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.

[Illustration: 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.

[Illustration: FIG. 31.—Oxygen Inhaling Apparatus]

[Illustration: 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.

[Illustration: 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 glottis) if exposure to its action has lasted

a sufficiently long time. Microscopic sections exhibit a diphtheritic

appearance of the mucous membrane, and inflammation of the lungs. The

effects upon the central nervous system (irritation of the medulla

and spinal cord) which are peculiar to ammonia compounds need not be

considered, as the corrosion of the respiratory passage is sufficient

alone to cause death. When the action of the gas is less intense, the

patient rallies from the first stage, but often severe symptoms come on

later affecting the lungs.

Lehmann in experiments upon himself could tolerate as much as 0·33 per

thousand NH₃ for thirty minutes; he found in gas works (with fairly

marked odour) hardly more than 0·1 per thousand NH₃ in the atmosphere,

and considers 0·5 per thousand distinct evidence of excess. He found

that he could produce in dogs acclimatisation up to 1·0 per thousand

NH₃ (five times as much as could at first be borne). About 88 per cent.

of the ammonia contained in the air is absorbed in breathing; ammonia

is said to exercise also a reducing action upon the oxygen of the blood

(oxyhæmoglobin).

Chronic poisoning by ammonia can hardly be said to occur. In those who

clean out sewers and drains, the inflammation of the eyes and digestive

disturbance attributed partly to ammonia are probably due more to the

action of sulphur compounds—ammonium sulphide and sulphuretted hydrogen.

Irritation due to solution of ammonia does not come into account in

industrial employment.

As regards treatment, fresh air or administration of oxygen is most

likely to be successful. Inhalation also of very dilute acetic acid

vapour, steam, or spray of sodium carbonate is advocated.

ALKALIS

The alkaline hydroxides (potassium and sodium hydroxide, KOH, NaOH)

have an albumen-dissolving and therefore caustic effect. Industrially

it occurs in the caustic action of concentrated (often hot) lyes upon

the skin or upon the eye—through splashing. Quicklime (CaO) has also a

caustic action, producing inflammation of the skin or eyes (especially in

those engaged in the preparation of mortar).

Under this head comes also the effect upon the respiratory

passages—described by several authors—caused in the production of

artificial manure discussed at length in Part I.

As regards treatment of the irritant effect of alkalis, what has been

said as to corrosives in general applies here (rinsing with water or weak

organic acids), and in inflammation of the eye caused by lime a drop of

castor oil is recommended.

_GROUP: METALS AND METAL-COMPOUNDS_

The various substances of this group differ markedly in their action.

Under this heading come principally chronic metal poisonings,

characterised by a general, often very intense, disturbance of nutrition,

which justifies their delineation as ‘metabolic poisons’; among these

poisons also are included certain others which produce chronic poisoning

accompanied by severe disturbance of the peripheral and central nervous

system.

The corrosive action common to the metal oxides (when acting in a

concentrated condition), attributable to the formation of insoluble

albuminates, need not, in industrial poisoning, be taken so much into

account. The corrosive effect is characteristic only of the compounds,

especially of the acid salts of chromium, which, as an acid-forming

element, may be classed in the preceding group. Disturbance of health

in workmen handling nickel compounds are also ascribed to the corrosive

action of these substances.

LEAD, LEAD COMPOUNDS

Lead poisoning is the most frequent and important chronic industrial

poisoning; the symptoms are very varied and associated with the most

different groups of organs. We shall describe the typical course of a

case of industrial lead poisoning, laying stress, however, on the fact

that numerous cases follow an irregular course, in that special symptoms

or complications of symptoms are in some especially accentuated, while in

others they become less marked or are absent altogether.

A premonitory indication of chronic lead poisoning is a blue line

on the gum, indicated by a slate gray or bluish black edging to the

teeth, the appearance of which is usually accompanied by an unpleasant

sweetish taste in the mouth. The cause of this blue line was for some

time disputed. It is obviously due to the formation and deposit of

sulphide of lead through the action of sulphuretted hydrogen arising from

decomposition in the mouth cavity. At the same time a general feeling of

malaise and weakness often comes on, occasionally accompanied by tremor

of the muscles and disinclination for food, at which stage the sufferer

consults the doctor. Frequently he complains also of pains in the

stomach, not difficult to distinguish from the lead colic to be described

later. Usually the patient already exhibits at this stage general

emaciation and marked pallor.

The blue line was formerly considered a characteristic early indication

of lead poisoning; but it has now been proved that occasionally it is

absent even in severe attacks. But although the blue line may fail as

an ‘initial symptom,’ it will nevertheless be a valuable aid to the

practitioner in the recognition of lead poisoning. It is worth while

to mention the fact that other metallic poisons produce a very similar

‘line,’ especially mercury, also iron and silver (as in the case of

argyria); it has been stated that the blue line can be simulated by

particles of charcoal on the gum. The pallor of the patient at the

commencement of lead poisoning drew attention to the condition of the

blood. The diminution in the amount of hæmoglobin often met with, which

under certain circumstances is accompanied by diminution of the red

blood cells, offers nothing characteristic. On the other hand, structural

changes in the red blood cells—presence of basophil granules in them—are

asserted by a number of writers to be characteristic of the first stages

of lead poisoning. The basophil granules are believed to be due to

regenerative changes in the nucleus. But these changes are also found in

pernicious anæmia, cancer, leucæmia, anæmia, tuberculosis, &c.; also in a

number of poisonings such as phenylhydrazine, dinitrobenzene, corrosive

sublimate, and others; they are therefore the less characteristic of

chronic lead poisoning, as occasionally they cannot be found in actual

lead poisoning, a point upon which I have convinced myself in the case

both of men and animals. Still, the appearance of much basophilia in the

red blood cells is a valuable aid to diagnosis, especially as the method

of staining to demonstrate them is simple.

Other anomalies of the blood observed in lead poisoning may here be

mentioned. Glibert found a striking diminution in the elasticity of the

red blood corpuscles, and experiments I have made point to the fact that

the power of resistance of the red blood corpuscles to chemically acting

hæmolytic agents, such as decinormal soda solution, is considerably

reduced.

The pulse is generally hard and of high tension, especially during the

attacks of colic. Further, cramp of the bloodvessels (also in the retinal

arteries) has been observed. To these functional disturbances in the

circulation are added sometimes definite changes in the vessel wall.

Later, obliterative arteritis comes on (in the brain arteries), and

arteriosclerosis.

The most important symptom of fully developed lead poisoning is colic,

which is usually preceded by the initial symptoms described (especially

the gastric symptoms), but not always so, as occasionally colic sets in

without any warning. The colic pains often set in with marked vehemence.

They radiate from the navel on all sides, even through the whole body;

the abdomen is contracted and as hard as a board. Pressure on the

lower part diminishes the pain somewhat, so that the sufferer often

involuntarily lies flat on his stomach. During the attack the pulse is

often remarkably slow. Constipation occurs, and often does not yield

to purgatives. The attacks last sometimes for hours, occasionally for

days, or the pains can (with remissions) even distress the patient for

weeks. The frequency of attacks is also very variable. Occasionally one

attack follows another, often there are intervals of weeks, even years,

according to the severity of the poisoning and duration of exposure.

If the patient is removed from the injurious action of lead, as a rule

recovery soon ensues.

[Illustration: FIG. 34.—Paralysis of the Ulnar Nerve in Lead Poisoning]

[Illustration: FIG. 34A.—Different Types of Paralysis of the Radial Nerve

in Hungarian Potters poisoned by Lead (_after Chyzer_)]

Often with the colic, or at any rate shortly after it, appear lead

tremor and arthralgia, paroxysmal pain mostly affecting the joints, but

occasionally also the muscles and bones. They are often the precursor of

severe nervous symptoms which affect the peripheral and central nervous

system. In a lead poisoning case running a typical course the predominant

feature is the peripheral motor paralysis of the extensors of the

forearms. Next the muscles supplied by the radial and ulnar nerves are

affected. Often the progress of the paralysis is typical; it begins with

paralysis of the extensor digitorum communis, passes on to the remaining

extensors, then to the abductor muscles of the hand; the supinator

longus and triceps escape. Sometimes the shoulder muscles are attacked;

also paralysis in the region supplied by the facial nerve and of the

lower extremities is observed. It appears plausible that overstrain of

single groups of muscles plays a decisive part; this seems proved by

the fact that paralysis first affects, among right-handed people, the

right hand (especially of painters), but in the case of left-handed,

the left hand; and among children the lower extremities are often

attacked first. Disturbance of sight increasing to amaurosis is often

an indication of severe brain symptoms. The view of some writers that

the cause of the sight disturbance lies in vasomotor influences (cramp

of the bloodvessels) is very probable, and supports the view that the

brain symptoms are entirely due to diseases of the arteries (arteritis).

These symptoms are distinguished by the collective name of saturnine

encephalopathy; they include apoplexy, hemiplegia, epilepsy, delirium,

and mania. The brain symptoms may cause death.

As later symptoms of lead poisoning may be mentioned lead gout and kidney

disease (lead nephritis). The genesis of both these diseases is much

disputed. It seems to be proved that the gout is true gout (with presence

of tophi) and that the contracted kidney is indistinguishable from

ordinary chronic Bright’s disease.

The kidney symptoms suggest that a regular excretion of lead through the

urine takes place which, if it were a fact, would have been an important

aid to diagnosis. But often analysis of urine for presence of lead is

negative. Excretion of lead by the skin is scarcely to be credited,

although occasionally affirmed. Elimination of lead is effected mainly

through the intestines (probably for the most part as sulphide of lead).

All lead compounds more or less are to be regarded as poisonous, although

the intensity of the action depends on the amount absorbed. For this its

solubility in water or in weak acids (hydrochloric acid of the gastric

juice) is the simplest test. According to this acetate of lead, lead

chloride, carbonate of lead (white lead), oxide of lead (lead dross),

minium (red oxide of lead) are relatively the most poisonous. Lead

sulphate and lead iodide are to be regarded as relatively less poisonous,

although by no means innocuous. The least poisonous, if not altogether

innocuous, is sulphide of lead, because it is an insoluble lead compound.

Treatment of lead poisoning ought to aim first and foremost at the

elimination of lead from the body. But unfortunately such attempts have

had little success. Treatment of symptoms is all that for the most

part is possible. Administration of iodide of potassium to assist the

excretion of lead has not been found the success which many anticipated.

This remedy however, can be tried; better results are to be expected

from careful regulation of the bowels by means of purgatives. During

colic administration of opium or morphia may be advisable to relieve pain

and overcome the probable cramp of the intestinal muscles. The cautious

administration of atropine (occasionally with cocaine) also serves

the same purpose. Hot compresses and mustard plasters may be applied,

and liquid diet should be given. Lead cachexia must be treated by

strengthening diet. Electrical treatment for lead paralysis is advocated.

From baths (sulphur baths) nothing more is to be expected than a bracing

effect—elimination of lead through increased diaphoresis is hardly to be

hoped for.

ZINC (ZINC ALLOYS)

Zinc (Zn) melts at 412° C. and distills at about 900° C.; exposed to

the air it burns, when heated, into zinc oxide. Older writers, when

investigating gastric and intestinal diseases and affections of the

nervous system observed in zinc smelters, regarded them as the result of

chronic zinc poisoning; but it may now be accepted as certain that these

symptoms are due to the lead always present in the zinc.

On the other hand so-called _brass-founders’ ague_ may be regarded as

a form of acute industrial zinc poisoning. Brass-founders’ ague occurs

exclusively in brass casters, and not in zinc workers. Sigel and Lehmann

have shown that founders’ ague is also caused by pure zinc if this is

heated so strongly that it burns.

Premonitory symptoms often occur before the onset of the disease; usually

they appear early, soon after casting has begun. The workman has general

malaise accompanied by slight cough, nausea, throat irritation, &c., but

these symptoms mostly disappear, returning again after a few hours with

renewed violence, often in the evening before going to bed. Frequently,

trembling sets in rather suddenly, often accompanied by headache, nausea,

and muscular pains, and soon develops into a pronounced shivering fit,

lasting generally about a quarter of an hour, but in severe cases for

several hours (with intervals). At the same time the breathing is hurried

and the heart’s action quickened (asthma and palpitation). Often the

temperature rises as high as 104° F. The attack ends with profuse

perspiration, and the patient sinks exhausted to sleep, awaking in the

morning generally quite restored or with but slight signs of fatigue;

only rarely is he unable to resume work.

It is noteworthy that some workmen are extraordinarily susceptible to

brass-founders’ ague, and are attacked again and again, while others

remain completely immune, so that idiosyncrasy and immunity both play

a part. Workmen who are susceptible to the disease, yet without marked

disposition (idiosyncrasy) towards it, can become acclimatised to the

poison. Lehmann has succeeded in artificially producing an attack in

a brass-caster who was highly susceptible. The symptoms in him were

the result of work with pure zinc in a burning condition. The proof,

therefore, is clear that brass-founders’ ague is due to zinc, and not, as

some authors have supposed, to copper or the simultaneous action of both

metals. The symptoms are produced through inhalation of zinc oxide, not

zinc fumes.

Lehmann conjectures that brass-founders’ ague may be a secondary fever

due to absorption into the system of the remains of cells in the

respiratory tract that have been killed by the action of the zinc.

The treatment can only be symptomatic; as the attack is so transient,

medical attendance is hardly necessary.

MERCURY, MERCURY COMPOUNDS

Mercury (Hg), on account of its volatility, is classed among industrial

poisons. Although boiling at 360° C. it is volatile even at ordinary

temperature. Industrial mercurial poisoning is caused by the frequent

inhalation of small quantities of vapour, sometimes, but more rarely, of

dust containing mercury, and assumes usually a chronic form.

Industrial mercurial poisoning often begins with inflammation of the

mucous membrane of the mouth and gums. There is increased flow of saliva,

a disagreeable metallic taste in the mouth, and foul breath. This may be

limited to a simple inflammation of the gum, or go on to ulceration with

falling out of teeth, or even to gangrene of the gum and mucous membrane

inside the mouth. Gastric attacks also occur in the early stages;

occasionally, however, they are absent.

The main symptoms of chronic mercurial poisoning are nervous and

psychical derangement, to which in severe cases are added general

disturbance of digestion and loss of strength.

Sometimes, after repeated attacks, more or less severe, a cachectic

condition is induced, showing itself in general emaciation, decrease

of strength, atrophy of the muscles, anæmia, and disturbed digestion,

which—often intensified by some intercurrent disease, such as

tuberculosis—lead to death. Slight cases of mercurialism recover, leaving

no evil results, if the patient is removed in time from the influence of

the poison.

The treatment of chronic mercury poisoning is symptomatic. To allay the

inflammation of the mucous membrane of the mouth the patient should use

a mouth wash of potassium chlorate and peroxide of hydrogen; the general

condition should be raised by strengthening, unstimulating food; for the

nervous symptoms baths and electricity should be tried; and for very

marked erythism and tremor recourse to narcotics may be necessary.

Industrial mercurial poisoning is produced not only by metallic mercury

but also by many compounds, of which industrially the oxides are the

most important. Nitrate of mercury (Hg₂(NO₃)₂) comes into account in the

treatment of fur. Mercury cyanide (HgCy₂) deserves mention, as small

quantities cause mercurial and large quantities cyanogen poisoning.

MANGANESE, MANGANESE COMPOUNDS

Manganese (Mn) or manganese compounds are used industrially in fine

powder; continuous absorption of dust containing manganese produces

chronic manganese poisoning. Instances of such poisoning are not very

numerous; altogether about twenty cases have been described. Recent

publications agree in asserting that only the dust rich in manganese

protoxide is dangerous.

Industrial manganese poisoning runs its course extraordinarily slowly,

and resembles chronic poisoning by other heavy metals, such as lead and

mercury, in that nervous and psychical symptoms, rather than digestive,

are prominent. Sometimes—but not always—the disease is introduced or

accompanied by psychical symptoms, both of excitement and depression

(hilarity, laughing, or depression and weeping). In the course of the

disease nervous disturbances arise, deafness, tingling, paralysis and

paræsthesia, in the arms and legs, giddiness, difficulty of walking,

tremor, increased knee-jerks and difficulty in speech. Often at the same

time swelling of the lower extremities (œdema) and loss of strength

(cachexia, marasmus) come on. Slight cases make a good recovery. An

interesting case of illness is described by Jaksch as manganophobia, in

which the symptoms were simulated, and were brought on solely by the fear

of manganese poisoning.

As regards treatment, electricity, massage, and baths are advocated to

allay the nervous symptoms, as in the case of chronic metal poisoning and

suitable strengthening food.

CHROMIUM, CHROME COMPOUNDS

Chromium trioxide (CrO₃) dissolves in water, forming chromic acid

(H₂CrO₄); of the salts of chromic acid the neutral and acid alkaline

salts concern our inquiry. These are normal and acid sodium or potassium

chromate (K₂CrO₄ and K₂Cr₂O₇). Chromate of lead (PbCrO₄) can cause lead

poisoning.

Poisoning can be produced by dust and by alkaline chromates, the

latter, when hot, giving off steam which, as has been proved, contains

excessively fine chrome particles. Chrome compounds attack especially the

surface of the body, the skin and the mucous membrane.

The bichromate and chromate dust produce ulcers where slight injuries

to the skin already exist. The ulcers develop slowly, and have a

smooth, heaped-up, undermined edge; deep-seated, they can even pierce

to the bone; they heal with great difficulty. Naturally they occur most

frequently on the uncovered parts of the body, especially on the arms

and hands. Characteristic also is an analogous ulceration attacking

the mucous membrane of the nose, from which hardly any chrome worker

(especially if brought into contact with chromate dust) is free.

Perforation and destruction of the cartilaginous septum of the nose is

very common. Ulcers on the mucous membrane at the entrance of the throat

(on tonsils and palate or in the larynx) have been occasionally observed.

Absorption of small quantities of chrome compounds into the body are said

to cause disturbances of digestion of an inflammatory character, and

especially inflammation of the kidneys.

The treatment of chrome ulcers is similar to that of other chronic

ulcers. An antidote for industrial chrome poisoning is not known.

OTHER METALS AND METAL COMPOUNDS

=Nickel Salts.=—Of late years in nickel-plating establishments an

eczematous inflammation of the skin has been described affecting

first of all the hands, and occasionally spreading over the arms and

even the whole body. The skin becomes inflamed, and vesicles appear

on the affected part. Some persons are extraordinarily susceptible

to this disease, others only become so after having worked for years

quite unaffected, and are then obliged to give up their occupation.

Probably the action of nickel salts (especially nickel sulphate) used

in electrolytic baths causes the disease. But it was in fact traced by

several writers to contact with benzene, petroleum, and lime by the

workmen. The simultaneous action of these substances upon the skin

would no doubt encourage its appearance. The application to the skin of

vaseline or cream is recommended. Careful cleanliness and attention to

the skin is on the whole by far the most reliable protection.

[=Nickel carbonyl= (Ni(CO)₄).—Mond, Langer, and Quincke in 1890

discovered that, on passing a current of carbon monoxide over finely

divided (pyrophoric) metallic nickel, a gaseous compound of nickel and

carbon monoxide was formed. When heated to 150° C. the gas decomposes

into its constituents and metallic nickel is deposited.

Nickel carbonyl is a clear, pale straw-coloured liquid, volatilising

at room temperature. It has a peculiar soot-like smell detectable when

present to the extent of about 1 vol. in 2,000,000, while the Bunsen

flame becomes luminous when nickel carbonyl is present in the air to the

extent of 1 vol. in 400,000—two facts of great importance in detecting

escape of the gas in the manufacture of pure nickel by the Mond process.

_Occurrence of poisoning by nickel carbonyl._—At the first introduction

of the process about 1902, before the dangerous properties of the gas had

been sufficiently recognised, some twenty-five men were poisoned, of whom

three died. Poisoning only occurred when, as a result of the breakdown

of the automatic working of the plant, hand labour took the place of

machinery.

This very rare form of poisoning has been very fully investigated by

H. W. Armit (_Journ. of Hygiene_, 1907, p. 526, and 1908, p. 565). The

symptoms in man, he says, were transient headache and giddiness and at

times dyspnœa, quickly passing off on removal to fresh air. After from

twelve to thirty-six hours the dyspnœa returned, cyanosis appeared, and

the temperature began to be raised. Cough with more or less blood-stained

sputum appeared on the second day. The pulse rate became increased, but

not in proportion to the respiratory rate. The heart remained normal.

Delirium of varying types frequently occurred. Death took place in the

fatal cases between the fourth and eleventh days. The chief changes

found post mortem were hæmorrhages in the lungs, œdema of the lungs, and

hæmorrhages in the white matter of the brain, while some doubt exists as

to whether any blood changes were present.

Precisely analogous results were found in experiments on animals

(rabbits, cats, and dogs).

The points Armit investigated experimentally were (1) Is the carbon

monoxide of the compound wholly or partly responsible for the symptoms,

or (2), is nickel carbonyl absorbed as such, or (3), is it the nickel

of the compound which produces the symptoms? His conclusions are that

the poisonous effects of nickel carbonyl are entirely due to the nickel

of the compound. The peculiar toxicity is due to the fact that, being

introduced in a gaseous form, the nickel is deposited as a slightly

soluble compound in a very fine state of subdivision over the immense

area of the respiratory surface. Nickel carbonyl when mixed with air

cannot be absorbed as such by an animal as it becomes split up into the

nickel containing substance (possibly hydrated basic carbonate of nickel)

and carbon monoxide before or soon after reaching the alveoli of the

lungs. The nickel is dissolved from the respiratory surface by the tissue

fluids and is then taken up by the blood. The hæmorrhages found after

death follow as the result of fatty degeneration of the vessel walls

which is the specific pathological change set up by nickel.]

=Copper.=—Symptoms which have been described by some writers as chronic

industrial copper poisoning are probably due to admixtures of other

poisonous metals, especially lead and arsenic. Although some copper

workers, especially those careless of cleanliness, exhibit hair and teeth

coloured by the action of copper compounds (green tinge on hair and edge

of teeth), symptoms of illness traceable to copper are not demonstrable.

_Brass-founders’ fever_, which by some earlier writers was ascribed to

copper or combined copper and zinc action, is traceable to zinc (see

Zinc).

=Ferro-silicon.=—The illnesses due to this are phosphoretted or

arseniuretted hydrogen poisoning (see pp. 191 and 197).

=Silver and Silver Compounds.=—Gradual absorption of small quantities

of a solution of silver may produce industrial argyria, often beginning

with the appearance of a black edge to the gums and darkening of the hair

and nails, followed by black spots on the skin which in severe cases

coalesce, so that the whole or almost the whole surface of the body

becomes black and glossy.

Argyria is due to the absorption of silver compounds into the

circulation, and subsequent deposition of the reduced silver in the body

(liver, kidneys, spinal cord, &c.). The black colouring of the skin is

caused by the action of light.

No interference with health worth mentioning is observed.

_GROUP: ARSENIC, PHOSPHORUS_

The poisons (gradually absorbed) belonging to this group are mainly such

as affect metabolism; they impair the processes essential to metabolism

(in especial the oxidation processes) and cause severe damage to the

cells, through destruction of albumen. The poisons of this group also

have a paralysing effect upon the central nervous system.

Generally speaking the effects produced by the poisons of this group vary

considerably. Among the arsenic compounds arseniuretted hydrogen, which

is supremely a blood poison, must be excluded from the group and included

among the blood poisons.

ARSENIC, OXIDES OF ARSENIC

Pure _metallic arsenic_ (As) is considered innocuous. _Oxides of arsenic_

especially are held to be industrial poisons such as arsenic trioxide

(As₂O₃), the anhydride of arsenious acid (H₃AsO₃), a white powder, which

is known under the name of white arsenic; _arsenic acid_ (H₃AsO₄), which

forms crystals easily soluble in water, and the salts of these acids,

especially copper arsenite, formerly employed in the production of dyes,

and also _arsenic chloride_ (arsenic trichloride, AsCl₃). _Arseniuretted

hydrogen_ will be treated separately as it has a completely different

poisonous effect from that of the oxidic compounds of arsenic. _Arsenic

sulphides_ (realgar, AsS₂, and orpiment, AsS₃) are regarded as innocuous

in consequence of their insolubility in a pure state. But it may be

remarked that arsenic sulphides (sulphur arsenic ores) which are used

industrially, and even metallic arsenic, are to be considered poisonous,

as they contain oxidic arsenic compounds in great quantity.

Chronic arsenical poisoning is caused by gradual absorption through the

respiratory or digestive tracts of small quantities of the oxidic arsenic

compounds either in solution or as dust or fumes.

The disease usually begins with digestive derangement which shows

itself in more or less severe gastric and intestinal catarrh (loss of

appetite, vomiting and diarrhœa); sometimes there are severe affections

of the respiratory tract,—pharyngeal and bronchial catarrhs; often the

illness is accompanied by skin affections of various kinds, rashes,

pustular eczema, loosening of the nails, abscesses, dark pigmentation

of particular parts of the skin, and other symptoms. The nervous

symptoms vary much according to the severity of the disease; first of

all, deafness and feeling of pins and needles, or loss of sensation

(paræsthesia and anæsthesia) of the extremities. Further, rheumatic

joint pains, weakness of the extremities and characteristic symptoms of

paralysis occur, with accompanying atrophy of the muscles, and gradual

loss of energy leading to total incapacity for work. Severe cases end in

general exhaustion and loss of strength, with signs of severe injury to

the central nervous system, such as epileptic fits, mental hebetude, &c.

PHOSPHORUS

_Phosphorus_ (P) is polymorphic; red (amorphous) phosphorus is innocuous,

while white or yellow is poisonous. Phosphorus at various stages of

oxidation is little if at all poisonous. White phosphorus is volatile

and fumes in the air—the fumes consisting of phosphorus, phosphoric and

phosphorous acids.

Chronic industrial phosphorus poisoning is produced by continued

inhalation of the fumes of white phosphorus resulting in inflammation

of the periosteum of the bone, with which necrosis and formation of new

bone are associated. It attacks especially the lower jawbone (ossifying

periostitis). The inflammation begins with increased flow of saliva,

painful swelling of the gums, which, as it increases, brings about the

death of the jawbone (necrosis, phosphorus necrosis). This becomes

covered again with newly formed bone substance from the periosteum. The

process ends with the formation of a fistula (a passage filled with pus),

which discharges outwards, and through which the dead bone (sequestrum)

is eventually cast off. Occasionally the process attacks the upper jaw,

rarely other bones.

With these characteristic symptoms of phosphorus necrosis, derangement of

nutrition together with anæmia, indigestion and bronchial catarrh, may

be associated. Further, a general brittleness of the bones (fragilitas

ossium) is observed with the result that the long bones of the leg or arm

sometimes break at relatively small exertion of force; such cases from

Bohemia came lately under my notice.

Some authorities regard caries of the teeth as the pre-disposing cause of

phosphorus necrosis; according to this view the carious teeth constitute

the means of entrance for the poison. Opposed to this so-called ‘local’

theory is the view that chronic phosphorus poisoning is a ‘general’ one.

The truth may lie midway. On the one hand phosphorus necrosis probably

arises partly from the general poisonous action of the phosphorus, and on

the other from local inflammation which leads to the occurrence of local

symptoms. The general symptoms of chronic phosphorus poisoning described

above support this view, especially the effect observed on the bones of

the skeleton. This view is also strengthened by the fact that workmen

with perfectly sound teeth, who had been exposed to phosphorus fumes for

many years, were attacked by necrosis only when traumatic inflammation

produced by chance injury was set up.

The treatment of phosphorus necrosis is surgical. Formerly the treatment

recommended was to wait for formation of new bone and exfoliation of the

dead bone (expectant treatment); the necrosed portions of bone were then

extracted through the fistula. Recently early operative interference has

succeeded in preserving the periosteum which enabled the new bone to form.

Phosphoretted Hydrogen

Industrial poisoning by gaseous phosphoretted hydrogen (PH₃) calls for

attention in connection with the preparation and employment of calcium

carbide (acetylene) and also of ferro-silicon.

Phosphoretted hydrogen is a dangerous poison. Even 0·025 per cent. in

the air is harmful to animals after a time; 0·2 per cent. PH₃ in the air

quickly causes death.

The poison produces changes in the lungs, though without injuring the

respiratory passages by corrosion, and finally has a paralysing effect

upon the central nervous system. It has no effect upon the blood. An

autopsy on a person who has died of phosphoretted hydrogen poisoning

reveals as a rule no characteristic sign, except centres of inflammation

in the lungs.

The symptoms of phosphoretted hydrogen poisoning are—difficulty of

breathing, cough, fainting fits, noises in the ears, and nausea;

in severe cases coma and death. Slight cases soon recover without

after-effects.

_GROUP: SULPHURETTED HYDROGEN, CARBON BISULPHIDE, AND CYANOGEN (NERVE

POISONS)_

In this group are comprised industrial poisons the principal effect of

which is upon the nervous system, especially the central nervous system.

The chemical composition of the separate members of the group differs

much.

SULPHURETTED HYDROGEN

Industrial poisoning by pure sulphuretted hydrogen (SH₂), the well-known

colourless, nauseous-smelling gas, occurs comparatively rarely. Poisoning

is generally acute, but chronic illness in workers has been traced back

to inhalation of the gas.

This poison exerts a paralysing action upon the central nervous system

and is slightly irritating to the mucous membranes and respiratory organs.

Its action can be described as follows: When absorbed into the blood

union of the poison with the alkaline constituents takes place with

formation of an alkaline sulphide. Presence of only slight quantities

of sulphuretted hydrogen in the air acts injuriously. Lehmann has shown

that about 0·15 to 0·2 per thousand sulphuretted hydrogen is not without

effect, and that prolonged inhalation of 0·5 per thousand becomes

dangerous. Continued exposure to the poison seems only to increase

susceptibility to its action. An almost complete absorption of the whole

of the sulphuretted hydrogen present in the air breathed takes place.

Continued inhalation of small quantities of sulphuretted hydrogen

produces irritation of the mucous membrane, cough, and lacrymation;

headache, giddiness, nausea, and mental dulness soon ensue; occasionally

also symptoms of intestinal catarrh follow; if at this stage—or after

a longer exposure to the action of a smaller amount—the patient is

withdrawn from its further influence, there still continue for some time

symptoms of irritation of the mucous membrane (such as inflammation of

the conjunctiva and of the respiratory passages).

Further exposure or absorption of greater amounts induces general

discomfort and passes on to a second stage of convulsions and delirium.

Inhalation of a large dose of sulphuretted hydrogen causes almost

instantaneous death; the affected person falls dead—often without

a sound—as if struck by a blow; occasionally a short stage of

unconsciousness, with symptoms of suffocation, precede death.

This acute form often occurs, especially in acute sewer gas poisoning.

Besides this, a sub-acute form of sewer gas poisoning is recognised

which is attributable, in part at least, to the action of sulphuretted

hydrogen, the prominent symptoms being irritation of the mucous membranes

and of the intestinal canal. In other severe cases symptoms of the

central nervous system preponderate (headache, giddiness, and delirium).

These forms of poisoning can be caused not only by sulphuretted hydrogen,

but also by other poisonous gases which are found in drains or sewers.

As regards treatment, continued inhalation of oxygen, supported by

artificial respiration, is often, in serious cases, effective. In severe

poisonings also saline injections and bleeding may be advocated. Other

symptoms (catarrh, &c.) must be treated symptomatically.

CARBON BISULPHIDE

Pure carbon bisulphide (CS₂) is a colourless, peculiar-smelling liquid

which boils at 46° C.

As Lehmann has shown, even 1·5 to 3·0 mg. CS₂ per litre of air produces

distress—with acute symptoms of poisoning (congestion, giddiness,

sickness, &c.).

Industrial carbon bisulphide poisoning is, however, chronic in nature and

induced by continuous inhalation of small quantities of the fumes. To

understand the action of carbon bisulphide, its capacity for dissolving

fats and fatty substances must be taken into account. Its injurious

effect extends to the nerve tissues (central and peripheral nervous

system) and the glandular tissues.

Throughout chronic industrial carbon bisulphide poisoning, which has

been described fully by Delpech, Laudenheimer, and others, nervous and

psychical symptoms predominate, together with severe chronic digestive

derangement.

The patient after exposure for some time suffers from violent headache,

giddiness, and sickness; he has sensations of cold, pains in the

limbs, a feeling of ‘needles and pins,’ and itching in different parts

of the body. Gradually a condition of general excitement develops.

Sleeplessness, cramps, and palpitation set in. At the same time the

nervous system becomes involved—hypersensitiveness, loss of sensation

or complete numbness of some parts of the skin, diminution of muscular

power, disturbances of movement, twitching, violent trembling, wasting

of the muscles, and paralysis; the sight also is sometimes affected.

The stage of excitement, in which the patient often becomes strikingly

loquacious without cause, passes gradually, as the nervous symptoms

develop, into the stage of depression; sometimes this takes weeks and

months; excitement and gaiety give place to deep depression; other

symptoms appear—weakness of memory, mental dulness, and difficulty in

speaking. The powers of sensation become affected, paralysis increases,

and digestive disturbances, anæmia, and general loss of strength are

manifest. Occasionally definite mental disease (psychosis, mania,

melancholia, dementia, &c.) develops.

Certain cases of chronic carbon bisulphide poisoning in indiarubber

workers have come under my notice, and some remarks concerning them

may be of interest. The characteristic symptoms are essentially as

follows: the invalid appears in the consulting-room in a bent position,

leaning upon a stick with head and hands shaking. The gait is clumsy

(spastic-paralysis) so that the patient ‘steps’ rather than walks. When

seated, the tremor ceases to some extent, but in purposive movements

increases rapidly, involving the whole body, so that an exact systematic

examination becomes impossible, and the invalid sinks back into the

chair exhausted and bathed in perspiration. He complains of cold in

the extremities. He looks pale; the skin of the upper extremities is

totally without feeling, as also is the upper part of the feet; the skin

of the head is hypersensitive; the muscular strength of the arms is

almost lost; testing the strength brings on marked shaking, followed by

a fainting-fit caused by exhaustion. The extremities of the patient are

cyanotic (livid); the knee jerks are exaggerated. The patient suffers

from indigestion, constipation, headache, and giddiness; he is irritable,

and depressed; his memory is weak; mental derangement cannot be proved.

Chronic carbon bisulphide poisoning is rarely fatal. Slight cases end in

recovery after more or less long continuance; in severe cases improvement

occasionally takes place, but serious nervous disturbance (paralysis,

weakness of the muscles, deterioration of intellect) usually persists.

Treatment is symptomatic, aiming especially at relieving the nervous

symptoms and improving the state of nutrition. If psychical disturbances

are prominent, treatment in an institution is necessary.

CYANOGEN AND CYANOGEN COMPOUNDS (CYANOGEN GAS, PRUSSIC ACID, CYANIDES)

Industrial cyanogen poisoning is not frequent. _Cyanogen gas_ (C₂N₂,

existing in small quantities in furnace gas, illuminating gas, and other

kinds of gas) and especially _hydrocyanic acid_ (CNH, prussic acid) are

considered industrial poisons; the latter is a very unstable, colourless,

pungent-smelling liquid, boiling at 27° C. Among the cyanides employed

industrially and having an effect similar to that of prussic acid must be

mentioned _cyanide of potassium_ and _cyanide of sodium_ (KCN and NaCN),

_cyanide of silver_ (AgCN) and _cyanide of mercury_ (Hg[CN]₂).

Cyanogen and cyanogen compounds are extraordinarily powerful poisons. The

minimum dose lies, as Lehmann has proved by experiments on animals, at

about 0·05 per thousand of hydrocyanic acid in the atmosphere breathed;

1-5 mg. per kg. weight is fatal to animals; to man about 60 mg. would be

fatal.

The poisonous action of cyanogen and cyanogen compounds depends upon

their power of preventing absorption of oxygen from the blood by the

tissues with the result that the venous blood flowing to the heart

retains the bright red colour which otherwise only arterial blood

exhibits. This effect is due to cessation of the gaseous exchange in the

body, and results in tissue suffocation. At the same time these poisons

have at first an exciting and then a paralysing effect upon the central

nervous system. In severe poisoning the nerve effect is masked by the

effect upon the exchange of gases in the blood, since this quickly leads

to death.

Most of the cases of industrial poisoning under this heading result from

inhalation; absorption of liquid cyanogen compounds through the skin can

rarely come into consideration.

If large quantities of hydrocyanic acid have been inhaled, death ensues

very quickly. The person affected falls down suddenly, breathes with

difficulty, the pulse soon becomes imperceptible, and after a more or

less long stage of deep unconsciousness (coma) life becomes extinct.

In slight cases of poisoning the patient feels a sensation of irritation

in the throat, giddiness, sickness, and difficulty in breathing;

occasionally such disturbances persist for some time.

Some writers have described symptoms in workers manipulating prussic

acid and cyanides, which they believe to be due to chronic prussic

acid poisoning. Complaint is made of oppression of the chest, throat

irritation, giddiness, difficulty in breathing, palpitation, hebetude,

exhaustion, and nausea and vomiting; in certain instances the attack,

aggravated by exhaustion and weakness, culminates in death. It is a

question whether such poisonings are chronic in the true sense of the

word. In view of the mode of action of hydrocyanic acid, such cases

of sickness should rather be accounted acute or sub-acute poisonings

through repeated action of small quantities of the poison.

It may be mentioned that in persons working with alkaline cyanides

(especially in electro-plating) skin affections occasionally occur; these

are traceable to the caustic effect of alkaline cyanides.

Treatment by oxygen inhalation with simultaneous artificial respiration

holds out most prospect of success. This holds good for acute poisoning

by the other poisons belonging to this group. Besides this, saline

injections and bleeding are recommended, and also the administration of

an infusion of sodium thiosulphate solution.

_GROUP: ARSENIURETTED HYDROGEN AND CARBONIC OXIDE (BLOOD POISONS)_

Included in this group, as in the former one, are substances chemically

very different from each other, but of which the action is especially

on the blood. Besides this common effect, these substances also produce

various other effects, such as local irritation, effect on the nervous

system, &c. The industrial blood poisons, which according to their

chemical constitution are classed among the aliphatic and the aromatic

series of organic compounds, will, for the sake of clearness, be

discussed in the following chapters.

ARSENIURETTED HYDROGEN

Acute arseniuretted hydrogen poisoning, produced by inhalation of

relatively very small quantities of arseniuretted hydrogen gas (AsH₃)

is in most cases industrial in origin. The absorption of an amount

corresponding to about 0·01 mg. arsenic suffices to produce severe

poisoning symptoms. The poisonous effect results chiefly from action upon

the red blood corpuscles, which are dissolved (hæmolysis). Arseniuretted

hydrogen is therefore a genuine blood poison. The effect upon the

blood, if not immediately fatal to life, is to cause the dissolved

blood-colouring matter to pass into the tissues where, though some is

deposited, most goes to, and acts injuriously on, the organs, especially

the liver, spleen, and kidneys. In cases running at once a fatal course,

the impoverishment of the blood caused by the lack of colouring matter

necessary to internal respiration produces tissue suffocation, which is

therefore the primary cause of death. In cases not immediately fatal, the

injury to the functions of the organs alluded to (for instance, cessation

of the functions of the kidneys, &c.) may lead to death secondarily.

Symptoms of the disease appear often only some time after the poisoning

has set in, and begin with general malaise, sickness, collapse, fainting

fits, and difficulty of breathing; after some hours the characteristic

signs follow—the urine becomes dark red to black, containing quantities

of blood colouring matter and dissolved constituents of the blood, and

later also bile colouring matter, so that a coppery jaundice comes on if

the illness is prolonged. The region of the liver, spleen, and kidneys

is painful. Severe cases often end fatally during the first stage of

the illness, more rarely later, with increased difficulty of breathing;

sometimes death occurs after a preceding comatose stage marked by

convulsions and delirium. In slighter poisoning cases the symptoms abate

in a few days and recovery follows.

The treatment of arseniuretted hydrogen poisoning is similar to that

adopted in the case of all other blood poisonings: in addition, if

possible, direct transfusion of blood from the artery of the giver into

the vein of the receiver, liquid nourishment, saline injections, and,

above all, prolonged oxygen inhalation.

CARBONIC OXIDE (CO)

Carbonic oxide (CO) is a colourless, odourless gas which frequently

causes both acute and, it is said, chronic industrial poisoning.

Carbonic oxide is a very poisonous gas; even as little as 0·5 per

thousand in the atmosphere breathed has a poisonous effect; about 2-3 per

thousand can be dangerous to life.

Its poisonous effect results from its power of combining with the

blood-colouring matter or hæmoglobin to form carboxy-hæmoglobin; the

affinity of carbonic oxide for the hæmoglobin of the blood is more than

200 times greater than that of oxygen, so that, however small the amount

of carbonic oxide in the air, it is inevitably absorbed by the blood and

retained. The blood so altered, assumes a cherry-red colour, is unable to

effect the necessary exchange of gases for internal respiration, and in

consequence of the lack of oxygen suffocation ensues.

Without doubt, however, carbonic oxide has also an immediate effect

upon the central nervous system (first excitation, followed quickly

by paralysis). It is maintained also that besides the action upon the

hæmoglobin it favours coagulation of the blood through the disintegration

of the blood corpuscles. The last-mentioned action is thought to account

for the sequelæ of carbonic oxide poisoning, but they can also naturally

be accounted for by the direct effect of the poison.

Onset of symptoms is very sudden if a large quantity of pure carbonic

oxide is inhaled. The affected person immediately falls down unconscious

and succumbs after drawing a few breaths with difficulty.

In less acute cases the illness begins with premonitory symptoms,

generally headache, sickness, giddiness, sleepiness, though in cases

of fairly rapid absorption these are absent, and are naturally absent

also when the poisoning creeps upon the affected persons while asleep,

as occasionally happens in cabins, &c., in factories. If the poisoning

continues, increasing mental dulness, accompanied by nausea and vomiting,

leads sometimes to a short stage of seemingly drunken excitement, which

preludes deep unconsciousness during which there is often a convulsive

stage, followed by complete loss both of sensation and of reflex action;

the breathing becomes shallow and intermittent, the pulse small and

irregular, and finally death ensues. Occasionally in the stage of

unconsciousness, death is hastened by entrance of vomited matter into the

respiratory passages. Bright red patches are seen on the body after death.

If persons affected by severe carbonic oxide poisoning are withdrawn

from the poisonous atmosphere after having reached the stage of

unconsciousness, they may recover, but often with difficulty; not

infrequently—in spite of suitable treatment—death occurs some

considerable time later from the symptoms described above. Still, in many

cases, under the influence of right treatment, gradual recovery has been

brought about, even after long unconsciousness accompanied by repeated

convulsions. In the rescued the symptoms described as characteristic of

the first stage often continue for at least a day. Further, they are

liable to a number of serious after effects, such as severe inflammation

of the lungs due to infection by the entrance of vomited matter into the

air passages, skin affections (rashes), and especially severe nervous and

mental affections. Frequently these develop from centres of softening

in the brain or from inflammation of the peripheral nerves (neuritis);

occasionally the poisoning may really only be the predisposing cause for

the outbreak of an existing psychical disease. It is not our task to

enumerate all the extremely varied disturbances which are observed after

carbonic acid gas poisoning. Neuralgias and paralyses have been described

as associated with the peripheral nerve symptoms over areas supplied

by different nerves; various forms of diseases of the brain and spinal

cord (poliomyelitis, paralysis, sclerosis, &c.); and finally a series of

psychoses (neurasthenia, melancholia, mania, &c.), occasionally passing

into dementia and imbecility. Glycosuria (sugar in the urine) has also

been noted as a sequela.

Chronic carbonic oxide poisoning, arising from continued inhalation of

small quantities of the gas, sets in usually with symptoms similar to

those of acute carbonic oxide poisoning; if the worker continues exposed

to danger, severe symptoms may arise which point to marked alteration of

the blood and later also of the digestion and bodily functions. Under

certain circumstances severe nervous and mental affections are said

to occur similar to those which we have mentioned as sequelæ of acute

carbonic oxide poisoning (convulsions, disturbances of mental activity,

symptoms which resemble progressive muscular atrophy, &c.).

In acute carbonic oxide poisoning oxygen inhalation indefatigably

continued and supported by artificial respiration is often successful.

The serious danger from this form of poisoning renders it very necessary

that in all premises where there is risk provision should be made for

the administration of oxygen. The sequelæ can of course only be treated

symptomatically.

OXYCHLORIDE OF CARBON (PHOSGENE)

Oxychloride of carbon (COCl₂), also called phosgene, is, at the ordinary

temperature, a colourless gas with a disagreeable smell. This decomposes

in moist air into carbonic oxide, hydrochloric acid, or chlorine, and

produces a strongly irritant local effect upon the mucous membranes.

Industrial poisoning by phosgene is characterised by great difficulty

in breathing and inflammation of the respiratory tract (bronchitis and

bloodstained expectoration).

Several cases have been treated successfully by oxygen inhalation.

NICKEL CARBONYL

The effects of nickel carbonyl are described on pp. 186-8.

CARBONIC ACID

Carbonic acid (CO₂), a colourless gas, is heavier than air (specific

weight, 1·526), and therefore, wherever it collects, sinks to the ground.

Carbonic acid is only very slightly poisonous; about 10 per cent.

carbonic acid in the air causes asphyxia. The extinguishing of a candle

flame will serve as an indication that the amount of carbonic acid in

the atmosphere has reached this point. Cases of industrial carbonic acid

asphyxia are sudden; they do not occur frequently.

The gradual action of the gas when mixed with air produces first a

tingling sensation on the surface of the body, reddening of the face,

irritation of the mucous membrane and the respiratory organs, after

which succeed difficulty in breathing, palpitation, fainting, and

unconsciousness.

Sudden and fatal poisoning occurs industrially. Upon entering places

filled with carbonic acid gas the affected person falls down dead almost

immediately. These are cases of asphyxia, in which the lack of oxygen

certainly plays the greatest part. If those affected by acute carbonic

acid poisoning are removed in time out of the dangerous atmosphere they

usually recover quickly.

Oxygen inhalations and artificial respiration are to be applied in

severer cases. There are no sequelæ.

_GROUP: HYDROCARBONS OF THE ALIPHATIC AND AROMATIC SERIES AND THEIR

HALOGEN AND HYDROXYL SUBSTITUTION PRODUCTS_

The industrial poisons comprised in this group have as their principal

general effect injurious action upon the functions of the central

nervous system (paralysis or causing excitation) which is prominent in

most of the cases of industrial poisoning caused by these substances.

This effect is most marked in the case of the readily volatile (low

boiling) hydrocarbons, while those less volatile and boiling at a higher

temperature often have collateral effects (such as local irritation).

The characteristic poisonous effect caused by the chlorine and

hydroxyl-substitution products (chloroform and alcohol group) is also

mainly on the central nervous system (narcosis).

HYDROCARBONS OF MINERAL OIL

BENZINE, LIGROINE, PETROLEUM, PARAFFIN, VASELINE

_Mineral oil_ (crude petroleum) has, according to its origin, differing

composition. Thus in American mineral oil hydrocarbons of the methane

series preponderate; in the Russian, hydrocarbons of the aromatic series.

Reference has been made in Part I. to this point, as well as to the

separation of crude petroleum into its different fractions.

The injury to health produced by crude petroleum and its derivatives is

of two kinds. Direct contact with liquid petroleum and the semi-liquid

and solid deposit after distillation (paraffin) cause local injury to the

skin. Inhalation of the volatile constituents of raw petroleum causes

symptoms affecting mainly the central nervous system. They have moreover

a markedly irritating effect upon the mucous membrane of the respiratory

organs. These substances clearly exhibit the characteristic we have

referred to, namely, that the hydrocarbons boiling at low temperature act

as nerve poisons, whereas those boiling at a higher temperature produce a

local irritant effect.

The skin affections take the form of inflammation of the hair follicles

(acne), eruptions with characteristic formation of vesicles, and

pimples and pustules which precede the deep-seated formation of ulcers,

abscesses, &c.

In paraffin workers the acne-like skin inflammations are known as

‘paraffin eczema.’ They develop sometimes into cancer of the skin (warty

and epitheliomatous growths).

In the general poisoning produced by inhalation of petroleum fumes the

effect upon the central nervous system is all the more plainly and

clearly marked when the irritant effect of the hydrocarbons boiling at

higher temperature is slight or absent; that is, in the case of poisoning

which arises solely from industrial products of low boiling hydrocarbons;

among these benzine is included.

Acute poisoning from inhalation of benzine fumes begins with headache,

sickness, and attacks of giddiness resembling alcoholic intoxication. If

very much has been inhaled, the patient quickly becomes unconscious, with

occasionally muscular tremors, convulsions, difficulty in breathing, and

cyanosis.

In cases of poisoning by inhalation of fumes of crude petroleum, these

symptoms may be complicated by coughing, intense inflammation of the

mucous membrane of the respiratory organs—congestion, bronchitis,

bloodstained expectoration, and inflammation of the lungs. In workers

who frequently remain long in an atmosphere filled with benzine fumes,

further symptoms of chronic benzine poisoning show themselves—mental

hebetude, pains in the limbs, trembling, weakness of the muscles, and

other disturbances of the nervous system; in such cases these may really

be signs of continued attacks of acute or sub-acute poisoning; many

benzine workers are anæmic.

The treatment of acute benzine poisoning consists in oxygen inhalation,

with simultaneous artificial respiration. Treatment of chronic

derangement of health is symptomatic.

HYDROCARBONS OF THE AROMATIC SERIES

BENZENE AND ITS HOMOLOGUES

_Benzene_ (C₆H₆) is a characteristically smelling (aromatic) liquid which

boils at 80·5° C. Acute benzene poisoning, which plays an important part

as an industrial poisoning, is caused by inhalation of benzene fumes. The

various kinds of benzol used commercially contain, besides benzene, alkyl

benzenes, especially _toluene_ (methylbenzene, C₆H₅.CH₃, boiling-point

111° C.); _xylene_ (dimethylbenzene, C₆H₄[CH₃]₂, boiling-point 140°

C.); _pseudocumene_ and _mesitylene_ (tri-methylbenzene, C₆H₃[CH₃]₃,

boiling-point 169° or 163° C.); the regular presence of _thiophene_

(C₄H₄S, boiling-point 84° C.) in commercial benzol must also be taken

into account. Industrial benzol poisoning arises, therefore, as a rule,

not from the action of pure benzene vapour, but from fumes which contain

a mixture of the compounds mentioned.

The course run by industrial benzol poisoning is often very acute, if

large quantities are inhaled—death occurring suddenly, after a short

illness with symptoms of vertigo. Gradual inhalation of lesser quantities

gives rise to headache, giddiness, malaise, then twitchings appear

which develop into convulsions, and lastly unconsciousness. In order to

ascertain in what manner the various substances contained in commercial

benzol share in the poisonous effect, experimental research seemed to me

to be indispensable, especially as published statements so far gave no

accurate data.

Two cases of industrial benzol poisoning have given rise to close

experimental research upon the poisonous nature of benzene.

Lewin undertook experiments on animals; which he confined under bells

and caused to inhale fumes of chemically pure and impure benzene. He

mentions that even at comparatively low concentration poisoning results,

and indeed more readily and certainly from the action of impure than pure

benzene. Lewin found that when air was made to flow slowly first through

benzene and then into the bell, symptoms of paralysis, convulsions,

and unconsciousness showed themselves in from four to six minutes.

After-effects by this means could not be observed. Lewin maintains,

however, that in man even slight acute action of benzene can be followed

by after-effects (giddiness, sickness, headache, distress in breathing,

and oppression of the heart).

Santesson made researches upon the poisonous action of benzene in

connection with occurrence of certain cases of poisoning through ‘impure

benzol’ (coal-tar benzene) in a rubber tyre factory. In the factory

mentioned nine young women were poisoned, of whom four died. The symptoms

shown were lassitude, anæmia, giddiness, headache, vomiting, and fever.

Post mortem, hæmorrhages and fatty degeneration of the endothelium of the

bloodvessels and various organs were found. Experimental research showed

that commercial benzol and chemically pure benzene had the same effect.

Santesson did not succeed in his experiments on animals in producing

chronic poisoning by inhalation of benzine and of benzene fumes (which

two completely different poisons he does not distinguish strictly from

each other, as is the case, unfortunately, with many other writers). My

experimental researches upon the poisonous effect of pure benzene, pure

toluene, cumene, thiophene, and the most important kinds of commercial

benzol gave the following results:

For rabbits the limit of toxicity is a proportion of 0·015 to 0·016 per

thousand pure benzene in the air, that is 0·015 to 0·016 c.c. benzene

vapour per litre of air.

A concentration of 0·056-0·057 per thousand pure benzene in the air

causes in rabbits at once—after one minute—twitching of the muscles;

after eight minutes, convulsions; after ten minutes, deep narcosis; and

after twenty-five minutes, coma. If the animal is taken out of the bell

in time, even if it has shown marked symptoms, it recovers very quickly

(in two to ten minutes) without manifesting any after effects. Even in

animals repeatedly exposed to the poison sequelæ were not observed.

Dogs are somewhat more susceptible to pure benzene than rabbits; 0·024

per thousand causes after ten minutes severe convulsions, which after

twenty minutes become continuous; 0·042 per thousand kills after twenty

minutes (sudden death in a state of tetanus).

Cats are less sensitive than dogs and more sensitive than rabbits;

0·03-0·04 per thousand causes after ten minutes attacks of cramp and,

after twenty minutes, convulsions; 0·05 per thousand at once brings on

poisoning symptoms. As regards the character of the symptoms (cramps,

convulsions, quick recovery, no after effects) the above statements apply

to all three kinds of animals (rabbit, dog, and cat).

Chloral hydrate completely checks the convulsions and enables animals to

tolerate higher concentrations of benzene for a longer time.

Benzene is thus to be counted among nerve irritant poisons. The

convulsions are probably provoked by excitement of the motor centres in

the brain.

In view of the fact that thiophene in a concentration of 0·03-0·05 per

thousand in the air was borne by animals for an hour without producing

any symptoms of poisoning, the proportion of thiophene in commercial

benzol must be looked upon as practically non-injurious.

The so-called 90 _benzol_—a commercial benzol of which 90 per cent.

distils at 100° C.—has naturally a somewhat weaker action, although, in

respect of the poisoning symptoms produced, it is similar to that of pure

benzene.

_Pure toluene_ (boiling-point 111° C.) and purified toluol (commercial

product, boiling-point 109°-112° C.) produce, when inhaled, gradually

increasing narcosis in the three kinds of animals referred to; they

produce no symptoms of convulsions or spasms.

After the animals have been taken out of the bell, recovery is not so

rapid as after benzine inhalation, but takes from half an hour to one

hour. In rabbits and cats 0·046-0·05 per thousand produces after fifteen

minutes staggering and paresis; after thirty minutes deep narcosis. The

dog is again somewhat more susceptible, as little as 0·034 per thousand

causing these symptoms in the same time.

‘Purified toluol’ (commercial product) acts somewhat less rapidly

than pure toluene, but this small difference in effect need hardly be

considered.

Other poisons were also investigated:—

_Solvent naphtha I_, a commercial product, of which 90 per cent.

comes over at 160° C.; it contains little toluene, chiefly xylene,

pseudocumene, and cumene.

_Solvent naphtha II_, of which 90 per cent. comes over at 175° C, it

contains besides xylene, chiefly pseudocumene, mesitylene, cumene, &c.

The fumes of solvent naphtha I cause, when inhaled by rabbits, dogs, and

cats, gradual narcosis, although not nearly so quickly as toluene at

similar concentrations; recovery usually takes over an hour after the

deeply narcotised animals have been removed from the bell. Rabbits and

cats are affected in about equal degree. The dog is the more sensitive.

Rabbits and cats can tolerate about 0·012-0·013 per thousand of the

fumes of solvent naphtha I in the atmosphere for a long time without any

symptoms. Only after breathing for fifty minutes air containing 0·0536

per thousand do they become narcotised. In the dog 0·036 per thousand

causes narcosis only after thirty minutes.

With the fumes of solvent naphtha II I could not affect rabbits at all.

The cat also, in spite of long inhalation of the heavy fumes, showed no

marked symptoms of poisoning. In the dog gradual narcosis came about only

after an hour’s inhalation of 0·048 per thousand.

The fumes of pure _xylene_ caused narcosis in rabbits after forty

minutes’ inhalation of 0·05 per thousand in the atmosphere; after being

taken out of the bell the animals recovered slowly (after half an hour to

one hour).

_Cumene_ causes no symptoms after one hour’s inhalation in a

concentration of 0·06 to 0·07 per thousand. This explains the effects of

solvent naphtha I (in which xylene preponderates) and solvent naphtha II

(in which pseudocumene, cumene, &c., preponderate). After effects were

not observed.

Benzol and toluol fumes, and particularly those of solvent naphtha,

exercise a distinctly irritant effect upon the mucous membrane, which,

however, passes off without after effects.

Pure benzene, therefore, proved the most poisonous of the substances

under investigation. When inhaled its effect (convulsions, with quick

recovery) differs essentially from that of toluene, solvent naphtha,

xylene, and cumene (gradual narcosis, slow recovery). The fumes of the

various kinds of commercial benzol (solvent naphtha) boiling at a higher

temperature are practically non-poisonous (solvent naphtha II). Pure

benzene fumes are, however poisonous, even in very small quantities in

the air. The limit for animals lies at 0·015-0·016 per thousand.

Lehmann has shown in a recent work that man, exposed to a mixture of

benzene and air, absorbs 80 per cent. of the benzene.

Treatment of acute industrial benzene poisoning consists in severe cases

of artificial respiration, with simultaneous administration of oxygen; in

slight cases it is sufficient to bring the patient into fresh air.

_Naphthalene._—Naphthalene, which is insoluble in water, has irritant

effect upon the mucous membrane and upon the skin when brought into

contact with it.

Long continuance in an atmosphere containing naphthalene as dust or fumes

causes headache, nausea, giddiness, &c.

HALOGEN SUBSTITUTION PRODUCTS

ALIPHATIC SERIES (NARCOTIC POISONS)

The halogen substitution products of the aliphatic series are not of

much account as industrial poisons. They have generally a narcotic

effect, that is, a paralysing effect upon the central nervous system,

usually preceded by a short stage of excitement. This effect shows itself

typically on inhalation of chloroform (methanetrichloride, CHCl₃), which

however plays no part as an industrial poison. The narcotic effect of

the other alkyl chlorides is less than that of chloroform. With carbon

tetrachloride (CCl₄) the narcotic effect is only half that of chloroform;

it causes, however, a more violent excitation; inhaling the fumes brings

on nausea, coughing, sickness, headache, &c.

_Methylchloride_ (CH₃Cl) has a less narcotising effect. On the other hand

it has a stronger local irritant action, which is indeed present also in

chloroform, though not so apparent. This gas, as is well known, is used

as a local anæsthetic in medicine.

Pure _methylene chloride_ (CH₂Cl₂) similarly is much less powerful than

chloroform. Severe poisoning, alleged to have resulted from methylene

chloride was caused by a mixture, called indeed methylene chloride, but

composed of methylalcohol and chloroform.

Of the remaining halogen substitution products of methane, _methyl

bromide_ (CH₃Br) and _methyl iodide_ (CH₃I) have given rise to industrial

poisoning.

These poisons also act in the same way as the alkyl chlorides, but the

excitement accompanying the narcosis is more marked—so far as the scanty

observations allow conclusions to be drawn. The symptoms first show

themselves in sickness, giddiness, hebetude, slowing of respiratory

movements and of the heart’s action; convulsions or delirium ensue.

Treatment consists in artificial respiration or promotion of breathing

by a plentiful supply of fresh air or oxygen; in pronounced narcosis

stimulating remedies should be applied.

BENZENE SERIES

_Chlorobenzene_, and _nitro-_ and _dinitro-chlorobenzene_ and

_benzoylchloride_, have given rise to industrial poisoning.

To chlorobenzene similar action is attributed as to benzene (headache,

fainting, rapid breathing, cyanosis); changes in the blood (methæmoglobin

formation) have also been observed.

Nitro- and dinitro-chlorobenzene are active poisons; the effect

corresponds in general to that of nitro- and dinitrobenzene, but in

addition the fumes or dust have markedly irritant action on the skin

(dermatitis).

_Benzoylchloride_ (C₆H₅COCl), a colourless, pungent-smelling liquid,

produces a violently irritant effect upon the mucous membrane,

decomposing into hydrochloric acid and benzoic acid.

Treatment is analogous to that of benzene poisoning, and in cases of

benzoyl chloride poisoning to that by hydrochloric acid.

It may be mentioned that chlorine rash is attributed to the action of

chlorinated tar products (chlorobenzene compounds).

HYDROXYL SUBSTITUTION PRODUCTS

FATTY SERIES (ALCOHOLS)

The hydroxyl substitution products of the fatty series belong mainly

to the narcotic poisons; the greater the molecular weight of the

alcohol, the more marked is usually the narcotic effect. According to

this propylalcohol is eighteen times as poisonous as ethylalcohol;

butylalcohol and amylalcohol have from 36 to 120 times as great a

narcotic effect as methylalcohol.

_Methylalcohol_ (wood spirit, CH₃OH) plays relatively the greatest part

among alcohols as an industrial poison, because it is employed as a

means of denaturing spirit. Its poisonous nature is relatively great,

being very persistent. Industrial poisoning by methylalcohol is due to

inhalation of the vapour and is rarely of a severe nature. The fumes

have a strongly irritant effect upon the mucous membrane, giving rise to

throat irritation, cough, hoarseness, and in severe cases bronchitis and

inflammation of the conjunctiva of the eye. In addition inhalation of

methylalcohol vapour causes headache, giddiness, nausea (inclination to

vomit), and occasionally also twitchings and tremor.

The _higher alcohols_ (propyl-, butyl-, amyl-alcohol, C₃H₇.OH, C₄H₉.OH,

and C₅H₁₁.OH) occur in fusel oil. They cause but slight (if any)

industrial poisoning. Cases of more severe industrial poisoning through

amylalcohol fumes have been described (in factories for smokeless

powder), with symptoms of sickness, headache, giddiness, with fatal

issue in some cases, preceded by severe nervous symptoms (convulsions or

delirium).

Beyond speedy removal out of the dangerous atmosphere, probably no

special treatment is needed in these cases of industrial poisoning from

alcoholic vapour.

_GROUP: NITRO AND AMIDO COMPOUNDS OF THE ALIPHATIC AND AROMATIC SERIES

(BLOOD POISONS WHICH FORM METHÆMOGLOBIN)_

Characteristic of the nitro and amido compounds of the aliphatic and

aromatic series of the organic substances is their action upon the

blood. The normal oxyhæmoglobin (blood-colouring matter) is changed

into methæmoglobin, with which the oxygen is so firmly combined that

the internal exchange of gases necessary to life becomes impossible.

Methæmoglobin has a dark chocolate-brown colour and a clearly defined

characteristic spectrum.

Of the poisons belonging to this group several are important. In so

far as these substances are volatile—and this is generally the case

with those causing industrial poisoning—effects are due to inhalation

of fumes, but it is proved that the poisons of this group in liquid

form can be absorbed by the intact skin, and this channel of absorption

is characteristic of industrial poisoning. Severe poisoning results

especially from wetting the skin by spilling on the clothes, &c.

The grey-blue discoloration of the mucous membrane, especially of the

lips, is characteristic; sometimes also the skin is altered in colour.

This discoloration is often noticed by others before the patient feels

unwell. Soon the person affected has general nausea, vomiting, headache,

giddiness, severe nervous symptoms, feeling of anxiety, and difficulty

of breathing; in severe cases unconsciousness comes on, and death occurs

with increasing cyanosis (lividity).

Treatment is naturally that which has been emphasised in the introductory

words to Part II, which hold for all blood poisonings. In mild cases

oxygen treatment has given good results. In all factories where such

poisoning can occur provision should be made for immediate oxygen

treatment. Besides this, the workers must be adequately instructed as to

the danger and symptoms of poisoning, especially of the characteristic

premonitory skin discoloration, in order to be able to assist their

fellows.

NITROCOMPOUNDS

ALIPHATIC SERIES

_Nitro-glycerin_ (triple nitric acid ester of glycerin, C₃H₅.[NO₃]₃),

the well-known oily explosive liquid, has also an irritant local effect.

When absorbed into the body, in addition to methæmoglobin formation, it

causes dilatation of the bloodvessels, slowing of the respiration and

heart’s action, and attacks of suffocation. The general remarks upon this

group apply here, but symptoms referable to central paralysis occur as

the methæmoglobin formation is slow. Industrial poisoning arises through

inhalation of gases containing nitro-glycerin and also by absorption

through the skin. Statements as to its poisonous nature are very varied.

Under certain conditions moistening the skin with small quantities of

nitro-glycerin suffices to produce symptoms. Probably the susceptibility

of different persons varies greatly.

_Amylnitrite_ (nitric acid amyl ester, C₅H₁₁NO₂), a characteristically

smelling liquid, acts similarly. The fumes of amylnitrite, even when

inhaled in small quantities, cause marked dilatation of the bloodvessels,

through paralysis of the muscular walls of the bloodvessels, thus causing

marked flushing of the face; the pulse becomes quick, then weak and slow.

NITRO AND AMIDO COMPOUNDS

AROMATIC SERIES

The substances of this group are important.

_Nitrobenzene_ (C₆H₅NO₂, named oil of mirbane), a yellowish liquid of

characteristic smell, induces especially the formation of methæmoglobin

in the blood; the effect upon the central nervous system (first

excitation, then depression) is often absent. The description of the

disease in general in the introductory words of this whole group is

characteristic. Occasionally signs of asphyxia show themselves; sometimes

there are twitchings, disturbance of the power of sensation, and

convulsions; early discoloration of the mucous membrane and the skin,

which assume a blue to grey-black colour, is characteristic.

Chronic poisoning is also attributed to nitrobenzene, showing itself in

lassitude, headache, malaise, giddiness, and other disturbances of the

nervous system.

_Nitrotoluene_ (C₆H₄CH₃NO₂), of which the ortho-compound acts most

powerfully, and also _nitroxylene_ (C₆H₃[CH₃]₂NO₂) have similar but less

marked effect.

The _dinitrobenzenes_ (C₆H₄[NO₂]₂) are stable bodies. Meta-dinitrobenzene

inhaled as dust or otherwise, can produce marked poisoning symptoms

essentially the same as those described. Especially characteristic is the

early dark discoloration of the skin.

Symptoms resembling nitrobenzene poisoning in general are caused by

_nitrophenols_ (C₆H₄.OH.NO₂), of which paranitrophenol is the most

toxic; also by _dinitrophenols_ (C₆H₃[NO₂]₂OH), solid crystalline

substances which melt at different temperatures, and the _mono-_ and

_di-nitrochlorobenzenes_ (C₆H₄.Cl.NO₂ and C₆H₃.Cl[NO₂]₂). In cases of

industrial poisoning by dinitrophenol, observed by Leymann, the workers

were taken suddenly ill, with symptoms of collapse, pains in the chest,

vomiting, distress of breathing, rapid pulse, and convulsions, and died

within a few hours. At the autopsy a yellow substance was found with

picric acid reaction which appeared to be di- or tri-nitrophenol. In

other cases, some fatal, of industrial nitrochlorobenzene poisoning, also

observed by Leymann, the typical grey-blue discoloration of the skin

was obvious, and the chocolate-brown colour of the blood produced by

methæmoglobin.

_Trinitrophenol_ (picric acid, C₆H₂[NO₂]₃OH) is a yellow crystalline

compound with bitter taste; poisoning by this substance exhibits clearly

strong local irritant action (upon skin, mucous membrane, and intestinal

canal, and especially upon the kidneys), besides effect on the blood and

central nervous system. Prolonged action of picric acid upon the skin

causes inflammation. Absorption of picric acid dust causes inflammation

of the mucous membrane of the respiratory passages and symptoms of

gastric and intestinal catarrh as well as inflammation of the kidneys.

A jaundice-like discoloration of the skin and darkening of the urine are

also characteristic; sometimes picric acid poisoning produces a rash

resembling that of measles and scarlet fever.

_Nitronaphthalene_ (C₁₀H₇[NO₂]) and _nitronaphthol_ (C₁₀H₆.NO₂.OH) in

addition to methæmoglobin formation have an irritant action. It is stated

also that dulness of the cornea is produced.

_Azobenzenes_ also, which are to be considered as intermediate between

nitrobenzene and aniline, form methæmoglobin (azobenzene, C₆H₅N = NH₅C₆).

_Aniline_ (amidobenzene, C₆H₅.NH₂), a colourless, oily liquid of aromatic

smell, has only slight local irritant effect. In the frequent cases

of industrial poisoning by ‘aniline oil’ or aniline hydrochloride, in

which the aniline enters through the skin or is inhaled in the form

of fume, there appear the typical symptoms common to this group, of

the action upon the blood through methæmoglobin formation: headache,

weakness, cyanosis, difficulty in breathing, &c., to which are added

nervous symptoms such as convulsions and psychical disturbance, although

these play a subordinate part in industrial poisoning. In severe cases

the typical symptoms of air hunger are shown. Occasionally recovery

only takes place gradually, and signs of irritation of the kidneys

and inflammation of the urinary organs are seen. These symptoms occur

only rarely in acute industrial poisoning, but are, however, in so far

worthy of notice because of the frequent occurrence of tumours in the

bladder among aniline workers. It is possible that here the irritant

action of the urine which contains aniline plays a part. The tumours

in the bladder operated upon, in some cases with success, were many of

them non-malignant (papillomata), but some were carcinomata (cancerous

new growths) running a malignant course, and recurring after operation.

In the urine the aniline combines with sulphuric acid, and is partly

excreted as paramidophenol sulphuric acid.

The treatment of aniline poisoning is the same as that for all the

poisons of this group. In view of the occurrence of tumours of the

bladder in aniline workers, they should be instructed to seek medical

aid on the first indications of trouble, so that a careful cystoscopic

examination may be made.

_Toluidine_ (C₆H₄.CH₃.NH₂), which is mixed with aniline for industrial

use, produces the same symptoms with marked irritation of the renal

organs.

Of the _nitroanilines_ (C₆H₄.NH₂.NO₂) _paranitroaniline_ is the most

poisonous. Characteristic of the action of this compound is methæmoglobin

formation, central paralysis and paralysis of the heart’s action.

Of the _benzenediamines_, _paraphenylene diamine_ (C₆H₄[NH₂]₂) may be

regarded as an industrial poison. The irritant action of this substance

is prominent; it induces skin affections, inflammation of the mucous

membranes, more especially of the respiratory organs, and sometimes

inflammation of the kidneys. They have been noted in workers using ursol

as a dye; here, doubtless, the action of diimine (C₆H₄.NH.NH.) must be

taken into account, which arises as an intermediate product and exercises

a markedly irritant action. Further, the general effect of paraphenylene

diamine is an irritant one upon the central nervous system.

_APPENDIX_

TURPENTINE, PYRIDINE BASES, ALKALOIDS

_Turpentine oil._.—Turpentine oil is a peculiar-smelling, colourless

liquid of the composition C₁₀H₁₆; different reactions show that

turpentine oil contains the aromatic nucleus (cymene). It is used in

the manufacture of varnish, and thus can cause industrial poisoning

by inhalation of fumes. Even from 3 to 4 mg. of vapour of turpentine

oil per litre of air brings on severe symptoms. Turpentine oil acts as

a local irritant, and when absorbed into the system has an exciting

effect upon the central nervous system. Inhalation of large quantities

of turpentine vapour cause rapid breathing, palpitation, giddiness,

stupor, convulsions, and other nervous disturbances, pains in the chest,

bronchitis, and inflammation of the kidneys. The last-mentioned symptom

also arises from the chronic action of turpentine vapours.

_Pyridine._—Pyridine (C₅H₅N), a colourless liquid of peculiar odour, is

employed as well as methylalcohol in denaturing alcohol. The disturbance

of health observed in workers occupied with the denatured spirit are

probably mainly due to the inhalation of fumes of methylalcohol. Pyridine

is comparatively innocuous. Eczema, from which persons suffer who

come into contact with denatured spirit, is ascribed to the action of

pyridine. Larger doses produce a paralysing effect, but this need not be

considered in its industrial use.

_Nicotine, tobacco._—According to various published statements, effects

among tobacco factory workers are attributed to the nicotine contained

in tobacco dust and to the aroma which fills the air. Nicotine in large

doses has at first an exciting followed by a paralysing effect upon the

central nervous system; it causes moreover contraction of the unstriped

muscles and has a local irritant effect.

The symptoms of illness ascribed to nicotine are: conjunctivitis, catarrh

of the air passages, palpitation, headache, want of appetite, and,

particularly, tendency to abortion and excessive menstruation. Severe

industrial poisoning due to nicotine has only been observed in workers

who chewed tobacco leaves.

_Poisonous wood._—The symptoms of disease noticed in workers who

manipulate certain kinds of wood are attributed by some writers to the

presence of alkaloids. Such knowledge as we have of the illness due to

them—they are evidently of the nature of poisoning—is referred to at the

end of Part I.