Pesticides as a cause of occupational skin disease in farmers

Radoslaw Spiewak

Department of Occupational Biohazards, Institute of Agricultural Medicine, Lublin, Poland

Source: Spiewak R. Pesticides as a cause of occupational skin disease in farmers. Ann Agric Environ Med 2001; 8 (1): 1-5.

 

Abstract: Pesticides are chemical substances used in agricultural production to protect crops against pests. They help to achieve better quality and quantity of crops; however, they also are capable of causing occupational diseases in farmers. Skin is the most exposed organ while spraying the pesticide on fields. Farmers are also exposed to pesticides while mixing, loading the pesticide as well as while cleaning the equipment and disposing of empty containers. Other activities associated with exposure are sowing pesticide-preserved seeds, weeding and harvesting previously sprayed crops.

During the first decades of using pesticides the main problem was the risk of acute intoxication among people occupationally exposed. With decrease in the toxicity of improved pesticides, attention was turned to chronic intoxication and environmental contamination. Nowadays, the problem of diseases not immediately related to the toxic potential of pesticides gains increasing interest. The majority of these non-toxic diseases are dermatoses. Most pesticide-related dermatoses are contact dermatitis, both allergic or irritant. Rare clinical forms also occur, including urticaria, erythema multiforme, ashy dermatosis, parakeratosis variegata, porphyria cutanea tarda, chloracne, skin hypopigmentation, nail and hair disorders. Farmers exposed to arsenic pesticides are at risk of occupational skin cancer, mostly morbus Bowen (carcinoma in situ), multiple basal cell carcinomas and squamous cell carcinomas. Non-arsenic pesticides, e.g. paraquat, are also potentially carcinogenic.

Key words: pesticides, occupational dermatoses, farmers, contact dermatitis, urticaria, erythema multiforme, ashy dermatosis, parakeratosis variegata, porphyria cutanea tarda, chloracne, skin hypopigmentation, nail and hair disorders, skin cancer.

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Pesticides are chemical substances used in agricultural production to protect crops against pests. These substances may be divided into insecticides (insect killers), fungicides (fungus killers), herbicides (weed killers), rodenticides (rodent killers), repellents (substances used to deter vermin from cultivated land), and fumigants (gaseous chemicals used for clearing plantations of microbes or insects). Pesticides help to achieve better quality and quantity of crops; however, they are capable of causing occupational diseases in farmers. Skin is the most exposed organ while spraying the pesticide on fields [65]. Farmers are also exposed to pesticides while mixing, loading the pesticide as well as while cleaning the equipment and disposing of empty containers [67]. Other activities associated with exposure are sowing pesticidepreserved seeds, weeding and harvesting previously sprayed crops. In the case of contaminating skin with pesticides in field, most farmers wash the skin and change their clothing only after having finished their work - the prolonged exposure increases risk of unwanted effects of these substances, both irritating, allergising and carcinogenic [68].

During the first decades of using pesticides the main problem was the risk of acute intoxication among people occupationally exposed to them. With the decrease of acute toxicity of improved pesticides, attention was turned to chronic intoxication and environmental contamination. Nowadays, the problem of diseases not immediately related to toxic potential of pesticides gains increasing interest. The majority of these non-toxic diseases are dermatoses.

The most common clinical form of pesticide-related skin diseases is contact dermatitis, both allergic or irritant. The less common diseases include contact urticaria, erythema multiforme, ashy dermatosis, occupational acne, porphyria cutanea tarda, hair and nail disorders, and skin cancer. These diseases will be described below. Many of the discussed pesticides are no longer in use because of rapid progress on the pesticide market. It cannot be excluded, however, that similar skin diseases may also appear due to some newly introduced pesticides because of structural similarities between the older and newer formulas.

CONTACT DERMATITIS

Pesticide-related contact dermatitis was first described by McCord and Kilkee in 1921 [42]. Pesticide-related contact dermatitis may be both allergic [11, 13, 38, 46, 61, 66] or irritant [37, 38]. Some pesticide components are capable of increasing the skin sensitivity to light which results in phototoxic reactions [26], or may undergo photoactivated chemical reaction which produces a derivative allergising to the skin (photoallergy) [54].

Among all 815 pesticide-related diseases (including poisoning) registered in Japan in 1968-1970, allergic contact dermatitis was diagnosed in 274 cases (33.6%) [41]. Among 122 Taiwanese fruit farmers who were spraying pesticides regularly, contact allergy to pesticides was found in 40%, and clinical symptoms of contact dermatitis - in 30% [22]. In Spain, the prevalence of contact allergy to mercury and carbamates which are compounds of many pesticides was three times as high among farmers compared to the control group [21]. Among 104 Polish farmers treated in a dermatology clinic for eczema, contact allergy to pesticides was found in two persons [45]. In an unselected population of 160 patients in another Polish dermatology clinic, contact allergy to pesticides was found in 46 persons (28.7%) [15]. Among 263 hop growers in eastern Poland, contact allergy to pesticides was found in 66 persons (25.1%) [39].

Some pesticides have shown a very high allergising potential. The organophosphorus insecticide parathion was used for producing experimental contact dermatitis [38]. There were "epidemics" of contact dermatitis among farmers, caused by pesticides with strong allergising properties. In the USA, such outbreaks of contact dermatitis were caused by pesticides Dyrene (2,4-dichloro-6-(o-chloroanilino)-s-triazine anilazine) [59] and Omite-Cr (propagite) [53]. In the district of Magdeburg (Germany), a significant increase of pesticide-related contact dermatits was noted after introduction of the pesticide Nematin which caused 18 of all 22 pesticide allergy cases registered from 1966-1980 [25].

Allergising or irritant properties of the pesticide preparations may be due to active substances themselves or due to additives like emulgators or preservatives. Moreover, skin reactions may be produced by the degradation product of the active substance or additives. This kind of skin reaction to degradation product was described in workers sorting potatoes for planting - the potatoes were previously impregnated with metham sodium (sodium N-methyl dithiocarbamate) which underwent hydrolytic decomposition into allergising methyl isothiocyanate [58].

Screening for, and diagnosis of pesticide-related contact dermatitis is very difficult because of constant changes in the preparations used. Each year, new pesticide preparations are allowed for trade and older products are banned from the market. However, even if a pesticide is no longer on the market, sensitisation to it may last for many years and eventually re-appear due to cross-reaction with a new pesticide structurally related to the primary sensitiser. Moreover, many products in daily use (rubber, medications, housekeeping means) contain pesticides or chemically related substances capable of provoking relapses of the disease.

URTICARIA

Urticaria is characterised by the presence of transient vascular reaction representing localised vascular oedema in the upper dermis, caused by dilatation and increased permeability of the capillaries following exposure to the eliciting agent. The clinical expression of the reaction are wheals. A case of occupational urticaria to the fungicide captan was described in a gardener, who reacted not only to the captan pulver and solution but also to captanpreserved tulip bulbs [18]. An insect repellent diethyltoluamide (used mostly in housekeeping) was also reported to cause contact urticaria [40]. A more recent case report describes a redwood plant nursery worker, who developed contact urticaria and anaphylactoid reaction to common fungicide chlorothalonil [19].

ERYTHEMA MULTIFORME

The clinical manifestation of this entity is a sudden onset of an erythematous eruption with presence of characteristic lesions called iris, bull's eye or target lesions, which consist of papules with two or more concentric rings of slightly differing colours. Two cases of erythema multiforme were described, in which the skin lesions appeared a few hours after coming in contact with the organophosphorus insecticide methyl parathion [4, 43]. Another case report describes development of target lesions after accidental massive exposure to another organophosphorus insecticide dimethoate in an ex-farmer [55].

ASHY DERMATOSIS

Ashy dermatosis, called also erythema dyschromicum perstans, is a skin disease occurring predominantly in dark-skinned individuals, characterised by the presence of single or multiple ashen macules of variable size and shape. The cause of the disease is by large unknown, however, in 39 banana farm workers the disease was probably caused by exposure to the fungicide chlorothalonil (TCPN) [47].

PARAKERATOSIS VARIEGATA

This is disease of unknown etiology, characterised by ashy dermatosis-like eruption at the onset, which progressively involves the entire skin and turns gradually into poikiloderma (skin atrophy with speckle-like discolorations). Two farmers with parakeratosis variegata were recently described, in whom the disease was attributed to the exposure to pesticides and fertilisers [50].

PORPHYRIA CUTANEA TARDA

This is the most common form of porphyria, characterised by cutaneous photosensitivity that causes scarring bullae, hyperpigmentation, excessive hair growth on the face, and sometimes skin thickening and hair loss. Pesticide-related porphyria cutanea tarda was described in three workers employed at production of herbicides 2,4-dichlorophenol (2,4-T) and 2,4,5-trichlorophenol (2,4,5-T) [7]. An outbreak of the disease from 1955-1959 was caused by eating wheat seeds which had been preserved with the fungicide hexachlorobenzene [56].

CHLORACNE

This is an inflammatory disease of pilosebaceous unit (complex of hair follicles and sebaceous glands) similar to ordinary acne, caused by chlorinated polycyclic aromatic hydrocarbons, among them by pesticides or their contaminants. Some researchers regard chloracne as a form of irritant contact dermatitis [23]. However, there is more evidence against this hypothesis [16]. Acnegenic properties of chlorine compounds are most apparent under regular exposure. Chloracne was found in over 80% of workers involved in production of the insecticide and herbicide pentachlorophenol [14, 31]. A case of chloracne following exposure to pentachlorophenol-impregnated wood has also been reported [17].

Pesticide spraying is also associated with risk of developing chloracne. A case of a young farmer was reported, who developed chloracne due to exposure to neburone in a herbicide [3]. In another case report, a 53- year old man developed chloracne after having worked for many years as a pesticide sprayer [49].

The assessment of acnegenic potential of a given preparation is very difficult because the final product may be contaminated with raw materials, intermediate compounds and decomposition products which are not specified on the label. During heating of chlorophenols in the production of pesticides, formation of unwanted chlorodioxins takes place which possess strong acnegenic properties and may contaminate the final product [20]. TCDD (2,3,4,8-tetrachlorodibenzo-p-dioxin) is a strong acnegenic substance of which is present as an impurity in the herbicide 2,4,5-trichlorophenol (TCP) [27]. Acnegenic activity of the chloraniline pesticides propanil, 3,4-dichloroaniline, and methazole is, in fact, attributed to their contaminants: 3,4,3',4'-tetrachloroazobenzene and 3,4,3',4'-tetrachloroazoxybenzene [34].

Chloracne is relatively uncommon among farmers and should be differentiated from elastosis with comedones, which may occur in outdoor workers [27].

HYPOPIGMENTATION OF THE SKIN

This is abnormally diminished coloration of skin resulting from decreased production of melanin, the natural skin dye, by melanocytes. In a pesticide sprayer, hypopigmentation was observed following contact dermatitis reaction to the carbamate herbicide Carbyne [9].

HAIR LOSS

Pesticide-related hair loss was described in a farmer spraying DDT. The hair loss was classified as diffuse alopecia of mixed type [35].

NAIL DYSTROPHY

This condition is characterised by discoloration, deformities, and eventually loss of the nails. Permanent nail dystrophy was described in pesticide sprayers and other persons exposed to herbicides and insecticides diquat, paraquat, and dinitroorthocresol [2, 8, 24].

SKIN CANCER

Of all surveys on cancer among farmers, eight of 12 studies have shown excess in melanoma incidence, and seven of eight studies have shown excess in other skin cancers, which is primarily attributed to sunlight exposure, but also to pesticides [5]. At their workplace, farmers are exposed to various carcinogens, including pesticides [6]. The International Agency for Research on Cancer (IARC) informs about the increased risk of developing skin and lip cancer among professional pesticide sprayers [28]. Workers employed at production of the herbicide paraquat were also found to be at higher risk of developing skin cancer [37].

Strong carcinogenic properties are attributed to arsenic pesticides [1, 63]. Arsenic is carcinogenic metal with a clear predilection for the skin [36]. Until 1960s, arsenic salts were widely used as insecticides and seed-impregnates, and prior to those times acute poisonings were very common which suggests high exposure in many pesticide sprayers [12]. Arsenic compounds were first introduced and widely used in vineyards, therefore the first reported cases of arsenic-related cancer were vintners [10, 52, 62]. A more recent case report of skin cancer related to longterm arsenic exposure was published in 1987 [30]. In a recent study from Costa Rica, skin cancers (lip cancer, melanoma, non-melanocytic skin and penile cancer) occurred in excess in coffee growing areas with extensive use of paraquat and lead arsenate [64].

The effect of arsenic compounds on skin becomes apparent many years after exposure. First cases of palmoplantar keratosis were reported 10-15 years after introduction of arsenic into agriculture [51]. Carcinogenic effect of arsenic may become disclosed many decades after cessation of exposure, as it is in patients who received arsenic as medication. Before World War II, arsenic was used as a drug administered both internally (syphilis treatment, "tonics" for malaise and neuroses) and externally (Fowler's solution for psoriasis) [32, 33, 57, 60]. In such patients, multiple skin cancer appeared 30-50 years after being treated with these arsenic drugs [44, 48]. This may suggest that farmers who were exposed to arsenic pesticides 40-50 years ago, are still at risk of developing skin cancer related to that exposure. Therefore, every farmer presenting to a doctor with skin cancer should be questioned for contact with arsenic compounds and other potentially carcinogenic pesticides. Typical signs of long-term arsenic exposure are palmoplantar keratosis (excessive thickening of hand palms and foot soles) and chronic skin inflammation of distal body parts (acrodermatitis atrophicans). Later on, morbus Bowen (carcinoma in situ), multiple basal cell carcinomas and squamous cell carcinomas with ulceration may appear [10, 29]. Occupational skin cancer should be considered in first range in farmers with multiple or recurrent skin cancer, who were involved in spraying of arsenic insecticides in the past. Such patients must be checked also for other epithelial tumours, especially lung cancer.

According to the IARC, spraying and application of nonarsenical insecticides also entail exposures that are probably carcinogenic to humans (Group 2A) [28].

CONCLUSIONS

Most pesticide-related dermatoses are contact dermatitis, both allergic or irritant.

Rare clinical forms are also possible, including urticaria, erythema multiforme, ashy dermatosis, parakeratosis variegata, porphyria cutanea tarda, chloracne, skin hypopigmentation, nail and hair disorders.

Farmers who were exposed to arsenic pesticides are at risk of occupational skin cancer, mostly morbus Bowen (carcinoma in situ), multiple basal cell carcinomas and squamous cell carcinomas.

Also non-arsenic pesticides are potentially carcinogenic.

REFERENCES

  1. Axelson O: Pesticides and cancer risk in agriculture. Med Oncol Tumor Pharmacother 1987, 4, 207-217.
  2. Baran RL: Nail damage caused by weed killers and insecticides. Arch Dermatol 1974, 110, 467.
  3. Barriere H, Gerault C, Bureau B, Mousset S: Acne chlorique par manipulation d'herbicides. Ann Dermatol Venereol 1985, 112, 369-370.
  4. Bhargava RK, Singh V, Soni V: Erythema multiforme resulting from insecticide spray. Arch Dermatol 1977, 113, 686-687.
  5. Blair A, Zahm SH: Cancer among farmers. Occup Med 1991, 6, 335-354.
  6. Blair A, Zahm SH: Agricultural exposures and cancer. Environ Health Perspect 1995, 103(Suppl 8), 205-208.
  7. Bleiberg J, Wallen M, Brodkin R, Applebaum IL: Industrially acquired porphyria. Arch Dermatol 1964, 89, 793-797.
  8. Botella R, Sastre A, Castells A: Contact dermatitis to paraquat. Contact Dermatitis 1985, 13, 123-124.
  9. Brancaccio R, Chamales MH: Contact allergy and depigmentation produced by the herbicide Carbyne. Contact Dermatitis 1977, 3, 108-109.
  10. Braun W: Carcinoma of the skin and the internal organs caused by arsenic. Germ Med Monthly 1958, 3, 321-324.
  11. Brown R: Contact sensitivity to Difolatan (Captafol). Contact Dermatitis 1984, 10, 181-182.
  12. Brzozowski J: Zatrucia srodkami ochrony roslin i nawozami sztucznymi In: Zahorski W (Ed): Zarys Chorob Zawodowych i Higieny Pracy. PZWL, Warszawa 1956.
  13. Camarasa G: Difolatan dermatitis. Contact Dermatitis 1975,1, 127.
  14. Cheng WN, Coenraads PJ, Hao ZH, Liu GF. A health survey of workers in the pentachlorophenol section of a chemical manufacturing plant. Am J Ind Med 1993, 24, 81-92.
  15. Chodorowska G, Luty S, Toruniowa S: Wystepowanie alergii kontaktowej na wybrane chemiczne srodki ochrony roslin u pacjentow Kliniki Dermatologicznej w Lublinie pochodzacych z regionu lubelskiego. Med Wiejska 1991, 26, 131-139.
  16. Coenraads PJ, Brouwer A, Olie K, Tang N: Chloracne. Some recent issues. Dermatol Clin 1994, 12, 569-576.
  17. Cole GW, Stone O, Gates D, Culver D: Chloracne from pentachlorophenol-preserved wood. Contact Dermatitis 1986, 15, 164-168.
  18. Croy I: Ein kasuistischer Beitrag zur Ätiologie der Urtikaria durch Pilzbekämpfungsmittel auf Captan-Basis. Z Ges Hyg 1973, 19, 710-711.
  19. Dannaker CJ, Maibach HI, O'Malley M: Contact urticaria and anaphylaxis to the fungicide chlorothalonil. Cutis 1993, 52, 312-315.
  20. Delvaux EL, Verstraete J, Hautfenne A, De Sart F, Goffin G: Les polychloro dibenzo-p-dioxines. Toxicology 1975, 3, 187-206.
  21. Garcia-Perez A, Garcia-Bravo B, Beneit JV: Standard patch tests in agricultural workers. Contact Dermatitis 1984, 10, 151-153.
  22. Guo YL, Wang BJ, Lee CC, Wang JD: Prevalence of dermatoses and skin sensitisation associated with use of pesticides in fruit farmers of southern Taiwan. Occup Environ Med 1996, 53, 427-431.
  23. Harvell JD, Lammitausta K, Maibach HI: Irritant contact dermatitis. In: Guin JD (Ed.): Practical Contact Dermatitis. McGraw-Hill, New York 1995.
  24. Hearn CE, Keir W: Nail damage in spray operators exposed to paraquat. Br J Ind Med 1971, 28, 399-403.
  25. Helmdach F, Schlenzka K: Die Entwicklung der Berufsekzeme in der Landwirtschaft des Bezirkes Magdeburg seit 1966. 1. Mitteilung. Dermatol Monatsschr 1984, 170, 625-631.
  26. Hindson C, Diffey B: Phtototoxicity of glyphosate in a weedkiller. Contact Dermatitis 1984, 10, 51-52.
  27. Hogan DJ, Tanglertsampan C: The less common occupational dermatoses. Occup Med 1992, 7, 385-401.
  28. IARC Working Group: Occupational exposures in spraying and application of insecticides. IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans 1991, 53, 45-92.
  29. Jackson R, Grainge JW.: Arsenic and cancer. Can Med Assoc J 1975, 113, 396-401.
  30. Jampel RM, Jerdan MS: Palmar lesions and a nonhealing ulcer of the ear in a former agricultural worker. Arsenical keratoses; invasive squamous cell carcinoma of the right ear; and bowenoid keratoses. Arch Dermatol 1987, 123, 253-256.
  31. Jirasek L, Kalensky J, Kubec K, Pazderova J, Lukas E: Chlorakne, Porphyria cutanea tarda und andere Intoxikationen durch Herbizide. Hautarzt 1976, 27, 328-333.
  32. Junge J, Moll I: Multiple Palmoplantarkeratosen, Basaliome und Porokarzinome nach Arsen-Therapie. Hautarzt 1995, 46, 198-201.
  33. Kastl J, Horacek J: Multiple Basaliome nach langfristiger Arseneinnahme. Dermatol Monatsschr 1985, 171, 158-161.
  34. Kimbrough RD: Human health effects of selected pesticides, chloroaniline derivatives. J Environ Sci Health B 1980, 15, 977-992.
  35. Kwiatkowska E, Plonka T. Przypadek wylysienia wywolanego przez DDT. Przegl Dermatol 1971, 58, 185-190.
  36. Lansdown AB: Physiological and toxicological changes in the skin resulting from the action and interaction of metal ions. Crit Rev Toxicol 1995, 25, 397-462.
  37. Li W-M: The role of pesticides in skin disease. Int J Dermatol 1986, 25, 295-297.
  38. Lisi P, Caraffini S, Assalve D: Irritation and sensitization potential of pesticides. Contact Dermatitis 1987, 17, 212-218.
  39. Luty S, Chodorowska G: Alergia kontaktowa na pestycydy u plantatorów chmielu i rolników. In: Zagórski J (Ed.): Choroby Zawodowe i Parazawodowe w Rolnictwie. Instytut Medycyny Wsi, Lublin 2000.
  40. Maibach HI, Johnson HL: Contact urticaria syndrome. Arch Dermatol 1975, 111, 726-730.
  41. Matsushita T, Nomura S, Wakatsuki T: Epidemiology of contact dermatitis from pesticides in Japan. Contact Dermatitis 1980, 6, 255-259.
  42. McCord CP, Kilkee CH: Pyrethrum dermatitis. J Am Med Assoc 1921, 77, 448-449.
  43. Meneghini CL, Angelini G: Secondary polymorphic eruptions in allergic contact dermatitis. Dermatologica 1981,163, 63-70.
  44. Murata K, Iwazawa T, Takayama T, Yamashita K, Okagawa K: Quadruple cancer including Bowen's disease after arsenic injections 40 years earlier: report of a case. Surg Today 1994, 24, 1115-1118.
  45. Niczyporuk W, :Wronski A, Poniecka H, Krajewska-Kulak E: Alergia kontaktowa u pracownikow zatrudnionych w rolnictwie i czlonkow ich rodzin. Med Wiejska 1990, 25, 240-248.
  46. Peluso AM, Tardio M, Adamo F, Venturo N: Multiple sensitization due to bis-dithiocarbamate and thiophthalimide pesticides. Contact Dermatitis 1991, 25, 327.
  47. Penagos H, Jimenez V, Fallas V, O'Malley M, Maibach HI: Chlorothalonil, a possible cause of erythema dyschromicum perstans (ashy dermatitis). Contact Dermatitis 1996, 35, 214-218.
  48. Piontek M, Hengels KJ, Borchard F, Strohmeyer G: Nichtzirrhotische Leberfibrose nach chronischer Arsenintoxikation. Dtsch Med Wochenschr 1989,114, 1653-1657.
  49. Poskitt LB, Duffill MB, Rademaker M: Chloracne, palmoplantar keratoderma and localized scleroderma in a weed sprayer. Clin Exp Dermatol 1994, 19, 264-267.
  50. Rogozinski TT, Zekanowski C, Kaldan L, Blaszczyk M, Majewski S, Jablonska S: Parakeratosis variegata: a possible role of environmental hazards? Dermatology 2000, 201, 54-57.
  51. Roth F: The sequelae of chronic arsenic poisoning in Moselle vintners. Germ Med Monthly 1957, 2, 172-175.
  52. Roth F: Über die chronische Arsenvergiftung der Moselwinzer unter besonderer Berücksichtigung des Arsenkrebses. Z Krebsforsch 1956, 61, 287-319.
  53. Saunders LD, Ames RG, Knaak JB, Jackson RJ: Outbreak of Omite Cr-induced dermatits among orange pickers in Tulare County, California. J Occup Med 1987, 29, 409-413.
  54. Savitt LE: Contact dermatitis due to benomyl insecticide. Arch Dermatol 1972, 105, 926-927.
  55. Schena D, Barba A: Erythema-multiforme-like contact dermatitis from dimethoate. Contact Dermatitis 1992, 27, 116-117.
  56. Schmid R: Cutaneous porphyria in Turkey. N Eng J Med 1960, 263, 397-298.
  57. Scholz S, Zschoch H, Scholz H: Multiples Plattenepithelkarzinom als Arsenspatschaden nach Psoriasisbehandlung. Z Arztl Fortbild Jena 1988, 82, 1201-1203.
  58. Schubert H, Würbach G, Prater E, Jung H-D, Tarnick M. Kontaktdermatitis auf Metham-Natrium. Dermatosen 1993, 41, 28-33.
  59. Schuman SH, Dobson RL: An outbreak of contact dermatitis in farm workers. J Am Acad Dermatol 1985, 13, 220-223.
  60. Schwäblein-Sprafke U: Multiple Basaliome als Spatfolge einer akuten iatrogenen Arsenvergiftung im Kindesalter. Dermatol Monatsschr 1985, 171, 443-448.
  61. Sharma VK, Kaur S: Contact sensitization by pesticides in farmers. Contact Dermatitis 1990, 23, 77-80.
  62. Thiers H, Colomb D, Moulin G, Colin L: Le cancer cutane arsenical des viticulteurs du Beaujolais. Ann Dermatol Syphiligr 1967, 94, 133-158.
  63. Vineis P, Settimi L, Seniori-Costantini A: Esposizione a fitofarmaci e rischio oncogeno. Med Lav 1990, 81, 363-372.
  64. Wesseling C, Antich D, Hogstedt C, Rodriguez AC, Ahlbom A: Geographical differences of cancer incidence in Costa Rica in relation to environmental and occupational pesticide exposure. Int J Epidemiol 1999, 28, 365-374.
  65. Wolfe HR, Armstrong JF, Durham WF: Pesticide exposure from concentrate spraying. Arch Environ Health 1966, 13, 340-344.
  66. Won JH, Ahn SK, Kim S-C: Allergic contact dermatitis from the herbicide Alachlor. Contact Dermatitis 1993, 28, 38-39.
  67. Yoshida K: Cutaneous exposure of pesticide spray applicators. In: Dosman JA, Cockcroft D (Eds): Principles of Health and Safety in Agriculture. CRC Press, Boca Raton 1989.
  68. Zahm SH, Blair A. Cancer among migrant and seasonal farmworkers: an epidemiologic review and research agenda. Am J Ind Med 1993, 24, 753-766.

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