Primary irritants cause inflammation. Inflammation is one of the body’s defence mechanisms. It
is the reaction of a tissue to harm which is insufficient to kill the tissue and is typified by constriction of the small vessels in the affected area, dilation of the blood vessels, increased
permeability of the vessel walls, and migration of the white blood and other defensive cells to the
invading harmful chemical. The aim is to concentrate water and protein in the affected area to
‘dilute’ the effect and wash away the chemical. Production of new cells is ...
Primary irritants cause inflammation. Inflammation is one of the body’s defence mechanisms. It
is the reaction of a tissue to harm which is insufficient to kill the tissue and is typified by constriction of the small vessels in the affected area, dilation of the blood vessels, increased
permeability of the vessel walls, and migration of the white blood and other defensive cells to the
invading harmful chemical. The aim is to concentrate water and protein in the affected area to
‘dilute’ the effect and wash away the chemical. Production of new cells is speeded up and
contaminated surface cells are shed.
The respiratory system is the main target organ for vapour, gas or mist. Readily-soluble chemicals,
e.g. chlorine or phosgene, attack the upper respiratory tract; less soluble gases, e.g. oxides of
nitrogen, penetrate more deeply into the conducting airways and, in some cases, may cause
pulmonary oedema, often after a time delay.
For example, sulphur dioxide is highly water soluble and tends to be absorbed in the airways
above the larynx. However, in
the presence of particulate catalysts and sunlight, conversion to sulphur trioxide occurs and the
irritant response is much more severe.
Other parts of the body are also vulnerable: the skin and eyes from direct contact/rubbing or
from exposure to airborne material including splashes; the mouth and pharynx by ingestion of
solid or liquid chemicals.
One effect of direct contact of liquid or solid, and less often vapour, with the skin is a contact
irritant dermatitis. Some dusts can also act as primary irritants. Even chemically-inert dusts, e.g.
from glass fibres, can induce a dermatitis due to abrasion; this is made worse if a reactive
chemical, e.g. a synthetic resin binder, is also involved. Examples of primary irritants include
acids; alkalis; defatting compounds, e.g. organic solvents, surfactants; dehydrating agents; oxidizing
agents and reducing agents.
In extreme cases irritant chemicals can have a corrosive action. Corrosive substances can also
attack living tissue (e.g. to cause skin ulceration and, in severe cases, chemical burns with
degradation of biochemicals and charring), kill cells and possibly predispose to secondary bacterial
invasion. Thus whilst acute irritation is a local and reversible response, corrosion is irreversible
cell destruction at the site of the contact. The outcome is influenced by the nature of the compound,
the concentration, duration of exposure, the pH and also, to some extent, by
individual susceptibility etc. Thus dilute mineral acids may be irritant whereas at higher concentrations
they may cause corrosion.
Note that this
includes many primary irritants, such as:
• Chemicals which give strong acid reactions, often on interaction with water, e.g. mineral acids.
Some organic acids can also be corrosive. Phenolics can result in local anaesthesia so that the
pain will be absent for a time, i.e. contact may go unheeded.
• Halogen compounds.
• Acid anhydrides/halides which react with water to form their parent acids.
• Common bases, which render aqueous solutions alkaline.
• Certain oxidizing/reducing compounds and salts which, in the form of solid (bulk or dust) or
as solution, can produce irritation by thermal burns.
Strong acids and alkalis produce effects within moments: e.g. sulphuric and nitric acids quickly
become hydrated by the water content of the skin/mucous membranes and combine with skin
protein to form albuminates, sometimes with charring. Some substances, e.g. certain organotins
or hydrofluoric acid, produce a more delayed reaction. Thus on the skin hydrofluoric acid produces
an effect which varies, depending on concentration and duration of exposure, from mild erythema
to severe burns and intense pain, sometimes delayed by several hours after the initial exposure. A
tough white lump forms over the area of skin damage under which progressive destruction of cell
tissue continues. Burns under the finger nails are notable in this respect because of the difficulties
of treatment. Similarly, inhalation of the vapour can cause corrosion of the respiratory system and
pulmonary oedema. If hydrofluoric acid is swallowed, burns to the mouth and pharynx can occur
with vomiting and ultimate collapse.