Oxford Handbook of Occupational Health (2 edn)
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Dermatitis 1
Epidemiology
Prevalence data1 suggest that 20000 people in the UK have skin problems that are caused or made worse by work. Occupational dermatitis (OD) makes up the greatest proportion of these. Data come from two main sources:
Voluntary reporting schemes for occupational physicians and dermatologists: the incidence of OD is falling steadily.2 Of 2055 new cases of occupational skin disease reported in 2010, 1497 (73%) were due to dermatitis. However, this is likely to be an underestimate as mild cases might not present to a dermatologist and many workplaces do not have access to OH services
Industrial Injuries Disablement Benefit: 55 awards in Great Britain in 2009/10, but these are a small proportion of the most severe OD.
Classification
Endogenous eczema
An inherited disorder often associated with other atopic conditions, such as rhinitis. Not primarily caused by work that may be exacerbated by exposures at work.
Acquired occupational contact dermatitis
Irritant contact dermatitis (IrCD): skin irritation from direct contact with irritant agents, e.g. chemicals or plants. Reversible impairment of the barrier properties and local inflammation of skin is dose related for mild (chronic) irritants
Allergic contact dermatitis (ACD): has an immune-mediated mechanism due to a type IV (cell-mediated) reaction. Sensitization can occur within 7–10 days of exposure; usually develops after months or years. Once sensitized, the individual can react to very low level exposures.
Clinical features
The clinical appearance of dermatitis derives from oedema of the epidermis and inflammatory infiltration in the dermis. Typically, onset is slow and >24h after exposure. There may be a temporal relationship to work, with improvement during holidays. IrCD is classically confined to areas of contact, usually the face and hands. With ACD, involvement of eyelids and spread to secondary sites, not directly exposed, is common. See HSE website for colour pictures of dermatitis is available at: 
http://www.hse.gov.uk/skin/imagelibrary.htm
Acute features
Redness
Pruritis
Vesiculation, exudation, and crusting
Dryness, cracking, and fissuring.
Chronic features
Cracking
Lichenification.
Complications
2° bacterial infection.
Causal exposures/industries
Exposures
Causal exposures often occur in combination
Chemicals or biological agents:
irritants (common examples include weak acids and alkalis, soaps and detergents, oxidizing and reducing agents, solvents)
sensitizing agents
Frequent hand washing (wet work)
Gloves and other PPE
Mechanical trauma
Radiation and UV light.
Jobs
Dermatitis can occur in any job, but is particularly common in:
Health care work
Cleaning
Engineering (cutting oils)
Hairdressing
Catering
Printing
Agriculture
Chemical manufacture.
Individual susceptibility
The response of normal skin to physical and mechanical damage and to irritant agents varies widely in the population
The risk of sensitization ↑ if the barrier integrity of skin is impaired, e.g. pre-existing skin conditions which lead to i antigen presentation
Risk of irritation and sensitization ↑ in those with a history of atopy.
Compensation
Non-infective dermatitis is prescribed for Industrial Injuries Disablement Benefit (D5) in workers whose skin is exposed to irritants. Dermatitis and skin ulceration (C30) is prescribed in those exposed to chromic acid, chromates, or dichromates.
Relevant legislation and further information
Occupational dermatitis is reportable under RIDDOR. A list of agents for which associated dermatitis would be reportable is given in the guidance document (see 
Appendix 3), but exposure to any known irritant or sensitizing agent would qualify
HSE (2011). Statistics on work-related skin disease. Available at: http://www.hse.gov.uk/statistics/causdis/dermatitis/skin.pdf
Dermatitis 2: management
Clinical investigation and treatment
Differential diagnosis
It can be difficult to distinguish IrCD and ACD from history and examination alone. Clues include exposure to a known irritant or sensitizing agent. However, always consider whether a previously unknown sensitizer might be responsible. Careful enquiry into exposures at home and work is important, but it can be difficult to identify the cause. A history of childhood eczema indicates endogenous dermatitis, but exacerbation by irritants or sensitizers at work should still be considered.
Skin patch testing is crucial in making a diagnosis. This should include common allergens, medicaments, and agents that are present at work. Patch testing is a specialized procedure. It should be carried out by an experienced dermatologist, particularly when investigating rare or possible new sensitizers, as standardized skin patch test reagents may not be available commercially. Care is needed in the standardization of tests in this context, and the interpretation of results. The occupational health team has an important role in:
Providing dermatologist with a list of possible workplace exposures
Ensuring that samples of products, excipients, and other potential causative agents are supplied to the investigating clinic.
Treatment The treatment of occupational dermatitis is the same as for endogenous eczema. Topical emollients and topical steroids.
Occupational health input
Advise the employer about primary prevention
Substitution of known sensitizing agents with suitable alternatives
Engineering controls (e.g. enclose computerized cutting operations to reduce contact between cutting oils and the skin of operators)
Use of PPE (gloves). 
Some components of gloves (typically carbamates and thiurams used as preservatives and accelerants) can themselves cause sensitization
Education about the risks and good hand care (see Box 8.1).
Ensure hands are not wet for >2h/day or >20 times each day. For potent irritants d these exposure limits
Avoid wearing gloves for >4h/day
Use tools that avoid wet-work or contact with irritants
Wash hands in warm (not cold or hot) water and dry thoroughly
Use protective gloves from the start of wet-work
Minimize glove use—induces dermatitis by occluding skin surface
If protective gloves used for >10min wear cotton gloves underneath
Keep gloves intact and dry inside
Avoid introducing irritants into the gloves
Do not wear rings at work—they trap water and contaminants
Use lipid-rich moisturizing creams at and after work.
Manage individual cases
Facilitate careful clinical investigation and diagnosis
Reinforce education about good hand care (see Box 8.1)
Advise about adjustments to work to reduce direct skin contact with irritants or allergens.
Epidemiological surveys
Sometimes it can be difficult to determine if a single case of dermatitis is occupational. It is useful to ascertain whether there is a higher incidence of dermatitis among the population of employees who have similar dermal exposures. Surveys are also useful for investigating unexplained clusters of cases. It is important to undertake epidemiological investigations ethically, and to involve the employees’ representatives.
Health surveillance
Skin surveillance is required under the COSHH Regulations where there is a significant risk of dermatitis. The detail of skin surveillance programmes is covered on p.
426, Skin surveillance. OH has a role in:
Advising employers about the need for and format of surveillance
Training competent persons
Follow-up of cases identified by routine surveillance.
Prognosis
Because irritant contact dermatitis is dose related, it is usually possible to manage by attention to exposure controls outlined here
Allergic contact dermatitis can be much more difficult to manage:
once an individual is sensitized, he/she reacts to very low levels of exposure; elimination of the allergen is not always possible
redeployment is sometimes required as a last resort if symptoms cannot be controlled by other means, but the risks of dermatitis need to be weighed carefully against the (often greater) health risks of losing employment completely
if the allergen is common in the environment outside work, symptom control is more difficult to achieve.
Further information and guidance
HSE (2004). Medical aspects of occupational skin
disease, guidance note MS24, 2nd edn. Available at: http://hse.gov.uk/pubns/ms24.pdf
HSE Skin at work. Available at: http://www.hse.gov.uk/skin/index.htm
Concise guidance to good practice: diagnosis, management, and
prevention of occupational contact dermatitis. Available at: http://www.nhsplus.nhs.uk/providers/images/library/files/guidelines/Dermatitis_concise_guideline.pdf
Dermatitis: occupational aspects of management—a national
guideline. (Full guideline and associated leaflets). Available at: http://www.nhsplus.nhs.uk/providers/clinicaleffectiveness-guidelines-evidencebased.asp
BOHRF (2012). Occupational contact dermatitis: evidence
review. Avaialble at: http://www.bohrf.org.uk/projects/dermatitis.html
Contact urticaria
Epidemiology
Data from the specialist physicians reporting schemes1 show that the annual incidence of reported new cases of occupational contact urticaria is declining; 56 cases were reported in 2010.
Clinical features
Wheal and flare: ‘nettle rash’, itchy skin lumps with erythema:
rapid onset within 20min of exposure
subsides within hours of exposure
see HSE website for colour pictures of urticarial. Available at: http://www.hse.gov.uk/skin/imagelibrary.htm
Associated with systemic features: asthma, GI symptoms, anaphylaxis.
Non-allergic contact urticaria
Tends not to have systemic features and is probably due to local release of histamines and bradykinins in response to direct stimulus.
Causal exposures
Certain arthropods, jellyfish, algae
Nettles and certain seaweeds
Benzoic acid, ascorbic acid.
Allergic contact urticaria
This is a classical type I (IgE-mediated) hypersensitivity reaction. It occurs when an individual who has been previously sensitized to an allergen is re-exposed.
Causal exposures/industries
Exposures:
latex (see p.
202, Latex allergy)
protein allergens, e.g. animal products
foods, spices, herbs, food additives (benzoic acid, cinamic acid)
resins
disinfectants
Industries:
health care
rubber manufacture
veterinary practitioners
food handlers
horticulture.
Investigation
Skin-prick testing
Total and specific IgE.
Management Allergen avoidance.
Skin cancers
Epidemiology
Types
Squamous cell carcinoma
Basal cell carcinoma
Melanoma.
Causal exposures/industries
UVA and UVB radiation: any occupation where work is predominantly outdoors, e.g. agricultural and construction workers
Ionizing radiation
PAHs: historically an important cause of skin cancer, but now rare because of good hygiene controls
Arsenic and arsenicals.
Clinical features and management
Skin nodule; itching or colour change in existing naevi
Surgical excision.
Prevention
Education and protection against the sun for outside workers
Reducing exposure to tar, pitch, and mineral oils through substitution and engineering controls
Control of ionizing radiation (see p.
20, Ionizing radiation 3: exposure control).
Compensation
Primary carcinoma of the skin is prescribed for Industrial Injuries Disablement Benefit (C21) in those who are exposed to arsenic or arsenic compounds, tar, pitch, bitumen, mineral oil (including paraffin), or soot.
Relevant legislation
Skin cancer that is attributable to occupational exposure is reportable under RIDDOR The EU directive on optical radiation requires health surveillance for workers who are exposed to optical radiation and are likely to have health effects.
Skin pigmentation disorders
Altered skin colour
Causal exposures
Silver and silver salts produces blue-grey skin pigmentation: argyria
Trinitrotoluene (TNT) causes orange staining of skin
A number of other chemicals can cause skin staining:
potassium permanganate
fluorescein, etc.
Hyperpigmentation
Causal exposures
Pitch, tars; associated with photosensitivity
Mercury compounds
Arsenic and arsenicals.
Hypopigmentation (vitiligo)
Can be localized or generalized, and is indistinguishable from naturally occurring vitiligo.
Causal exposures
Hydroquinones
Phenols
Catechols.
Screening
Using a Woods lamp, loss of melanin can be detected before it is apparent in white skin. This method is useful for detection of occupational vitiligo in exposed workers.
Compensation
Vitiligo is prescribed for Industrial Injuries Disablement Benefit (C25) in those exposed to paratertiarybutylphenol, paratertiarybutylcatechol, para-amylphenol, hydroquinone, monobenzyl ether of hydroquinone, or monobutyl ether of hydroquinone.
Folliculitis and acne
Epidemiology
Data from the specialist physicians reporting schemes1 show that reported new cases of occupational folliculitis and acne are declining. Three cases were reported in 2009 and no cases in 2010.
Clinical features
Oil folliculitis
Papules and pustular lesions
Discoloration of the hair follicles
Comedone formation with marked inflammatory component
Typically occurs on thighs and forearms, where prolonged contact with oil saturates clothing.
Chloracne
Pale comedones and cysts (unlike the inflamed lesions of oil acne)
Typically on the face: cheeks, forehead, and neck
Less commonly on the trunk, limbs, and genitalia
Larger inflammatory lesions in chronic cases.
Coal tar acne
Comedone formation
Photosensitivity
Skin pigmentation.
Causal exposures
Oil folliculitis
Cutting oils
Lubricants.
Chloracne
Chlorinated naphthalenes (used as a synthetic insulating wax)
Polychlorinated biphenyls (PCBs), e.g. chlorinated dibenzodioxins and dibenzofurans (used as heat insulator in electric transformers and capacitors).
Coal tar acne
Coal tar and products (used in roofing and civil engineering).
Prevention
The incidence of oil acne has reduced drastically because of exposure controls, particularly the decrease in use of cutting oils, use of safer products, and better hygiene. The use of PCBs has been greatly restricted in the UK.
Compensation
Oil folliculitis and acne are prescribed for Industrial Injuries Disablement Benefit under D5 (non-infective dermatitis).
Photodermatitis
Some occupational exposures can give rise to skin damage through interaction with UV light.
Polycyclic aromatic hydrocarbons
Coal tar
Pitch
Creosote
Industries:
gas production
coke oven work
roofing
production of graphite from pitch.
Plants
Many plants cause dermatitis that is triggered by sunlight.
Compositae
Umbelliferae:
giant hogweed
celery, etc.
Some lichens
Gardeners and grounds men are at risk when handling plants, but particularly when using lawn strimmers to cut verges, etc.
Others
Methylene blue causes dermatitis through a phototoxic reaction.
Scleroderma
Occupational scleroderma is rare.
Causal exposures
Inhalation of vinyl chloride monomer (VCM)
Scleroderma-like changes have been reported in association with exposure to the following:
Pesticides
Epoxy resins
Perchlorethylene and trichloroethylene
Silica.
Clinical features
Thickened shiny skin on the fingers.
VCM disease
Occurs as part of a syndrome which includes the following:
Acro-osteolysis: resorption of the terminal phalanges on X-ray
Raynaud’s phenomenon: digital vascular spasm giving rise to blanching in cold conditions
Associated features of VCM exposure include:
hepatic fibrosis
angiosarcoma of the liver.
Prevention
VCM disease has been virtually eliminated by good hygiene controls (enclosure) in the PVC manufacturing industry.
Compensation
Sclerodermatous thickening of the skin of the hands is prescribed for Industrial Injuries Disablement Benefit (C24b (iii)) in those who are exposed to vinyl chloride monomer in the manufacture of PVC.
Occupational skin infections
Occupation can be a risk factor for skin infection because of either association with environmental conditions that favour microbial overgrowth or exposure to specific organisms.
Epidemiology
Data from the specialist physicians reporting schemes1 show that new cases of infective skin disease due to occupation have been declining over the past decade—26 cases were reported in 2010.
Saturation diving
Divers who live for prolonged periods in dive chambers are susceptible to infections of the skin and ear because of the persistently warm humid conditions. Pseudomonas species are a particular problem. Prevention of otitis externa requires meticulous aural toilet.
Zoonotic skin infections
These are a hazard for agricultural workers, veterinary practitioners, abbatoir, and fish-processing workers. They include Orf, Herpes Simplex, Anthrax, Scabies, Lyme Disease.
Multi-resistant Staphylococcus aureus
Persistent carriage of MRSA has been described in HCWs. This has mainly been described as nasal colonization on repeated swabbing, and is mostly asymptomatic. It usually clears with topical antibiotic treatment for the nose and chlorhexidine body washes. However, true infections (e.g. of skin lesions) are potentially serious and difficult to treat. Those who are at increased risk of multi-resistant Staphylococcus aureus (MRSA) carriage include HCWs with hand eczema or persistent respiratory tract infection (e.g. sinusitis or bronchiectasis).
There is no definitive guidance on exclusion of HCWs who are at risk of MRSA colonization or infection, or those who are chronically colonized. Decisions to restrict from work where there is a high risk of acquiring MRSA, or transmitting infection to patients (e.g. care of surgical wounds) should be made on an individual basis. There is little hard evidence to guide such decisions, and the risk of legal challenge in the event of loss of employment is significant.
Compensation
Certain occupational zoonoses that affect skin are prescribed for Industrial Injuries Disablement Benefit.
Cutaneous anthrax (B1)
Glanders (B2)
Orf (B12).
Relevant legislation
Any infection that is clearly attributable to occupation is reportable under RIDDOR.
