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Electrochemical characterization of supercapacitor electrodes

Chapter 5: Modification of Carbon Electrodes via Covalent Strategies

5.2 Functionalization of carbons via Friedel-Crafts reaction with p-BQ

5.2.3 Electrochemical characterization of supercapacitor electrodes

Carcinogen Industry or exposure Example(s)

Outdoor workers Farmers

Fisherfolk

Construction workers

Open-cut miners

Industrial UV Welders

Germicidal lamps

Ultraviolet light

UV curing processes

Nuclear industry Reactor workers Ionising radiation

Health care Radiologists Coal, coke, gas industries Coke oven workers

Tar distillers

Pitches and tars (polyaromatic hydrocarbons)

Coal gas manufacture

Fuel manufacture Briquette making

Creosote users Tile workers

Oil refining Still cleaners

Engineering Tool setters

Lathe operators

Oils

Cotton industry Mule spinners

Arsenic Agriculture Insecticide application

Animal dips

abundant dilated skin vessels close to the surface of the skin (telangiectasiae) and flat, reddened, scaling, premalignant sun keratoses.

Basal cell carcinoma is a tumour of the epidermal epithelial cells which also demonstrates a close association between site of tumour and exposure to sunlight.

However, unlike squamous cell tumours up to a third of basal cell carcinomas may develop on skin that is not chronically exposed to sunlight. Further, many of these tumours have a tendency to cluster around the skin of the eyes, nose and mouth.

Most nonmelanoma skin cancers (80–90%) occur on the head and trunk. These tumours rarely metastasise and a large proportion respond well to treatment, indicating that they have a high incidence, but a low mortality. On the other hand, the majority of melanomas are found on the trunk and limbs, even though the causative agent is invariably sunlight. Conversely, rates of melanoma are lower in outdoor workers than in indoor workers, suggesting that gradual exposure to sunlight during spring and early summer, and the build-up of skin tan may be protective factors. The higher rates of

melanoma in indoor workers may be related to the massive (but short-lived) exposures to sunlight at weekends or on annual vacations. Indeed, melanoma may be related more to previous skin damage through sunburn and blistering than to direct sunlight exposure itself.

Melanoma is a tumour of melanocytes. It is a cancer of white people, and is very rare in black people. The cancer tends to be pigmented in an initially flat lesion. As the cancer spreads out irregularly and superficially in the skin the pigmentation can become irregular (Fritschi and Siemiatycki 1996).

The only satisfactory curative treatment for melanoma is surgical excision. The likely outcome depends on the depth of the tumour, the site of the tumour, the gender of the individual, and other factors. The likely success of this treatment (surgery) is much greater when the cancer is thin, in its early stages. Cure is possible in 90% of patients if the cancer is removed before it is less than 0.75mm thick. The cancer is lethal in 60% of cases where it has been allowed to invade vertically into the skin to a thickness of 4mm or more by the time it is treated.

Epidemiological surveys show an increased risk for the development of squamous cell, basal cell or melanoma-type tumours among fair-skinned populations as geographic location approaches the equator. The migration of fair-skinned populations during recent centuries to those regions of the world with high sunlight exposure has meant that those individuals (and their families) are more likely to develop skin cancer, a factor confirmed in the medical and scientific literature. Indeed, Australia, now with a predominantly European-based population, has one of the highest incidences of melanoma, particularly in those states with tropical climates.

Prevention of occupational skin disorders

Determination of the agents and risk factors that cause occupational skin disorders is crucial to their prevention (Mathias 1990). However, this can be problematic, especially for skin allergens. As with many workplace risks, the process of occupational risk management (identify, assess, control) are necessary in prevention. Obviously prevention of dermatoses in the workplace would ideally be accomplished through total elimination of skin exposure to dermatitic risk factors (Cooley and Nethercott 1994). However, this is not always possible. Therefore a multidimensional approach to occupational skin disorders is needed, involving:

■ recognition of potential cutaneous irritants and allergens

■ recognition that some individuals may be more susceptible to exposure than others (atopy)

■ elimination, substitution, or engineering controls to control skin exposure

■ personal protection, appropriate clothing and barrier creams to prevent skin exposure

■ appropriate information and training of workers and managers

■ monitoring and health surveillance (including pre-employment screening)

■ personal hygiene

■ better systems for diagnosis, treatment and reporting of occupational skin disorders

■ regulation of established allergens and irritants.

A comprehensive preventive program of this type requires cooperation of workers, employers, product manufacturers and suppliers, safety and occupational health practitioners, the medical profession and government agencies.

Finally, it is important to promptly and accurately diagnose the cause of the dermatitis for the speedy rehabilitation of the worker. A worker who has been incorrectly diagnosed with work-related dermatitis often finds it difficult to accept a later diagnosis of constitutional dermatitis. The confusion, and sometimes hostility, such conflicting diagnoses produce can result in greatly delayed healing of the skin disease.

Summary

A wide variety of agents encountered in the workplace may cause injury, cell death, irritation, sensitisation, infection, discolouration or other changes to the skin of workers.

Further, some agents induce cancerous changes to the skin. The term occupational dermatoses is commonly used for all of these abnormalities resulting from, or aggravated by, the work environment.

In addition to being a target organ, the skin may also serve as an entry route to the body for toxic chemicals by percutaneous absorption.

Causal agents in the development of occupational skin disorders may be categorised as:

■ chemical: a wide range of corrosives, acids, alkalis, organic and inorganic compounds

■ physical: mechanical effects, heat and cold, humidity, sunlight and other radiation

■ biological: bacterial, viral, fungal infections, parasite infestations, plants and plant products.

Chemical agents are the greatest cause of occupational skin disorders. Sometimes a combination of several chemical agents, or of chemical and other agents (for example, sunlight) is responsible. The multicausal nature of occupational dermatoses significantly complicates its diagnosis and control in the workplace. While the symptoms of a skin disorder are visibly apparent, accurate diagnosis linking the disorder to occupation requires a high level of clinical skill and expertise in taking occupational histories and in physical examination. Establishing the relative contributions of exposures outside work can also prove difficult and complex.

Hot humid conditions and sun exposures associated with tropical and subtropical climates, in particular combined with the use of personal protective equipment, can exacerbate skin disorders.

As with exposure to all occupational risks, assessment of risks and application of the hierarchy of controls will assist in eliminating or reducing risk. These measures include:

■ removal of known dermatoxic agents from the workplace

■ substitution of hazardous materials for less hazardous materials (for example, allergen replacement in epoxy resins by high molecular weight chemicals)

■ control at source such as enclosed dipping instead of spray painting

■ safe working procedures such as reuse of cutting oils in lathe operations

■ personal administration, such as adequate supervision, training and information (labels and material safety data sheets), provision of personal hygiene controls (for example, ensuring that skin is washed when contaminated)

■ personal protective equipment, including hats, eye protection, work overalls, gloves, aprons, footwear, barrier creams.

Other approaches, such as monitoring and health surveillance, will identify problems as they arise and assist in control. Epidemiological studies may sometimes be helpful in establishing causal relationships with occupational skin diseases (for example, skin cancer).

References

Adams, R.M. (ed.) (1990) Occupational Skin Diseases, 2nd edn. Philadelphia: W.B. Saunders.

ATSDR (1996) Skin lesions and environmental exposures. Agency for toxic substances and disease registry. Aust. Ass. Occup. Health Nursing 44:529–540.

Burry, J.N. (1982) Clinical epidemiology and preventive dermatology: A sample of 1,000 cases in South Australia. Aust. J. Dermatol. 23:14–17.

Coenraads, P.J., Foo, S.C., Phoon, W.O. and Lun, K.C. (1985) Dermatitis in small scale metal industries. Cont. Derm. 12:155–160.

Cooley, J.E. and Nethercott, J.R. (1994) Prognosis of occupational skin disease. Occup. Med. State Art Rev. 9:19–24.

Draize, J.H., Woodard, G. and Calvery, H.O. (1944) Methods for the study of irritation and toxicity of substances applied topically to the skin and mucous membranes. J. Pharmacol. Exp. Ther.

82:377–390.

Emmett, E.A. (1987) Occupational skin cancers. Occup. Med. State Art Rev. 2:165–177.

Freeman, S. (1991) Occupational skin diseases: Diagnosis and differential diagnosis. J. Occup.

Health Safety—Aust. NZ 7:229–235.

Fritschi, L. and Siemiatycki, J. (1996) Melanoma and occupation. Results of a case-control study.

Occupat. Environ. Med. 53:168–173.

Halkier-Sorensen, L. (1996) Occupational skin diseases. Cont. Derm. 35:(Suppl) 1–120.

Lachapelle, J.M. (1986) Industrial airborne irritant or allergic contact dermatitis. Cont. Derm.

14:137–145.

Linn Holness, D. (1994) Characteristic features of occupational dermatitis: Epidemiologic studies of occupational skin disease reported by contact dermatitis clinics. Occupational Skin Disease.

In: Nethercott, J.R. (ed.) Occup. Med. State Art Rev. 9:45–52.

Lushniak, B.D. (2000) Occupational skin diseases. Prim. Care 27:895–916.

Maibach, H.I. (ed.) (1987) Occupational and Industrial Dermatology, 2nd edn. Chicago: Year Book Medical.

Maibach, H.I. (2000) Toxicology of the Skin. London: Taylor and Francis.

Mathias, C.G.T. (1990) Prevention of occupational contact dermatitis. J. Am. Acad. Dermatol.

23:742–748.

Mathias, C.G.T. (1994) Occupational dermatoses. In: Zenz, C., Dickerson, O.B. and Horvath, E.P.

(eds) Occupational Medicine, 3rd edn. St Louis: Mosby, pp. 93–131.

Nethercott, J.R. (ed.) (1994) Occupational skin disease. Occup. Med. State Art Rev. 9: 1–125.

NOHSC (1989) National Strategy for the Prevention of Skin Disorders. National Occupational Health and Safety Commission/AGPS, Canberra.

Rosen, R.H. and Freeman, S. (1992) Occupational contact dermatitis in New South Wales. Aust. J.

Dermatol. 33:1–10.

Rycroft, R.J.G., Menne, T., Frosch, P.J. and Lepoittevin, J.-P. (eds) (2001) Textbook of Contact Dermatitis. New York: Springer-Verlag.

Shama, S.K. (1988) Occupational skin disorders. In: McCunney, R.J. (ed.) Handbook of Occupational Toxicology. Boston: Little, Brown and Co, pp. 216–235.

Stevenson, C.J. (1989) Occupational skin disease. Postgrad. Med. J. 65:374–380.

Vestey, J.P., Gawkrodger, D.J., Wong, W.-K. and Buxton, P.K. (1986) An analysis of 501 consecutive contact clinic consultations. Cont. Derm. 15:119–125.

Zugerman, C. (1990) Chloracne: Clinical manifestations and etiology. Dermatol. Clin. 8: 209–213.