Cause Of Allergic Contact Dermatitis Research Articles

The frequency of fragrance allergy in a patch-test population over a 17-year period.

Fragrances are widely encountered in our daily environment and are known to be a common cause of allergic contact dermatitis. We have reviewed our patch test data from 1980 to 1996 to establish whether the pattern of fragrance allergy has changed with time. During this period, 25,545 patients (10,450 male, 15,005 female) were patch tested with the European standard series. The mean annual frequency of positive reactions to the fragrance mix was 8.5% in females (range 6.1-10.9) and 6.7% in males (range 5.1-12.9). Females were 1.3 times more likely to be allergic to fragrance (P < 0.001, 95% confidence interval, CI 1.17-1.41). Males with fragrance allergy were older than females by 5.6 years (mean age 48.2 vs. 42.6 years; P < 0.001, 95% CI 3.9-7.3). The incidence of a concomitant positive patch test to balsam of Peru in fragrance-sensitive patients showed wide variation, suggesting that it is not a reliable marker of fragrance allergy. There was a positive correlation between the isomers isoeugenol and eugenol. Oak moss remained the most common overall allergen throughout the study, positive in 38.3% of females and 35.6% of males who were tested to the constituents of the fragrance mix. During the period of the study the incidence of positive tests to oak moss increased by 5% yearly (P = 0.001, 95% CI 2.2-8.7). The frequency of allergic reactions to eugenol and geraniol remained relatively constant. Isoeugenol and alpha-amyl cinnamic aldehyde sensitivity increased and hydroxycitronellal showed a slow decline. There was a striking reduction in the frequency of sensitivity to cinnamic aldehyde (by 18% yearly; P < 0.001, 95% CI 14.3-21.0) and cinnamic alcohol (by 9% yearly; P < 0.001, 95% CI 5.2-12.9); these are now uncommon fragrance allergens. These data show temporal trends which may reflect the frequency of population exposure to individual fragrances.

Contents of fragrance allergens in children's cosmetics and cosmetic-toys.

Fragrances are one of the major causes of allergic contact dermatitis from use of cosmetics. The aim of the current study was to assess the possible exposure of infants and children to fragrance allergens from cosmetic products and "toy-cosmetics". 25 children's cosmetics or toy-cosmetic products were analysed by gas chromatography - mass spectrometry. Target substances were the fragrance allergens from the fragrance mix and 14 other fragrance substances, most of which have been described as contact allergens. The fragrance mix ingredients were either not present in children's shampoos/shower gels and cream/lotions, or they were present in fairly low concentrations. In hydro-alcoholic products, such as eau de parfum, eau de toilette, several ingredients of the fragrance mix were found: geraniol was present in 7/7 products, hydroxycitronellal in 6/7 and isoeugenol in 2/7 products. Isoeugenol was present in a maximum concentration of 0.07%. In one cosmetic-toy, cinnamic alcohol was present at 3.7% which exceeds the current industry guideline for safe products by a factor of 5. In all types of products other fragrance allergens were frequently found. In conclusion, children are already exposed at an early age to well-known allergens, sometimes at concentrations which are considered to be unsafe. As contact allergy usually persists for life, manufacturers of children's cosmetics should be aware of their special responsibility and apply the highest possible safety standards.

Increase in occupational skin diseases of dental personnel.

Occupational diseases of dentists and dental nurses were compiled from the Finnish Register of Occupational Diseases. The cases were recorded during 3 3-year observation periods, namely 1982-1984, 1986-1988, and 1992-1994 (i.e., 9 observation years). The relative risk of developing occupational allergic contact dermatitis in different occupations was calculated from the statistics of the years 1986-1991, and was expressed as the age-standardized rate ratio (SRR). During the 9 observation years, the majority of registered occupational diseases of dentists and dental nurses were skin diseases (221/312; 70.8%), followed by occupational repetitive strain injuries (61/312; 19.6%) and occupational respiratory diseases (20/312; 6.4%). The incidence rate (IR) for allergic contact dermatoses/10,000 workers (contact urticaria included) increased from 26 (95% confidence interval (CI) 16-40) in 1982-1984 to 79 (95%, CI 64-97) in 1992-1994. The IR/10,000 of allergic contact dermatoses increased especially for dentists, from 5.4 (95% CI 0.7-19) in 1982 to 67 (95% CI 45-95) in 1992-1994. The increase of the IR/10,000 dental nurses was smaller: from 43 (95%, CI 26-66) in 1982-1984 to 87 (95% CI 67-111) in 1992-1994. There was no increase in the IR/10,000 cases of irritant dermatoses. The most common causes of allergic contact dermatitis were plastics, disinfectants and antimicrobials, rubber chemicals, and mercury/mercury salts. The most common causes of irritant contact dermatitis were detergents, wet and dirty work, plastic chemicals and antimicrobials. Currently, Finnish dentists have the highest risk and dental nurses have the 4th highest risk of any occupation for developing occupational allergic contact dermatitis: the risk was 6.4-fold (SRR 6.4) in dentists and 6.1-fold in dental nurses, as compared to the general working population. It is evident that safer acrylics and protective gloves, better product declarations and material safety data sheets, as well as more information about protective measures, including non-touch working techniques, are needed.

Occupational dermatoses from plastic composites

Occupational dermatoses caused by plastic composites based on polyester resins, epoxy resins and vinyl ester resins (epoxy diacrylates) were reviewed. Common causes of irritant contact dermatitis are glass-fibre reinforcement and dust from product-finishing processes. Irritant contact dermatoses are also caused by resins, styrene, acetone, benzoyl peroxide, etc. Diglycidyl ether of bisphenol A (DGEBA) epoxy resin, amine hardeners, dicarboxylic (phthalic) anhydride hardeners and reactive epoxy diluents are common causes of allergic contact dermatitis. Non-DGEBA epoxy resins, tetraglycidyl-4,4′-methylenedianiline (TGMDA) and triglycidyl-p-aminophenol (TGPAP) used in carbon fibre reinforced composites may cause sensitization from prepregs. Diethylene glycol maleate is a new allergen in polyester resin cement. Natural rubber latex in protective gloves, and low molecular weight chemicals such as the epoxy resin hardener methyl tetrahydrophthalic anhydride (MTHPA) are causes of immunologic contact urticaria. Patch-testing with materials used by the patients at work, together with chemical analysis, is often needed to find the causative allergen, in addition to patch testing with standard test trays. Avoidance of skin contact with resin compounds, use of protective gloves, local ventilation, proper working methods, and informing the workers, are needed to lower the prevalence of occupational dermatoses in the manufacture of plastic composites. Copyright © 1999 John Wiley & Sons, Ltd.

Chloroxylenol causing hand dermatitis in a plumber

Chloroxylenol use has increased and is found in many over-the-counter preparations. Although not a common sensitizer, chloroxylenol's role as a contact allergen and relevance, when positive patch tests are found, is often high. Pre-patch test assessment generally does not identify chloroxylenol as a causative agent. It is increasingly found in liquid soaps particularly in industry and specifically in the health care environment. Even as a wash-off product, this allergen can be a hidden cause of allergic contact dermatitis.

Allergic Contact Dermatitis From Aromatherapy

Allergic contact dermatitis secondary to aromatherapy has been only rarely reported. We present 39-year-old woman who had used aromatherapy products for approximately 2 to 3 years who presented with an erythematous eruption on her face and chest. Patch testing showed a positive reaction to neomycin and fragrance mix. On cessation of her aromatherapy products, her eruption rapidly resolved. Aromatherapy products containing essential oils may need to be considered as a cause of allergic contact dermatitis because of the increasing popularity of this treatment.

Allergic contact dermatitis from aromatherapy

Allergic contact dermatitis secondary to aromatherapy has been only rarely reported. We present 39-year-old woman who had used aromatherapy products for approximately 2 to 3 years who presented with an erythematous eruption on her face and chest. Patch testing showed a positive reaction to neomycin and fragrance mix. On cessation of her aromatherapy products, her eruption rapidly resolved. Aromatherapy products containing essential oils may need to be considered as a cause of allergic contact dermatitis because of the increasing popularity of this treatment.

Occupational Dermatitis Transferred With Job Duties

Astroemeria is an increasingly common cause of allergic contact dermatitis. We report a case of occupational contact dermatitis that was transferred with job duties. When advising patients about their risk, it is advisable to discuss the risk to others in the setting as well.

Occupational dermatitis transferred with job duties

Astroemeria is an increasingly common cause of allergic contact dermatitis. We report a case of occupational contact dermatitis that was transferred with job duties. When advising patients about their risk, it is advisable to discuss the risk to others in the setting as well.

METAL (HARDWARE) IMPLANT “ALLERGY”

An essential attribute of all implanted surgical material must be an inherent inertness. Whereas to surgical implants are at times suspected, definitive association of a reaction caused by implant material is only rarely documented. Because there is no single source describing the incidence, clinical manifestations, pathogenesis, diagnosis, and management of such reactions, this article reviews the literature and attempts to interpret such reactions in light of the present knowledge of allergic and irritant contact metal of the skin and bone. Although the true incidence of contact from orthopedic implants may be rare, contact to metals is one of the most common causes of allergic contact dermatitis (ACD), as reported by both the North American Contact Dermatitis Group (NACDG) and the International Contact Dermatitis Research Group (ICDRG). 45 Nickel, cobalt, and chromium are the most constant offenders of all the allergenic metals. Nickel is the most frequent of all reported metal allergies 10 ; 10% of females are reported to be allergic to nickel. Dotterud and Falk 10 noted an increasing prevalence of nickel sensitivity in 201 school girls, which they ascribed to the higher incidence of ear piercing. They found the prevalence of nickel in girls with pierced ears to be twice as high as in girls without pierced ears (30.8% versus 16.3%, respectively). Nickel sensitivity in 223 boys was much lower, with but a few boys having pierced ears (11/223, or 5%). Nickel has also been reported to be one of the most frequent causes of occupational dermatoses. Of 853 hard-metal workers (485 males and 368 females), approximately 5% (2 males and 38 females) were positive to nickel on patch testing. Eighty-eight percent of the positives reported a history of costume jewelry allergy prior to their employment in the hard-metal industry. Forty percent of those allergic to nickel developed a recalcitrant hand eczema during the first year of employment, and 36 of 38 nickel-sensitive women had pierced ears. 43 Not only does nickel produce an eczematous (delayed-type hypersensitivity) reaction, but it has also been reported to cause immediate-type (IgE/mast-cell-induced) allergic reactions. The divalent nickel ion can be antigenic via contact, by ingestion, or by inhalation. The latter antigenic presentations may also cause clinical reactions, such as urticaria, with or without wheezing. Cobalt compounds can produce a wide range of immunologic reactions, plus pose an irritant-type problem of skin toxicity, especially in the workplace. Cobalt has been noted to occur concomitantly with nickel allergy. Rystedt and Fisher 43 report an incidence of 25% of nickel-sensitive individuals were also allergic to cobalt. Chromium is one of the less toxic heavy metals, but its salts can induce an irritant contact dermatitis (ICD). Trivalent chromium is the least reactive because of its relative inability to penetrate the skin. Hexavalent chromium, however, is the compound mostly associated with ICD. Many hexavalent chromium compounds are corrosive irritants, sensitizers, and respiratory carcinogens. 19 Sensitization to chromium enhances cobalt sensitization, which frequently occurs in nickel-sensitive individuals. These are not considered to be cross-reactions, but more likely distinctive, unique sensitizations to each individual metal. 24 The prevalence of these metals in the environment is high.

Analysis of allergens for dermatitis in textile products and its application to the determination of the cause of allergic contact dermatitis by spectrophotometry and GC/MS.

Analysis of allergens for dermatitis in textile products and its application to the determination of the cause of allergic contact dermatitis by spectrophotometry and GC/MS.

Corticosteroid usage and binding to arginine: determinants of corticosteroid hypersensitivity

Hypersensitivity to topical corticosteroids is a common cause of allergic contact dermatitis. The development of contact allergy is dependent on individual susceptibility, exposure to the potential allergen and the ability to penetrate the epidermis and react with epidermal protein. We looked at corticosteroid binding to arginine and relative usage of corticosteroids to see if these variables explain the number of allergic reactions seen to these structurally similar chemicals. A linear relationship was found between a measure of corticosteroid binding to arginine, the log of relative corticosteroid usage and the log of the relative number of corticosteroid allergies. Using multiple regression this association was significant (P = 0.01). Statistically, these two variables accounted for 73% of the variation in the results. Our results showed that the number of corticosteroid allergic reactions was dependent on usage and the intrinsic ability of the corticosteroid to degrade and bind to arginine. While total corticosteroid usage is unlikely to change, the prescription of individual corticosteroids with a reduced potential to degrade and bind to protein, but with equal efficacy, might reduce the overall prevalence of corticosteroid hypersensitivity.

Prevention of poison ivy and poison oak allergic contact dermatitis by quaternium-18 bentonite

Background: Poison ivy and poison oak are the most common causes of allergic contact dermatitis in North America. Objective: We investigated whether a new topical lotion containing 5% quaternium-18 bentonite prevents experimentally induced poison ivy and poison oak allergic contact dermatitis. Methods: A single-blind, paired comparison, randomized, multicenter investigation was used to evaluate the effectiveness and safety of quaternium-18 bentonite lotion in preventing experimentally induced poison ivy and poison oak allergic contact dermatitis in susceptible volunteers. One hour before both forearms were patch tested with urushiol, the allergenic resin from poison ivy and poison oak, 5% quaternium-18 bentonite lotion was applied on one forearm. The test patches were removed after 4 hours and the sites interpreted for reaction 2, 5, and 8 days later. The difference in reactions between treated and untreated patch test sites was statistically analyzed. Results: Two hundred eleven subjects with a history of allergic contact dermatitis to poison ivy and poison oak were studied. One hundred forty-four subjects had positive reactions to urushiol. The test sites pretreated with quaternium-18 bentonite lotion had absent or significantly reduced reactions to the urushiol compared with untreated control sites ( p < 0.0001) on all test days. When it occurred, the reaction consistently appeared later on treated than on control sites ( p < 0.0001). One occurrence of mild, transient erythema at the application site was the only side effect from the quaternium-18 bentonite lotion. Conclusion: Quaternium-18 bentonite lotion was effective in preventing or diminishing experimentally produced poison ivy and poison oak allergic contact dermatitis.

Analysis of patients with allergic patch test reactions to a plastics and glues series

839 patients were patch tested with a series of 31 plastics and glues allergens at a dermatologic clinic over a period of 7 years. 52 (6%) had a positive patch test reaction to 1 or more such allergens. Clinic charts of 47 patients (out of 52) were available for the study. All but 3 patients had dermatitis on their hands: 17 had only hand dermatitis. 25 (53%) patients' test results were of present or past relevance to their skin diseases. 11 patients (68%) with occupational allergic contact dermatitis (ACD) and 14 (45%) with non-occupational dermatitis had relevant reactions. p-tertiary-butylphenol-formaldehyde resin was the most common allergen (9 cases). 7 patients reacted to diaminodiphenylmethane. 5 patients, who had colophony allergy, reacted to abietic acid and 4 to abitol. There was no reaction to 14 test substances. Special series, such as this plastics and glues series, reveal the cause of ACD less frequently than standard series. However, there is no other way to confirm allergy to these usually industrial allergens, which can also sensitize through non-occupational exposure during hobby working or through unpolymerized monomer left in the finished plastic product.

Screening allergens for acrylate dermatitis associated with artificial nails

Background: Acrylates are increasingly observed to be a cause of allergic contact dermatitis (ACD), especially in the cosmetic industry. Patients suspected of acrylate allergy are generally tested to 33 acrylates, and acrylate-allergic patients commonly react positively to many of these allergens. Objective: The objective of the study was to develop a short list of screening acrylates to diagnose acrylate allergy in patients wearing artificial nails. Methods: Twenty-three patients with ACD to acrylates were studied and their patch test reaction rates to 33 acrylates analyzed to identify the acrylates that were most frequently positive. Results: Based on the frequency with which each acrylate was positive in a group of 11 patients wearing artificial nails and the known use of specific acrylates in the nail industry, ethyl acrylate, 2-hydroxy ethyl acrylate, etylene glycol dimethacrylate, ethyl α cyanoacrylate, and triethylene glycol diacrylate were identified as screening acrylates. Conclusion: The pattern of acrylate cross-reactivity among the most frequently positive acrylates suggests that a functional group that is a “carboxy ethyl side group” may be requisite for ACD to acrylates.

Adhesion molecules in the nickel allergic reaction.

Nickel is the major cause of allergic contact dermatitis, and to increase our understanding of this immune reaction we studied changes in the expression of adhesion molecules on mononuclear cells during nickel stimulation in vivo and in vitro. Nickel-induced lymphocyte cultures were used in vitro, the cells being examined with monoclonal antibodies (Mabs) and by flow cytometry. Mononuclear cells from skin biopsies of in vivo cutaneous nickel reactions were studied with Mabs and immunohistochemistry. The expression of adhesion molecules in vitro was differential: the number of cells carrying CD11c, CD29, CDw49b, CDw49d, CDw49e, CDw49f, CD54, CD56 and ELAM-1 being significantly overrepresented among the nickel-induced lymphoblasts whereas the number of blasts carrying CD44 was underrepresented and those of CD11a, CD18, CD58 and LAM-1 remained unchanged. CD4+ cells gained adhesion molecules during nickel-induced blast transformation whereas CD8+ cells lost most of their adhesion molecules. The in vivo results were in agreement with the in vitro ones except that CDw49b, CDw49f, CD56 and ELAM-1 could not be detected in a 96-hour nickel reaction in vivo. In conclusion, the nickel allergic reaction favors the expression of certain adhesion molecules, and this expression is induced on CD4+ cells while CD8+ cells tend to lose such molecules. The changes were more sensitively detected with the in vitro method.

Clioquinol Inhibits Allergic Contact Dermatitis Due to Nickel

Nickel sensitivity is one of the most common causes of allergic contact dermatitis. It is seen mostly as a result of nickel-containing jewelry. While

Oral manifestations of gold allergy

Sensitization to gold in a large group of patients suspected of clinical allergy to this metal has not been reported. Two hundred patients with symptoms of persistent oral mucosal or cutaneous lesions that were possibly related to allergy to constituents of gold alloys or gold jewelry were patch tested to determine the frequency of sensitization. Patch testing was performed with the European standard series and a series of dental materials including three different salts of gold. A persistent papular reaction to gold-(tri)chloride was considered a positive reaction. In 17 patients (8.5%, all women, mean age 50.2 years) persistent papular patch test reactions to both 0.5% and 1.0% gold(tri)chloride were observed. In five of seven patients with oral lichen planus (OLP) and in one of six patients with the burning mouth syndrome, gold in the dentures was replaced. Particularly in patients with OLP, a significant but variable improvement was observed. In all cases in which gold was replaced and improvement occurred, the patients were sensitized to 0.5% gold(tri)chloride. One patient with allergic contact stomatitis and one patient with allergic contact dermatitis healed completely after gold had been replaced. Sensitization to gold should be considered as a possible cause of allergic contact dermatitis and allergic contact stomatitis as well as a pathogenic or triggering factor in OLP.

An arm immersion model of compromised skin (II). Influence on minimal eliciting patch test concentrations of nickel.

The transition metal nickel is a very common cause of allergic contact dermatitis (ACD). In the general population, adults with hand eczema have a high incidence of allergy to nickel, and nickel allergy is high in occupational dermatoses and is often linked to wet work. Nickel may be found as a trace contaminant in some consumer products, e.g., household cleaning agents. It has therefore been debated whether these levels, whilst not a primary cause, might be sufficient to maintain ACD. The minimal concentration of nickel in patch tests on normal skin that will elicit an allergic reaction in highly sensitised subjects is 1-10 ppm. This trial assessed whether reactivity to nickel was altered on compromised dorsal forearm skin and compared this to normal skin on the contralateral dorsal forearm and on the back. Skin damage consequent upon arm immersion in sodium dodecyl sulphate (SDS) greatly enhanced reactivity to nickel on the forearm, with the dorsal aspect reacting most both in number of reactions at each concentration and in the minimal eliciting concentration, which was 0.5 ppm in 2/20 under the conditions of a 48 h occluded patch.

Nickel hypersensitivity in the orthodontic patient

Nickel is one of the most common causes of allergic contact dermatitis and produces more allergic reactions than all other metals combined. Currently, several brands of orthodontic wires are made of nickel titanium alloy and potentially have a high enough nickel content to provoke manifestations of allergic reactions in the oral cavity. The objectives of this study were (1) to determine if standard orthodontic therapy can sensitize patients to nickel, and (2) to assess gingival response to nickel-containing orthodontic appliances in patients who are nickel sensitive before treatment. Nickel sensitivity patch tests were conducted to confirm hypersensitivity to nickel. Twenty-nine patients from the Division of Orthodontics, Albert Einstein/Montefiore Medical Center were tested, ranging in age from 12 to 48 years. Of the 29 patients, there were 18 female and 11 males. Five of the patients had a positive nickel patch test, a rate of 18.5%. The five patients that tested positive were all female, meaning that the overall rate for females was 27.7% (5:18). The five female patients sensitive to nickel were followed monthly by intraoral photos and gingival and plaque index scores. The remaining patients began routine orthodontic therapy and were retested 3 months into treatment to see whether sensitization occurred. Two patients converted from an initial negative patch test to a positive test. There may be a risk of sensitizing patients to nickel with long-term exposure to nickel-containing appliances as occurs in routine orthodontic therapy.