment by oxygen in cases of
industrial poisoning through gaseous blood poisons, as this treatment is attended
with good results. Apparatus for the administration of oxygen should be kept
wherever there exists the possibility of such poisoning, especially in mines, smelting
works, chemical factories, and chemical laboratories.
Oxygen treatment rests on the fact that by raising the pressure of the oxygen
from 113 mm., as it is generally in ordinary air, to 675 mm., which is reached in
presence of pure oxygen, the quantity of oxygen absorbed in the blood rises from
0·3 to 1·8 per 100 c.c. Further, the saturation of the hæmoglobin, the colouring
matter of the blood, undergoes an increase of 2·4 per cent. This increase of oxygen
in the blood can save life in cases where through poisoning a deficiency of oxygen
has resulted.
 The introduction of oxygen is done by special apparatus which acts essentially on
the principle that during inhalation oxygen is pressed into the lungs which are below
normal physiological pressure, while exhalation is effected by a deflating
arrangement when the poisoned individual no longer breathes of his own accord.
When natural breathing begins, the introduction of oxygen without special apparatus
generally suffices.

Fig. 30.—Dräger’s Oxygen Box

I Oxygen cylinder; A Valve on

cylinder; B Manometer; C Key for
opening and closing the flow of
oxygen; F Economiser; H
Facepiece.

Dräger’s oxygen apparatus (fig. 30) consists of a small oxygen cylinder provided
with a closing valve, a small manometer, a so-called ‘automatic’ reducing valve with
an arrangement for opening and closing the oxygen supply, a bag to act as a
receiver or economiser, a breathing mask, and a metal tube connecting the
breathing mask with the other parts of the apparatus. The oxygen cylinder, when
filled, contains about 180 litres of oxygen, and the manometer allows the
manipulator to control at any time whatever oxygen it still contains. The automatic
arrangement not only reduces the pressure but at the same time controls the supply
of oxygen. This dose is fixed at three litres of oxygen per minute, so that the
apparatus with the same oxygen cylinder will last for sixty minutes. The oxygen is
not inhaled pure, but is mixed with atmospheric air according to need, and in order
to make this possible the breathing mask is provided with a small hole through
which atmospheric air finds entrance.
 Fig. 31.—Oxygen Inhaling Apparatus

Fig. 32.—Showing apparatus in use (Siebe, Gorman & Co.)

As the oxygen flows continuously from the cylinder waste during exhalation is prevented by the
economiser, in which, during exhalation, the inflowing oxygen accumulates, to be absorbed again in
inhalation. A small relief valve in the screw head of the bag prevents the entrance into it of exhaled air.
 Fig. 33.—Dräger’s Pulmotor (R. Jacobson)

Another oxygen inhaling apparatus for resuscitating purposes, that of Siebe, Gorman & Co., is
illustrated in figs. 31 and 32.
Dräger also constructs an apparatus called the ‘Pulmotor’ which simultaneously accomplishes the
introduction of oxygen and artificial respiration.
Inflation and deflation are effected by an injector driven by compressed oxygen; this alternately
drives fresh air enriched with oxygen into the lungs and then by suction empties them again. While with
the mechanical appliances of resuscitation belonging to older systems the hand of the helper regulated
the rate of breathing, in the case of the Pulmotor the lungs, according to their size, automatically fix the
rate of breathing; as soon as the lungs are filled the apparatus of its own accord marks the moment for
‘deflation,’ and as soon as they are emptied of ‘inflation.’ This automatic reversal is effected by a little
bellows which is connected with the air tubes. During inflation the same pressure is exerted in the
bellows as in the lungs. As soon as the lungs are filled, the pressure in the bellows increases and it
expands, its forward movement causing the reversal to deflation. When the lungs are emptied the
bellows contracts, and through this contraction results the reversal to inflation.
If, in an exceptional case, the breathing for some reason does not act automatically, the hand of the
helper can manipulate it by means of a backward and forward movement of a lever. According to
choice, either a nose-mask or a mask covering both mouth and nose can be worn.
Combined with the regular apparatus for resuscitation is an ordinary apparatus for the inhalation of
oxygen; by the simple altering of a lever, either the one or the other can be employed.

II. INDUSTRIAL POISONING IN PARTICULAR INDUSTRIES

After the foregoing general remarks we may now consider various points of view in regard to
classification of industrial poisonings into groups:

(1) Toxicological, based on the action of the poisons.

(2) Chemical, based on the chemical composition of the poisons.
 (3) Physical, based on the varying density of the poisons. (Division into solid (in
form of dust), gaseous, and liquid poisons.)

To which may be added:

(4) Classification according to the source of the poisoning and therefore

according to industry, upon which Part I is mainly based.

In this section (Part II) a system is adopted which takes into consideration as far as possible all the
principles of division mentioned above, in order to classify industrial poisonous substances in such a
manner that general practical conclusions can be clearly drawn, and supervision rendered easy.

GROUP: MINERAL ACIDS, HALOGENS, INORGANIC HALOGEN COMPOUNDS, ALKALIS

Common to this group is a strong corrosive and irritant effect, varying however in degree; as gases
this group corrode or inflame the mucous membrane of the respiratory passages, and in liquid form or
in solution, the skin.
Besides this superficial effect single members of this group, especially those containing nitrogen,
produce a remote effect upon the blood.
After absorption of the acids a decrease in the alkalinity of the blood can take place and in its power
to take up carbonic acid, thus vitally affecting the interchange of gases in the body, and producing
symptoms of tissue suffocation.
As regards treatment in the case of acids and alkalis, neutralisation has been already mentioned;
further, oxygen treatment may be recommended in cases where the blood has been injuriously affected.
In cases of poisoning through breathing in acid vapours, inhalation of extremely rarefied vapour of
ammonia or of a spray of soda solution (about 1 per cent.) is advisable.

MINERAL ACIDS

Hydrochloric Acid (HCl) is a colourless, pungently smelling gas which gives off strong white fumes.
Experiments on animals, carefully carried out by Leymann, produced the following symptoms.
Even in a concentration of 2-5 per thousand clouding of the cornea ensues, and after about an hour
inflammation of the conjunctiva, violent running from every exposed mucous membrane with marked
reddening, and frequently inflammation (necrosis) of the septum of the nose; the lungs are distended
with blood, here and there hæmorrhages occur in the respiratory and also in the digestive tracts. The
animal dies of œdema (swelling) of the lungs and hæmorrhage into the lungs if exposed long enough to
the action of HCl, even though (according to Lehmann) there may not be accumulation of HCl in the
blood; the chief effect is the irritant one; 1·5-5 per thousand parts HCl in the air suffices, after three or
four hours’ exposure, to affect smaller animals (rabbits) so much that they die during the experiment or
shortly after it. Man can tolerate an atmosphere containing 0·1 to 0·2 per thousand HCl; a somewhat
greater proportion of HCl produces bronchial catarrh, cough, &c.
The solution of hydrochloric acid in water is about 40 per cent. Simply wetting the skin with
concentrated solution of hydrochloric acid does not generally have an irritant effect unless persisted in
for some time; the action of the acid, when continued, has a marked effect upon the mucous
membranes and upon the eyes.
The same treatment already recommended in the introductory remarks on poisoning by inhalation of
acid fumes in general applies.
Hydrofluoric Acid (HFl), a pungently smelling, colourless gas, causes even in weak solutions (0·02
per cent.) irritant symptoms (catarrh of the mucous membrane of the respiratory organs, lachrymation,
&c.). Stronger solutions set up obstinate ulcers, difficult to heal, in the mucous membrane and the skin.
Silico-fluoric Acid (H₂SiFl₆) produces an analogous though somewhat less marked corrosive action.
As regards treatment the reader is again referred to the introductory sentences on this group.
Sulphur Dioxide (SO₂) is a colourless, pungently smelling gas which, acting in low concentration or
for a short period, causes cough and irritation of the mucous membrane of the respiratory passages and
of the eyes; acting for a longer period, it sets up inflammation of the mucous membrane, bronchial
catarrh, expectoration of blood, and inflammation of the lungs.
As Ogata and Lehmann have proved by experiments—some of them made on man—a proportion of
0·03-0·04 per thousand of sulphur dioxide in the air has a serious effect on a person unaccustomed to
it, while workmen used to this gas can tolerate it easily.
As sulphur dioxide probably does not affect the blood, treatment by oxygen inhalation is useless.
Otherwise the treatment spoken of as applying to acid poisonings in general holds good.
Sulphuric Acid (H₂SO₄). Concentrated sulphuric acid occasionally splashes into the eye or wets the
skin, causing severe irritation and corrosion, unless the liquid is quickly washed off or neutralised. If the
action of the acid persists, the corrosive effect becomes deepseated and leads to disfiguring scars.
Nitrous Fumes, Nitric Acid.—Nitric oxide (NO) oxidises in the air with formation of red fumes
composed of nitrogen trioxide (N₂O₃) and nitrogen peroxide (NO₂). These oxides are contained in the
gases evolved from fuming nitric acid and where nitric acid acts upon metals, organic substances, &c.
Industrial poisoning by nitrous fumes is dangerous; unfortunately it frequently occurs and often runs
a severe, even fatal, course; sometimes numerous workers are poisoned simultaneously. The main
reason why nitrous fumes are so dangerous is because their effect, like that of most other irritant gases,
is not shown at once in symptoms of irritation, such as cough, cramp of the glottis, &c., which would at
least serve as a warning to the affected person; on the contrary, generally no effect at all is felt at first,
especially if the fumes are not very concentrated. Symptoms of irritation usually appear only after some
hours’ stay in the poisonous atmosphere. By this time a relatively large quantity of the poisonous gas
has been absorbed, and the remote effect on the blood induced.
The first symptoms of irritation (cough, difficulty of breathing, nausea, &c.) generally disappear when
the affected person leaves the charged atmosphere, and he then often passes several hours without
symptoms, relatively well. Later severe symptoms supervene—often rather suddenly—difficulty of
breathing, fits of suffocation, cyanosis, and copious frothy blood-stained expectoration with symptoms
of inflammation of the bronchial tubes and lungs. These attacks may last a longer or shorter time, and
in severe cases can lead to death; slight cases end in recovery, without any sequelæ.
In poisoning by nitrous acid fumes, oxygen inhalation, if applied in time, undoubtedly holds out hope
of success, and should always be tried. Chloroform has been repeatedly recommended as a remedy.
Probably its inhalation produces no actual curative effect, but only an abatement of the symptoms
through the narcosis induced.
Nitric acid (HNO₃) in solution has an irritant corroding action if, when concentrated, it comes into
contact with the skin or mucous membrane.

THE HALOGENS (CHLORINE, BROMINE, IODINE)

Chlorine (Cl) is a yellow-green, pungently smelling gas, Bromine (Br) a fuming liquid, and Iodine (I)
forms crystals which volatilise slightly at ordinary temperatures.
According to Lehmann’s experiments on animals the effect of chlorine gas and bromine fumes is
completely similar. Lehmann and Binz assume that chlorine has a twofold effect: (1) narcotic, paralysing
the outer membrane of the brain, and (2) the well-known irritant action upon the mucous membrane,
producing a general catarrh of the air passages, and inflammation of the lungs; it is, however, only the
latter which causes menace to life. Other writers do not mention the narcotic effect upon the brain and
assume that the halogens when brought into contact with the mucous membrane are quickly converted
into halogen hydrides, and, as such, produce a corrosive effect. According to Lehmann, even 0·01 per
thousand Cl or Br in the air is injurious, even 0·1 per thousand produces ulceration of the mucous
membrane, and one or two hours’ exposure to the poison endangers life. Lehmann has further tested
(on dogs) acclimatisation to chlorine, and finds that after a month the power of resistance to chlorine
appears to be increased about ten times. In a further series of experiments the same author has proved
that even the smallest quantities of chlorine present in the atmosphere are completely absorbed in
breathing.
Continued or frequent action of chlorine upon the organism produces symptoms which have been
described as chronic chlorine poisoning—such as anæmia and indigestion, in addition to catarrhal and
nervous symptoms. Further, in factories where chlorine is produced by the electrolytic process, workers
were found to be suffering from the so-called chlorine rash (first observed by Herxheimer). This skin
disease consists in an inflammation of the glands of the skin, with occasional development of ulcers and
scars. Severe cases are accompanied by digestive disturbance. Bettmann, Lehmann, and others
maintain that it is not caused by chlorine alone, but by chlorinated tar products, which are formed in the
production of chlorine and hydrochloric acid.
In acute cases of chlorine poisoning oxygen treatment should be tried, but in any case the patient
should have free access to pure air. Approved remedies are inhalation of soda spray or very dilute
ammonia, or of a vapourised solution of sodium hypochlorite. If the patient is in great pain, he may be
allowed to inhale cocaine solution (0·2 per cent.).
The administration of arsenic (solutio arsenicalis) is recommended, especially in cases of acne. In
general the usual treatment for diseases of the skin is followed; salicylic acid lotions, sulphur baths, and
sulphur ointments may be made use of.
Chlorides.—Chlorides of Phosphorus, Phosphorus-trichloride (PCl₃), and Phosphorus oxychloride
(POCl₃), are strong-smelling liquids, fuming in the air, and when brought into contact with water
decomposing into phosphorous acid and hydrochloric acid. These halogen compounds of phosphorus
have a violently irritant action upon the respiratory organs and the eyes, in that they decompose on the
mucous membrane into hydrochloric acid and an oxyacid of phosphorus. Inhalation of the fumes of
these compounds causes cough, difficulty of breathing, inflammation of the respiratory passages, and
blood-stained expectoration.
Treatment is similar to that for acid poisoning in general and hydrochloric acid in particular.
Similar to that of the chlorides of phosphorus is the action of chlorides of sulphur, of which sulphur
monochloride (S₂Cl)₂ is of industrial hygienic importance as it is employed in the vulcanising of
indiarubber. It is a brown, oily, fuming liquid, which, mixed with water or even in damp air, decomposes
into sulphur dioxide and hydrochloric acid. The fumes of sulphur monochloride have therefore a marked
irritant effect, like that of hydrochloric acid and sulphur dioxide. The action of sulphur chloride was
thoroughly studied by Lehmann. Industrial poisoning by sulphur chloride is mentioned by Leymann and
also in the reports of the Prussian factory inspectors for 1897. The latter case ended fatally owing to the
ignorance of the would-be rescuers: a workman had spilt trichloride of phosphorus upon his clothes,
and the by-standers, not knowing its dangerous action when combined with water, poured water on
him.
Treatment is similar to that of poisoning from hydrochloric acid or sulphur dioxide.
Chloride of zinc (zinc chloride, ZnCl₂) likewise has corroding and irritant action upon the mucous
membrane of the respiratory organs.

AMMONIA

Ammonia (NH₃) is a colourless, pungent-smelling gas which dissolves to the extent of about 33 per
cent. in water. Inhaled, it first produces violent reflex coughing, then irritation and corrosion of the
mucous membrane of the respiratory organs, and finally death through suffocation (spasm of the