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Occupational Dermatitis in Government Workers*
OCCUPATIONAL DERMATITIS IN GOVERNMENT WORKERS* S. WILLIAM BECKER, JR. MS., M.D.I
This paper presents a summary of occupational dermatitis occurring in government employees treated at the United States Public Health Service Outpatient Clinic from July, 1951 to July, 1952. Since many persons did not seek medical care for minor eruptions or were treated at the Health Units in the government agencies, this series of patients does not include all of those with occupational dermatitis but does represent a fair sample. Table I presents the principle causes of the occupational dermatoses. The figure of thirty four per cent for allergic dermatoses (Group I, Table I) is somewhat higher than that usually found. Schwartz (1) stated that about twenty per cent of industrial dermatoses are allergic. Table II shows the substances to which patients were shown to be allergic. The most common causes of allergic contact dermatitis were the chemicals used in printing and allied fields (2). A breakdown of the figures according to occupation showed that one-third either worked in the Bureau of Engraving and Printing or as printers, engravers, cartographers, photographers, etc., in other agencies. The high percentage of patients exposed to chromates (chrome ink, various chrome etches and bichromate solutions) and other sensitizing chemicals seems to explain the high incidence of allergy. Patients with chromate dermatitis were difficult to treat. No protective cream including BAL ointment (3) gave satisfactory protection. Silicone cream (4) was unsatisfactory because the numerous organic solvents used by the patients removed the cream. Most of the patients sensitive to chromate were plate printers at the Bureau of Engraving and Printing. After the presses were supplied with automatic feed, takeoff and wipers so that the contact with the ink was lessened, the number of patients with chrome dermatitis decreased. The patients with dermatitis caused by plants were gardeners and workers in the National Capital Parks and Department of Agriculture. Forty three percent of the dermatoses (Group II, Table I) were due to primary irritants. Most patients were exposed to more than one primary irritant but the two greatest offenders were organic solvents and cleansing agents. The solvents (causing dermatitis in 65 patients) included type wash, blanket wash, ink, lacquer and paint solvents, gasoline, kerosene and others, but varsol (5) (a high boiling point petroleum solvent similar to Stoddards solvent) caused the most difficulty. Varsol was widely used as a degreaser, inkremover, cleanser and paint thinner and caused eczema of the hands by defatting the skin (6). A few patients who * From the United States Public Health Service Outpatient Clinic, 4th & D Sts., S. W. Washington, D. C. 1951—1953.
t Senior Assistant Surgeon (R) U.S.P.H.S. and dermatologist U.S.P.H.S. The opinions expressed in this article are those of the author and not necessarily those of the Public Health Service. Received for publication December 14, 1953. 249
250
THE JOtJRNAL OF INVESTIGATIVE DERMATOLOGY
TABLE I Principle causes of the dermatoses TYPE OF DERMATITIS
NUMBER OF PATIENTS
I. Allergic dermatitis
34
A. Chemical B. Physical
64 1
C. Plant II. Primary irritant dermatitis
III. IV. V.
VI.
23 43
A. Chemical B. Physical Irritation of preexisting dermatitis. . Infections Insect bites Occupational but exact cause undeter.
mined
VII. Resulting from injury
Total
PER CENT OF TOTAL
.
104 9
25
10
16
6 4
11
5 2
2
260
100
1
spilled varsol on their skin and could not remove it immediately developed acute dermatitis. Cleansing agents (some of which contained solvents) were the primary irritants in thirty-six patients. Sixteen of these were exposed to soap used in cleaning floors or special cleansing agents used to remove ink, ditto-paper stains or grease. Twenty-one patients developed dermatitis from hand soap (bar, liquid and granular). This latter group washed their hands excessively, as many as ten to fifteen times a day, and had a tendency to agrophobia. All of the dermatitides in the primary irritant group occurred on the hands and in most instances there was some exposure to both solvents and cleansing agents. The nine patients with physical irritation were burned by a variety of substances such as hot ashes, hot tar, etc. The preexisting dermatitis that was irritated by work (Group III, Table I) con-
sisted entirely of dermatitis of the hands and almost all of the patients had dyshidrotic eczema. There were a few patients with nummular eczema and one with a trichophytid. Soap, solvents and infection all played a part in irritating the hands of these individuals. The infections seen in these patients (Group IV, Table I) were staphylococcal and usually arose in an area where there had been some physical or chemical irritation. The insect bites (Group V, Table I) seen in the clinic were not unusual. Five patients (Group VI, Table I) had dermatitis which became worse when they worked but the exact cause was never determined. Two individuals (Group VII, Table I) developed stasic dermatitis after traumatic injury to the legs. Although many persons with similar occupations whose dermatitis had an identical cause were seen, there was great variation in the number of recurrences. One small group of patients had almost continuous difficulty. These individuals knew the causative agent and could have avoided the irritants, but did not do so.
OCCUPATIONAL DERMATITIS IN GOVERNMENT WORKERS
TABLE
251
II
Causes of allergic contact dermatitis NUMBER OS CASES
CAUSATIVE SUBSTANCE
Chemical Chromate
24
Non-chromate inks Rubber Developing chemicals Plastics Carbon paper Penicillin
10
9 3 2 2 2
Glue
Formaldehyde
T.N.T
Floor polish Brass Dyes Nickel
D.D.T Lacquer Lacquer thinner Glass eraser Physical Allergy Photosensitization from digitalis seed Plant Allergy Poison ivy Poinsettia
2 1 1 1 1 1 1 1 1 1 1 1
22 1
Psychiatric investigations of these patients was not possible but they seemed to
form an "accident prone" group (8) who purposely (consciously or subconsciously) exposed their skins to irritating substances. Explanation and education had little or no effect. SUMMARY
Occupational dermatitis found in two hundred and sixty government workers is presented and its etiology is discussed. These patients showed a higher percent-
age of allergic and a lower percentage of irritant dermatitis than was found in industrial surveys. The explanation appears to be the exposure to sensitizing chemicals of the patients working in printing and allied fields. There was a group of patients who seemed to fear dirt and used so much soap that dermatitis was produced. A small group of patients who suffered repeated exacerbations appeared to comprise an "accident prone" category. REFERENCES 1. SCHWARTZ, L.: Occuptational Dermatoses, in MeKenna, Modern Trends in Dermatology, New York, Paul B. Hoeber, Inc. 1948, pp. 253—274. 2. SCHWARTZ, L.; TULIPAN, L.; AND PECK, S. M.: Occupational Diseases of the Skin, Phila-
delphia, Lea and Febiger 1947, second edition, p. 449.
252
THE JOURNAL OF INVESTIGATIVE DERMATOLOGY
3. COLE, H. N., Ja.: Use of dimecaprol (BAL) ointment in chronic chrome dermatitis. Arch. Dermat. & Syph. 67: 30—36, 1953. 4. SMITH, C.; DAY, T. F.; AND ZIMMERMAN, E. H.: Studies of nitrocellulose silicone cream
as a skin protectant against eczematogenous contact allergens. J. Invest. Dermat. 21: 111—120,
1953.
5. Reference No. 2 PP. 532. 6. ANDERSON, N. P.: Contact dermatitis: Its relation to petroleum products. Industrial Medicine & Surgery, 22: 270—273, 1953.
7. RATTNER, H.: Occupational dermatitis. Industrial Medicine & Surgery 22: 198—201, 1953.
8.
Aasous, A. G., AND KEEEICI-I, J. E.: The phenomenon of accident proneness. Industrial Medicine & Surgery, 22: 141—148, 1953.
THE JOURNAL OF INVESTIGATIVE DERMATOLOGY
94
linolenic acid extract. Arch. This pdf is a scanned copy UV of irradiated a printed document.
24. Wynn, C. H. and Iqbal, M.: Isolation of rat
skin lysosomes and a comparison with liver Path., 80: 91, 1965. and spleen lysosomes. Biochem. J., 98: lOP, 37. Nicolaides, N.: Lipids, membranes, and the 1966.
human epidermis, p. 511, The Epidermis
Eds., Montagna, W. and Lobitz, W. C. Acascopic localization of acid phosphatase in demic Press, New York. human epidermis. J. Invest. Derm., 46: 431, 38. Wills, E. D. and Wilkinson, A. E.: Release of 1966. enzymes from lysosomes by irradiation and 26. Rowden, C.: Ultrastructural studies of kerathe relation of lipid peroxide formation to tinized epithelia of the mouse. I. Combined enzyme release. Biochem. J., 99: 657, 1966. electron microscope and cytochemical study 39. Lane, N. I. and Novikoff, A. B.: Effects of of lysosomes in mouse epidermis and esoarginine deprivation, ultraviolet radiation and X-radiation on cultured KB cells. J. phageal epithelium. J. Invest. Derm., 49: 181, 25. Olson, R. L. and Nordquist, R. E.: Ultramicro-
No warranty is given about the accuracy of the copy.
Users should refer to the original published dermal cells. Nature, 216: 1031, 1967. version of1965. the material. vest. Derm., 45: 448, 28. Hall, J. H., Smith, J. G., Jr. and Burnett, S. 41. Daniels, F., Jr. and Johnson, B. E.: In prepa1967.
Cell Biol., 27: 603, 1965.
27. Prose, P. H., Sedlis, E. and Bigelow, M.: The 40. Fukuyama, K., Epstein, W. L. and Epstein, demonstration of lysosomes in the diseased J. H.: Effect of ultraviolet light on RNA skin of infants with infantile eczema. J. Inand protein synthesis in differentiated epi-
C.: The lysosome in contact dermatitis: A ration. histochemical study. J. Invest. Derm., 49: 42. Ito, M.: Histochemical investigations of Unna's oxygen and reduction areas by means of 590, 1967. 29. Pearse, A. C. E.: p. 882, Histochemistry Theoultraviolet irradiation, Studies on Melanin, retical and Applied, 2nd ed., Churchill, London, 1960.
30. Pearse, A. C. E.: p. 910, Histacheini.stry Thearetscal and Applied, 2nd ed., Churchill, London, 1960.
31. Daniels, F., Jr., Brophy, D. and Lobitz, W. C.: Histochemical responses of human skin fol-
lowing ultraviolet irradiation. J. Invest. Derm.,37: 351, 1961.
32. Bitensky, L.: The demonstration of lysosomes by the controlled temperature freezing section method. Quart. J. Micr. Sci., 103: 205, 1952.
33. Diengdoh, J. V.: The demonstration of lysosomes in mouse skin. Quart. J. Micr. Sci., 105: 73, 1964.
34. Jarret, A., Spearman, R. I. C. and Hardy, J. A.:
Tohoku, J. Exp. Med., 65: Supplement V, 10, 1957.
43. Bitcnsky, L.: Lysosomes in normal and pathological cells, pp. 362—375, Lysasames Eds., de Reuck, A. V. S. and Cameron, M. Churchill, London, 1953.
44. Janoff, A. and Zweifach, B. W.: Production of inflammatory changes in the microcirculation by cationic proteins extracted from lysosomes. J. Exp. Med., 120: 747, 1964.
45. Herion, J. C., Spitznagel, J. K., Walker, R. I. and Zeya, H. I.: Pyrogenicity of granulocyte lysosomes. Amer. J. Physiol., 211: 693, 1966.
46. Baden, H. P. and Pearlman, C.: The effect of ultraviolet light on protein and nucleic acid synthesis in the epidermis. J. Invest. Derm.,
Histochemistry of keratinization. Brit. J. 43: 71, 1964. Derm., 71: 277, 1959. 35. De Duve, C. and Wattiaux, R.: Functions of 47. Bullough, W. S. and Laurence, E. B.: Mitotic control by internal secretion: the role of lysosomes. Ann. Rev. Physiol., 28: 435, 1966. the chalone-adrenalin complex. Exp. Cell. 36. Waravdekar, V. S., Saclaw, L. D., Jones, W. A. and Kuhns, J. C.: Skin changes induced by
Res., 33: 176, 1964.
This paper presents a summary of occupational dermatitis occurring in government employees treated at the United States Public Health Service Outpatient Clinic from July, 1951 to July, 1952. Since many persons did not seek medical care for minor eruptions or were treated at the Health Units in the government agencies, this series of patients does not include all of those with occupational dermatitis but does represent a fair sample. Table I presents the principle causes of the occupational dermatoses. The figure of thirty four per cent for allergic dermatoses (Group I, Table I) is somewhat higher than that usually found. Schwartz (1) stated that about twenty per cent of industrial dermatoses are allergic. Table II shows the substances to which patients were shown to be allergic. The most common causes of allergic contact dermatitis were the chemicals used in printing and allied fields (2). A breakdown of the figures according to occupation showed that one-third either worked in the Bureau of Engraving and Printing or as printers, engravers, cartographers, photographers, etc., in other agencies. The high percentage of patients exposed to chromates (chrome ink, various chrome etches and bichromate solutions) and other sensitizing chemicals seems to explain the high incidence of allergy. Patients with chromate dermatitis were difficult to treat. No protective cream including BAL ointment (3) gave satisfactory protection. Silicone cream (4) was unsatisfactory because the numerous organic solvents used by the patients removed the cream. Most of the patients sensitive to chromate were plate printers at the Bureau of Engraving and Printing. After the presses were supplied with automatic feed, takeoff and wipers so that the contact with the ink was lessened, the number of patients with chrome dermatitis decreased. The patients with dermatitis caused by plants were gardeners and workers in the National Capital Parks and Department of Agriculture. Forty three percent of the dermatoses (Group II, Table I) were due to primary irritants. Most patients were exposed to more than one primary irritant but the two greatest offenders were organic solvents and cleansing agents. The solvents (causing dermatitis in 65 patients) included type wash, blanket wash, ink, lacquer and paint solvents, gasoline, kerosene and others, but varsol (5) (a high boiling point petroleum solvent similar to Stoddards solvent) caused the most difficulty. Varsol was widely used as a degreaser, inkremover, cleanser and paint thinner and caused eczema of the hands by defatting the skin (6). A few patients who * From the United States Public Health Service Outpatient Clinic, 4th & D Sts., S. W. Washington, D. C. 1951—1953.
t Senior Assistant Surgeon (R) U.S.P.H.S. and dermatologist U.S.P.H.S. The opinions expressed in this article are those of the author and not necessarily those of the Public Health Service. Received for publication December 14, 1953. 249
250
THE JOtJRNAL OF INVESTIGATIVE DERMATOLOGY
TABLE I Principle causes of the dermatoses TYPE OF DERMATITIS
NUMBER OF PATIENTS
I. Allergic dermatitis
34
A. Chemical B. Physical
64 1
C. Plant II. Primary irritant dermatitis
III. IV. V.
VI.
23 43
A. Chemical B. Physical Irritation of preexisting dermatitis. . Infections Insect bites Occupational but exact cause undeter.
mined
VII. Resulting from injury
Total
PER CENT OF TOTAL
.
104 9
25
10
16
6 4
11
5 2
2
260
100
1
spilled varsol on their skin and could not remove it immediately developed acute dermatitis. Cleansing agents (some of which contained solvents) were the primary irritants in thirty-six patients. Sixteen of these were exposed to soap used in cleaning floors or special cleansing agents used to remove ink, ditto-paper stains or grease. Twenty-one patients developed dermatitis from hand soap (bar, liquid and granular). This latter group washed their hands excessively, as many as ten to fifteen times a day, and had a tendency to agrophobia. All of the dermatitides in the primary irritant group occurred on the hands and in most instances there was some exposure to both solvents and cleansing agents. The nine patients with physical irritation were burned by a variety of substances such as hot ashes, hot tar, etc. The preexisting dermatitis that was irritated by work (Group III, Table I) con-
sisted entirely of dermatitis of the hands and almost all of the patients had dyshidrotic eczema. There were a few patients with nummular eczema and one with a trichophytid. Soap, solvents and infection all played a part in irritating the hands of these individuals. The infections seen in these patients (Group IV, Table I) were staphylococcal and usually arose in an area where there had been some physical or chemical irritation. The insect bites (Group V, Table I) seen in the clinic were not unusual. Five patients (Group VI, Table I) had dermatitis which became worse when they worked but the exact cause was never determined. Two individuals (Group VII, Table I) developed stasic dermatitis after traumatic injury to the legs. Although many persons with similar occupations whose dermatitis had an identical cause were seen, there was great variation in the number of recurrences. One small group of patients had almost continuous difficulty. These individuals knew the causative agent and could have avoided the irritants, but did not do so.
OCCUPATIONAL DERMATITIS IN GOVERNMENT WORKERS
TABLE
251
II
Causes of allergic contact dermatitis NUMBER OS CASES
CAUSATIVE SUBSTANCE
Chemical Chromate
24
Non-chromate inks Rubber Developing chemicals Plastics Carbon paper Penicillin
10
9 3 2 2 2
Glue
Formaldehyde
T.N.T
Floor polish Brass Dyes Nickel
D.D.T Lacquer Lacquer thinner Glass eraser Physical Allergy Photosensitization from digitalis seed Plant Allergy Poison ivy Poinsettia
2 1 1 1 1 1 1 1 1 1 1 1
22 1
Psychiatric investigations of these patients was not possible but they seemed to
form an "accident prone" group (8) who purposely (consciously or subconsciously) exposed their skins to irritating substances. Explanation and education had little or no effect. SUMMARY
Occupational dermatitis found in two hundred and sixty government workers is presented and its etiology is discussed. These patients showed a higher percent-
age of allergic and a lower percentage of irritant dermatitis than was found in industrial surveys. The explanation appears to be the exposure to sensitizing chemicals of the patients working in printing and allied fields. There was a group of patients who seemed to fear dirt and used so much soap that dermatitis was produced. A small group of patients who suffered repeated exacerbations appeared to comprise an "accident prone" category. REFERENCES 1. SCHWARTZ, L.: Occuptational Dermatoses, in MeKenna, Modern Trends in Dermatology, New York, Paul B. Hoeber, Inc. 1948, pp. 253—274. 2. SCHWARTZ, L.; TULIPAN, L.; AND PECK, S. M.: Occupational Diseases of the Skin, Phila-
delphia, Lea and Febiger 1947, second edition, p. 449.
252
THE JOURNAL OF INVESTIGATIVE DERMATOLOGY
3. COLE, H. N., Ja.: Use of dimecaprol (BAL) ointment in chronic chrome dermatitis. Arch. Dermat. & Syph. 67: 30—36, 1953. 4. SMITH, C.; DAY, T. F.; AND ZIMMERMAN, E. H.: Studies of nitrocellulose silicone cream
as a skin protectant against eczematogenous contact allergens. J. Invest. Dermat. 21: 111—120,
1953.
5. Reference No. 2 PP. 532. 6. ANDERSON, N. P.: Contact dermatitis: Its relation to petroleum products. Industrial Medicine & Surgery, 22: 270—273, 1953.
7. RATTNER, H.: Occupational dermatitis. Industrial Medicine & Surgery 22: 198—201, 1953.
8.
Aasous, A. G., AND KEEEICI-I, J. E.: The phenomenon of accident proneness. Industrial Medicine & Surgery, 22: 141—148, 1953.
THE JOURNAL OF INVESTIGATIVE DERMATOLOGY
94
linolenic acid extract. Arch. This pdf is a scanned copy UV of irradiated a printed document.
24. Wynn, C. H. and Iqbal, M.: Isolation of rat
skin lysosomes and a comparison with liver Path., 80: 91, 1965. and spleen lysosomes. Biochem. J., 98: lOP, 37. Nicolaides, N.: Lipids, membranes, and the 1966.
human epidermis, p. 511, The Epidermis
Eds., Montagna, W. and Lobitz, W. C. Acascopic localization of acid phosphatase in demic Press, New York. human epidermis. J. Invest. Derm., 46: 431, 38. Wills, E. D. and Wilkinson, A. E.: Release of 1966. enzymes from lysosomes by irradiation and 26. Rowden, C.: Ultrastructural studies of kerathe relation of lipid peroxide formation to tinized epithelia of the mouse. I. Combined enzyme release. Biochem. J., 99: 657, 1966. electron microscope and cytochemical study 39. Lane, N. I. and Novikoff, A. B.: Effects of of lysosomes in mouse epidermis and esoarginine deprivation, ultraviolet radiation and X-radiation on cultured KB cells. J. phageal epithelium. J. Invest. Derm., 49: 181, 25. Olson, R. L. and Nordquist, R. E.: Ultramicro-
No warranty is given about the accuracy of the copy.
Users should refer to the original published dermal cells. Nature, 216: 1031, 1967. version of1965. the material. vest. Derm., 45: 448, 28. Hall, J. H., Smith, J. G., Jr. and Burnett, S. 41. Daniels, F., Jr. and Johnson, B. E.: In prepa1967.
Cell Biol., 27: 603, 1965.
27. Prose, P. H., Sedlis, E. and Bigelow, M.: The 40. Fukuyama, K., Epstein, W. L. and Epstein, demonstration of lysosomes in the diseased J. H.: Effect of ultraviolet light on RNA skin of infants with infantile eczema. J. Inand protein synthesis in differentiated epi-
C.: The lysosome in contact dermatitis: A ration. histochemical study. J. Invest. Derm., 49: 42. Ito, M.: Histochemical investigations of Unna's oxygen and reduction areas by means of 590, 1967. 29. Pearse, A. C. E.: p. 882, Histochemistry Theoultraviolet irradiation, Studies on Melanin, retical and Applied, 2nd ed., Churchill, London, 1960.
30. Pearse, A. C. E.: p. 910, Histacheini.stry Thearetscal and Applied, 2nd ed., Churchill, London, 1960.
31. Daniels, F., Jr., Brophy, D. and Lobitz, W. C.: Histochemical responses of human skin fol-
lowing ultraviolet irradiation. J. Invest. Derm.,37: 351, 1961.
32. Bitensky, L.: The demonstration of lysosomes by the controlled temperature freezing section method. Quart. J. Micr. Sci., 103: 205, 1952.
33. Diengdoh, J. V.: The demonstration of lysosomes in mouse skin. Quart. J. Micr. Sci., 105: 73, 1964.
34. Jarret, A., Spearman, R. I. C. and Hardy, J. A.:
Tohoku, J. Exp. Med., 65: Supplement V, 10, 1957.
43. Bitcnsky, L.: Lysosomes in normal and pathological cells, pp. 362—375, Lysasames Eds., de Reuck, A. V. S. and Cameron, M. Churchill, London, 1953.
44. Janoff, A. and Zweifach, B. W.: Production of inflammatory changes in the microcirculation by cationic proteins extracted from lysosomes. J. Exp. Med., 120: 747, 1964.
45. Herion, J. C., Spitznagel, J. K., Walker, R. I. and Zeya, H. I.: Pyrogenicity of granulocyte lysosomes. Amer. J. Physiol., 211: 693, 1966.
46. Baden, H. P. and Pearlman, C.: The effect of ultraviolet light on protein and nucleic acid synthesis in the epidermis. J. Invest. Derm.,
Histochemistry of keratinization. Brit. J. 43: 71, 1964. Derm., 71: 277, 1959. 35. De Duve, C. and Wattiaux, R.: Functions of 47. Bullough, W. S. and Laurence, E. B.: Mitotic control by internal secretion: the role of lysosomes. Ann. Rev. Physiol., 28: 435, 1966. the chalone-adrenalin complex. Exp. Cell. 36. Waravdekar, V. S., Saclaw, L. D., Jones, W. A. and Kuhns, J. C.: Skin changes induced by
Res., 33: 176, 1964.