Controversies in Allergy

This paper is one of a prospective series dealing with controversies in allergy. Publication of this and subsequent papers in the series should not be regarded as an endorsement of content by the editors of Immunology & Allergy Practice or by the American Association for Clinical Immunology and Allergy.

Chemical Sensitivity and the Environment

William J. Rea, MDCDirector, Environmental Control Unit, Carrollton Community Hospital, and Clinical Associate Professor of Thoracic Surgery, Southwestern Medical School, University of Texas Health Science Center, Dallas Monte J. Mitchell, BACDoctoral candidate in Clinical Psychology, University of Texas Health Science Center, Dallas.

This study is supported by grants from the Human Ecology Research Foundation of the Southwest and the Hillcrest Foundation.

Source: Immunology & Allergy Practice, Sept/Oct 1982, pp. 157-167


The rapidaly accelerating rate of growth of modern technology has been accompanied by a proliferation of chemical entities that supports the view that ours is a chemical environment. Whether isolated from natural products or synthesized for commercial usage, the ubiquitous nature of the chemical agent is widely appreciated; it has been estimated that as many as 2,000 new compounds are introduced annually. The growing realization of the widespread presence of hazardous chemicals in our environment has rendered critical the problem of chemical susceptibility originally described by Randolph almost 30 years ago.1 While celebrated instances of gross contamination through industrial waste have long been the object of professional attention, it is only recently that literally thousands of chemical products heretofore believed innocuous have been incriminated as agents of homeostatic dysfunction . With the discovery that the chemical incitant may trigger a maladaption response in virtually any of the four smooth muscle systems (cardiovasacular, respiratory, gastrointestinal, genitourinary) or the skin, has come the realization of the gravity of chemical sensitivity.2 Moreover, current reserach identifies disease onset with incitant sensitization and not with the end stage process, as has been done previously. Over the past three years, some 700 reports have isolated instances of chemical sensitivity to commonly encountered environmental incitants. An attempt will be made in the discussion which follows to present the problem of chemical susceptibility as it is encountered in three major components of our environmentCair, food, and water.

In the past two years, hundreds of reports have testified to the dangers of chemical agents, and the problems in isolating these incitants. This matter is complicated by the fact that sensitivity to one chemical often triggers a host of other sensitivities to both chemicals and foods. As Zschunke3 observes, the rate of technological growth has greatly complicated the already difficult job of tracing environmental chemical incitants. Nevertheless, countless reports continue to emerge which affirm previous findings and define an increasing number of new sensitivities to chemical agents long considered harmless.

Current data affirm the view that conventional methods for the isolation of chemical incitants may no longer be effective. With the findings that sensitivities occur in association with subthreshold and picomolar quantities of chemical agents,4 has come the discovery that standard procedures such as skin tests often fail to demonstrate positive reactions which are clinically verifiable.5

Recent literature verifies previous findings regarding the harmful effects of certain chemical incitants, such as formaldehyde,6 phenol,7 chlorine, and petroleum alcohol.8 Commonly encountered chemicals such as glycine,9 chlorphenothane, toluene and turpentine,10 have been associated with the triggering of a plethora of vascular alterations, and some chemicals, such as hydralazine have been found to induce advanced-stage disease processes.11

The growing awareness of the significant chemical contamination of our air and water supplies is illustrated by the increasing body of research which has attempted to isolate environmental incitants. Water contaminants have been shown to trigger vascular alterations,12 while air pollutants such as suspended particulates, formaldehyde, and ozone have been associated with dysfunctions ranging from mild respiratory distress to severe central nervous system disorders.13

A number of familiar metals have been incriminated, among them nickel, cobalt, chromium,14, aluminum,15 mercury,16 and platinum.17 Other common environmental chemical incitants include xylene,18 various acylates,19 and acrylated prepolymers,20 benzoyl peroxide, carbon tetrachloride,21 sulfates,22 dithiocarbamates,23 and isocyanates.24

While the list of potential chemical incitants is far too extensive to explore in detail, an attempt will be made to elucidate the hazards present for the chemically sensitive individual in a variety of circumstances.

Chemcial Contamination in Foods The widespread contamination of our urban water and food supplies is witnessed by the increasing use of food additives, preservatives, and dyes in the manufacturing and processing of commercially available food products. Recent research has made it increasingly apparent that many chemicals in products which we consume must be viewed as incitants capable of triggering a wide variety of disease processes.

The literature on the dangerous effects of alcohol and tobacco has long been well documented and accepted. Nevertheless, research continues to elucidate the role played by both substances in the mediation of an ever-increasing number of symptoms. Gong25 presents evidence of ethanol-induced bronchospasm, and reports of chemical sensitivity to tobacco glycoproteins,26 of tobacco dermatitis,27 and of tobacco-induced Raynaud=s phenomenon28 are not uncommon.

The literature abounds with reports of chemical sensitivities29,30 to many food and water contaminants in the form of additives. The notion of food allergy has become immensely complicated with the discovery of food-contaminant sensitivity, forcing researchers to define more clearly the nature of the incitant, not only as it is encountered in foods, but in the air and water as well. Bell31 has reported urticarial reactions and immunological changes as a function of exposure to a number of food additives. Condemi32 and Bell both suggest that food dyes may trigger reactions in sensitive individuals; such reactions may even include psychiatric conditions commonly though to be psychogenic, such as certain forms of hyperactivity. Lindemayer33 has presented data which associate urticarial reactions with several additives, such as p-hydroxybenzoic acid methylester, p-hydroxybenzoic acid propylester, benzoic acid, sodium benzoate, ponceau rouge, and indigo carmine. Monroe=s34 data indicate a causal role played by tartrazine azo dyes and salicylates in the provocation of vascular alterations. Other additives, including sodium nitrite and sodium glutamate, have been found to trigger migraine phenomena in susceptible patients.35

The ability of food preservatives such as sulfur dioxide and sodium salicylate to provoke asthmatic reactions continues to receive documentation36,37 and some data incriminate aspirin additives and aspirin-like food contaminants and dyes in the triggering of symptoms ranging from urticaria and angioedema to bronchoconstriction and purpura.38 An even wider variety of symptoms, including severe gastrointestinal disorders, has been associated with sensitivities to aniline, commonly found in rapeseed oil.39

Current research is expanding awareness of the role of chemical incitants in mediating what have long been considered food allergies. Data reported by Bell suggest that the study of chemicals which are the digestive by-products of common foods such as wheat and milk may provide a greater understanding of this interface between food and chemical sensitivities.

Chemical Incitants in the Home Environment Recent attention focused on the analysis of indoor air pollution has led to the discovery of a multitude of sensitivities to chemicals confronted in the home environment. Over the past few years articles of personal hygiene, clothing, furnishings, and countless commonly used household products have been incriminated as triggering agents of homeostatic dysfunction.

Time and space limitations allow only a cursory review of the numerous hygienic products which have been revealed as noxious for the chemically susceptible individual. Among these are a wide variety of cosmetics,40,41 particularly those containing glycerin, propylene, glycol, or butylene glycol,42 perfumes,43,44 and hair products such as dyes,45,46 creams,47 sprays,48 and shampoos.49 Moreover, sensitivities have been demonstrated to occur in association with lip salve,50 fingernail preparations,51 soaps,52 sanitary napkins,53 mouthwash,54 antiperspirants,55 contact lenses,56 contact lens solutions,57 and suntan lotions.58

Reports of sensitivities to textiles and to those chemicals used in the processing of clothing continue to apear. ElSaad59 reports sensitivities to synthetic acrylic fibers, and Burrows= data indicate the existence of contact dermatitis secondary to polyester spin finishes.60 Recently, the epoxy resins used in manufacturing many trousers have been isolated as triggering agents, and reports on synthetic clothing as environmental antigens are widespread.61 Products such as spray starch used in the maintenance of fabrics may also be considered toxic for the chemically sensitive individual,62 for whom, as Larsen=s interesting study suggests, even the metallic buttons on blue jeans may trigger reactions to nickel.63

Many household cleaning products, particularly those containing formaldehyde, have been shown to be hazardous for many. Several laundry products and detergents may be identified as household incitants,64 as well as a number of products used to clean and polish furniture.65

It is increasingly apparent that the very construction of many homes may prove dangerous for the chemically sensitive patient. A considerable amount of data suggests that chemicals contained in wood preservatives are environmental incitants capable of triggering a variety of symptoms.66-68 Frigas69 has reported asthma secondary to household insulation containing urea formaldehyde foam, and scattered reports suggest that petrochemical contaminants in construction products such as plaster70 and cement71 may also trigger chemically induced reactions.

Other products commonly encountered in the home have been identified as environmental incitants. Current data support earlier findings regarding the hazards of pesticides72 such as 2,4 DNP and fungicides.73 Moreover, research increasingly suggests the possibility of sensitivities to apparently innocuous items such as rubber bands,74 coins,75 epoxy,76 and countless paper products.77,78

The current emphasis on indoor air pollution has sparked research on other apparently benign features of the home environment. Thus, numerous house plants,79,80 and common insects81 are now viewed as environmental incitants of homeostatic dysfunction. In addition, sensitivities to cold and heat,82 and to contaminants in household water supplies have been associated with symptoms ranging from urticaria to severe respiratory distress. It is now clear that, in the face of increasing amounts of data which point to previously unsuspected household incitants, a more cautious attitude should be adopted regarding the issue of environmental safety in the home.

Chemical Incitants in the Occupational Environment For years, the hazards of occupational exposure to chemicals have been studied by researchers from various fields; however, until recently, attention has been focused primarily on a small number of extremely dangerous products encountered in work places generally acknowledged to be hazardous. In the past few years, however, research has exposed the dangers inherent in an ever-widening circle of work environments including numerous settings commonly thought to be safe. Many workers= symptoms are improved during evening hours and weekends,83 hence the conviction that heretofore Asafe@ occupations must be re-evaluated for their potential hazards. The manufacturing industry is replete with examples of chemical contamination. Car factory workers exposed to polyurethane foam have been shown to be at significant risk,84 and this industry is loaded with chemicals capable of triggering sensitivities, such as chrome, rubber, nickel and isocyanates in spray paints.85-86 Numerous other industries, including electronics,87 textiles,88 and food processing89 burgeon with incitants which threaten the susceptible individual.

But dangers are not confined to the metropolitan industrial setting; recent reports suggest that occupationally-related respiratory diseases are common among grain elevator workers90 and farm workers who evidence symptoms ranging from rhinitis to asthma.91

A number of familiar trades have come to be associated with chemical risks in recent years, among them carpentry92 (in which contact sensitivities to woods are reported widely), painting, identified with severe respiratory symptoms,93 and bricklaying, where sensitivities to chemicals such as cobal are now extensively described.94

There are increasing reports of chemically induced reactions among beauticians,95 and researchers have now incriminated a vast number of chemicals to which such workers are exposed on a daily basis, among them nickel sulfate, pellidol, and cobal chloride.96 Bakery work has come to be identified with risks in the form of chromium exposure through contact with a chromium compound in flour,97 as well as exposure to gas from the ovens; photographers and those responsible for developing photographs now appear at high risk for chemically induced respiratory disease,98 as well as cerebral and vascular dysfunction.

The list of occupations in which exposures to potentially hazardous chemicals may occur seems endless. It is now clear that physicians, laboratory technicians,99 nurses100 and others in direct contact with numerous drugs and chemicals face potential dangers. What is remarkable, however, is the extent to which seemingly safe occupations are fraught with risks; witness Fisher=s101 report of a chemically-triggered reaction in a concert violinist caused by contact with his rosin.

It would, of course, be impossible to discuss here all of the chemical agents encountered in the occupational environment to which reactions have been observed; the spectrum of incitants ranges from organic chemicals102 and inhalants103 to natural dyes104 and synthetic compounds.105 Symptoms have been found to be provoked by natural metals such as zinc and cobalt,106 as well as industrial chemicals, among them chloramine,107 formalin,108 paraformaldehyde, zylene,109 and the persulfates.110 Moreover, an array of reactions has been reported in association with common industrial agents such as the diisocyanates111 and toluenes.112 It is of critical importance to consider the chemicals confronted in occupational products which are apparently benign: recent reports have isolated chemical contaminants in cement,113 printing paper,114 and even latex surgical gloves.115

The spectrum of disease processes secondary to occupational incitant exposure is a broad one. Over the past three years, some 60 reports have associated dermatitis with chemical sensitivity in the work environment. It has been observed that occupational dermatitis may range from mild discomfort to permanent incapacity; such reactions have been found in association with a multitude of occupations: physician, dentist,116 medical technician,117 metalworker,118 musician,119 florist,120 caterer,121 office worker,122 and retail salesperson.123 Against the backdrop of present research it seems clear that a virtually infinite number of occupational milieus contain dangers for the susceptible patient. Data clearly reveal the necessity of environmental control for the evaluation and treatment of such occupational sensitivities.

Other disease processes that may assume the dimensions of an occupational illness include erythema and vesiculation,124 thrombocytopenic purpura,125 Raynaud=s phenomenon,126 and coronary artery spasm.127 A number of environmentally-triggered respiratory symptoms have been noted, among them bronchoconstriction,128 airway obstruction,129 pneumonitis,130 dyspnea,131 alveolitis,132 and asthma.133 Recent data also suggest that CNS dysfunctions, including depression, fatigue, and sleep disturbances,134 and even some forms of carcinoma135 may exist secondary to occupational chemical exposure.

Chemical Hazards in Drugs and Medical Procedures Current data are replete with reports of sensitivities to the chemicals contained in a multitude of drugs. The histamine-releasing properties of numerous drugs used in anesthesia and surgery have been known for some time, but only recently have marked sensitvities been shown to a rapidly increasing number of medications, among them neomycin, ethylenediamine, benzocaine,136 betanol,137 alpha-methyldopa,138 potassium iodide139 and succinylcholine.140 Such sensitivities assume a multitude of forms, ranging from dermatitis and edema to asthma.

Of all commonly used medications, aspirin has, more than any other in recent years, been associated with a wide variety of homeostatic reactions. Among the chemically induced reactions to aspirin are asthma,141,142 chronic rhinitis,143 urticaria,144 angioedema,145 and angina.146 Anderson reports sensitivities to a number of common drugs used topically,147 and data burgeon with reports of dermatitis secondary to commonly used health aids, such as medicated bandages148 and hearing aids.149

Numerous reports over the past two years have described the causal roles played by drugs in the mediation of migraine phenomena. Oral contraceptives,150 vasoconstrictors,151 and a host of monoamines and opiates152 have been incriminated. Purpura and petechiae have been demonstrated to occur secondary to exposures to anticoagulants153 and vaccines,154 while urticaria and advanced stage vascular alterations have been associated with many drugs, among them antibiotics, sedatives, tranquilizers, laxatives, diuretics,155 cancer therapeutic drugs,156 and hallucinogens.157 The role of oral contraceptives in provoking venous thromboembolism has been known for sometime. Recently, cloxacillin,158 diazepam, penicillamine,159 nitroprusside and dopamine160 have been shown to exhibit phlebitogenic properties. Coronary artery spasm may be provoked by epinephrine, methacholine and imipramine,161 and Raynaud=s phenomeon may exist secondary to chemicals contained in vinblastine, bleomycine,162 and sulphasalazine,163 among others.

A number of medical and surgical procedures have now been associated with chemically triggered reactions. Nickel sensitivity has been reported secondary to the use of skin clips,164 and hemodialysis has been associated with necrotizing dermatitis, a function of exposure to the epoxy resin in the needles,165 and to the polyvinyl-chloride tubing.166 Countless dental procedures have also come to be identified as triggering agents of chemical sensitivites.167,168 Procedures involving implants169,170 and prostheses appear riddled with difficulties for the chemically sensitive individual; metal sensitivities are widely reported and are incriminated in the failure of joint prostheses.171

This paper attempts to present the implications of environmental contamination for the chemically susceptible individual. It is hoped that this review will lead to a fuller comprehension of the potential hzatards represented by the ever increasing number of chemical entities in our environment; the need for environmental control becomes apparent as this comprehension is broadened. The clinician=s use, both in the office and in the hospital, of a controlled environment in which to diagnose and treat susceptible patients greatly simplifies the process of isolating the incitant. Modern technology has afforded the practitioner access to procedures such as mass spectrometry and gas chromatography which greatly facilitate the process of assessing environmental contamination. The efficacy of such control is illustrated in the operation of an environmental control unit within the hospital. Such a facility promotes symptom clearance by allowing patients to avoid contact with virtually all incitants. Rooms in the unit are constructed of inert materials, and chemically less contaminated foods, purified air, and purified waters are constantly monitored to insure their relative freedom from chemical contaminants.

By establishing such a control, the clinician affords himself a baseline in relation to which reactions to environmental incitants may be judged; chemical challenge under such conditions allows the establishment of a cause-effect relationship between incitant and homeostatic response. The elegance of environmental control lies in the fact that the diagnostic procedures which develop out of it also serve as treatment strategies. Avoidance of the incitant and the construction of a chemically safe home environment represent the primary intervention procedures which are critical to the treatment of chemical sensitivity.

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92. Conde-Salazar L, Garcia Diez A, Rafeensperger F, Hausen BM: Contact allergy to the Brazilian rosewood substitute Machaerium scleroxylon Tul. (Pao ferro). Contact Dermatitis 6(4):246-50, June 1980.

93. Clarke CW, Aldons PM: Isophorone diisocyanate induced respiratory disease (IPDI). Aust NZ J Med 11(3):290-2, June 1981.

94. Camarasa JG, Alomar A: Photosensitization to cobalt in a bricklayer. Contact Dermatitis 7(3):154-5, May 1981.

95. Kuhl M: Nickel allergy among beauticians. Zentralbl Arbeitsmed Arbeitsschutz Prophyl 29(6):159-60, June 1979.

96. Landthaler M, Burg G, Zirbs S: Dye and nickel allergy in the hairdressing salon. Hautarzt 32(6):281-4, June 1981.

97. Heine A, Fox G: Baker=s eczema through chromium compound in flour. Derm Beruf Umwelt 28(4):113-5, 1980.

98. Lam S, Chan-Yeung M: Ethylenediamine-induced asthma. Am Rev Respir Dis 121(1):151-5, Jan 1980.

99. Lindemayr H, Jager S: Occupational immediate type allergy to hemp pollen and hashish. Derm Beruf Umwelt 28(1):17-9, 1980.

100. Machado L, Zetterstrom O, Fagerberg E: Occupational allergy in nurses to a bulk laxative. Allergy 34(1):51-5, Feb 1979.

101. Fisher AA: Allergic contact dermatitis in a violinist. The role of abietic acidCa sensitizer in rosin (colophony)Cas the causative agent. Cutis 27(5):466,468,473, May 1981.

102. From the NIH: Occupational asthma from a low-molecular-weight organic chemical. JAMA 244(15):1667-8, Oct 10, 1980.

103. Cordasco EM, Lira R, Demeter S, Wagner W: Industrial technology includes hazardous inhalants. Occup Health Saf 49(2):42-4, Feb. 1980.

104. Burge PS, O=Brien IM, Harries MG, Pepys J: Occupational asthma due to inhaled carmine. Clin Allergy 9(2):185-9, Mar 1979.

105. Burge PS, O=Brien IM, Harries MG: Peak flow rate records in the diagnosis of occupational asthma due to isocyanates. Thorax 34(3):317-23, June 1979.

106. Roto P: Asthma, symptoms of chronic bronchitis, and ventilatory capacity among cobalt and zinc production workers. Scand J Work Environ Health 6 Suppl 1:1-49, 1980.

107. Bourne MS, Flindt ML, Walker JM: Asthma due to industrial use of chloramine. Br Med J 2 (6181):10-2 July 7, 1979.

108. Baur X, Fruhmann G: Bronchial asthma of allergic or irritative origin as an occupational disease. Prax Klin Pneumol 33 Suppl 1:317-22, Apr 1979.

109. Cockcroft DW, Cartier A, Jones G, Tarlo SM, Dolovich J, Hargreave FE: Asthma caused by occupational exposure to a furan-based binder system. J Allergy Clin Immunol 66(6):458-63, Dec 1980.

110. Fruhamann G: Occupational asthma. New findings on work related obstructive respiratory diseases. MMW 123(8):299-303, Feb 20, 1981.

111. Lubach D: Diseases caused by diisocyanates. 2. Diisocyanate asthma. Derm Beruf Umwelt 27 (1):5-10, 1979.

112. Butcher BT, Karr RM, O=Neil CE, Wilson MR, Dharmarajan V, Salvaggio JE, Weill H: Inhalation challenge and pharmacologic studies of toluene diisocyante (TDI)-sensitive workers. J Allergy Clin Immunol 64(2):146-52, Aug 1979.

113. Czarnecki N: The persistence of chromate allergy in cement eczema. Hautarzt 30(2):80-3, Feb 1979.

114. Nurse DS: Sensitivity to thiourea in plan printing paper. Contact Dermatitis 6(1):153-4, Jan 1980.

115. Forsterom L: Contact urticaria from latex surgical gloves. Contact Dermatitis 6(1):33-4, Jan 1980.

116. Warin AP: Radiodermatitis of the hands in a dental practitioner. Clin Exp Dermatol 4(1):129-32, Mar 1979.

117. Rudzki E: Occupational dermatitis among health service workers. Derm Beruf Umwelt 27(4):112-5, 1979.

118. Rycroft RJ: Bacteria and soluble oil dermatitis. Contact Dermatitis 6(1):7-9, Jan 1980. 119. Tennstedt D, Cromphaut P, Dooms-Goossens A, Lachapelle JM: Dermatoses of the neck affecting violin and viola players (Afiddlers= neck,@ and contact dermatitis). Derm Beruf Umwelt 27(6):165-9, 1979. 120. Van Grutten M: Carnation dermatitis in a flower seller. Contact Dermatitis 6(4):289, June 1980 121. Hjorth N: Occupational dermatitis in the catering industry. Br J Dermatol 105 Suppl 21:37-40, Sept 1981.

122. Calnan CD: Carbon and carbonless copy paper. Acta Derm Venereol (Suppl) (Stockh) 59(85):27-32, 1979.

123. Pedersen NB: Occupational hand eczema from formaldehdye in price labels. Contact Dermatitis 6(1):57-8, Jan. 1980.

124. De Koning GA, Notowicz A, Stolz E: Phototoxic reactions to 8-methoxypsoralen as occupational dermatosis. Hautarzt 30(1):27-9, Jan 1979.

125. Nishioka K, Sarashi C, Katayama I: Chronic pigmented pupura induced by chemical substances. Clin Exp Dermatol 5:213-18, 1980.

126. Lelbach Wk, Marsteller HJ: Vinyl chloride associated disease. Ergeb Inn Med Kinderheilkd 47:1-110, 1981.

127. Pichard AD, Ambrose J, Mindich B, Midwall J, Gorlin R, Litwak RS, Herman MV: Coronary artery spasm and perioperative cardiac arrest. J Thorac Cardiovasc Surg 80:249-254, 1980.

128. Jones RN, Butcher BT, Hammad YY, Diem JE, Glindmeyer HW 3d, Lehrer SB, Hughes JM, Weill H: Interaction of atopy and exposure to cotton dust in the bronchoconstrictor response. Br J Ind Med 37(2):141-6, May 1980.

129. Fuchs E: Obstructive diseases of the respiratory tract caused by industrial allergens. Prax Klin Pneumol 33(11):1089-100, Nov 1979.

130. Evans WV, Seaton A: Hypersensitivity pneumonitis in a technician using Pauli=s reagent. Thorax 34(6):767-70, Dec 1979.

131. Novey HS, Keenan WJ, Fairshter RD, Wells ID, Wilson AF, Culver BD: Pulmonary disease in workers exposed to papain: Clinico-physiological and immunological studies. Clin Allergy 10(6):721-31, Nov 1980.

132. Belin L: Sawmill work and extrinsic allergic alveolitis. Scand J Work Environ Health 6(3):230-1, Sept 1980.

133. Butler J, Culver BH, Robertson HT: Meat wrappers= asthma. Chest 80 (1 Suppl):71-3, July 1980. 134. Bell I, King D: Psychological and physiological research relevant to clinical ecology: An overview of the recent literature. Archives of Clinical Ecology 1:15-25, Spring 1982.

135. Hartmann A, Schlegel H: Health hazards caused by wood in Switzerland. Schweiz Med Wochenschn 110(8):278-81, Feb 23, 1980.

136. Prystowsky SD, Allen AM, Smith RW, Nonomura JH, Odom RB, Akers WA: Allergic contact hypersensitivity to nickel, neomycin, ethylenediamine, and benzocaine. Relationships between age, sex, history of exposure, and reactivity to standard patch tests and use tests in a general population. Arch Dermatol 115:959-962, 1979.

137. Nater JP, Grosfeld JC: Allergic contact dermatits from Betanal (phenmedipham). Contact Dermatitis 5(1):59-60, Jan 1979.

138. Harries MG, Taylor AN, Wooden J, McAusland A: Bronchial asthma due to alpha-methyldopa. Br Med J 1(6176):1461, June 2, 1979.

139. Huang TY, Peterson GH: Pulmonary edema and iododerma induced by potassium iodide in the treatment of asthma. Ann Allergy 46(5):264-6, May 1981.

140. Morrow, JG 3d: Allergy to succinylcholine. Anesth Analg (Cleve) 60(6):456-7, June 1981. 141. Szmidt M, Grzelewska-Rzymowska I, Rozniecki J, Kowalski ML, Rychlicka I: Histaminemia after aspirin challenge in aspirin-sensitive asthmatics. Agents Actions 11(102):105-7, Apr 1981.

142. Chand N, Altura BM: Lipoxygenase pathway and hydroperoxy acids: Possible relevance to aspirin-induced asthma and hyperirritability of airways in asthmatics. Prostaglandins Med 6(2):249-56, Feb 1981.

143. Settipane GA: Aspirin intolerance presenting as chronic rhinitis. RI Med J 63(3):63-5, Mar 1980. 144. Settipane RA, Constantine HP, Settipane GA: Aspirin intolerance and recurrent urticaria in normal adults and children. Epidemiology and review. Allergy 35(2):149-54, Mar 1980.

145. Szczeklik A, Czerniawska-Mysik G, Serwonska M, Kuklinski P: Inhibition by ketotifen of idiosyncratic reactions to aspirin. Allergy 35(5):421-4, July 1980.

146. Miwa K, Kambara H, Kawai C: Exercise-induced angina provoked by aspirin administration in patients with variant angina. Am J Cardiol 47(6):1210-4, July 1980.

147. Andersen KE, Maibach HI: Allergic reaction to drugs used topically. Clin Toxicol 16(4):415-65, 1980. 148. Fisher AA: Paraben dermatitis due to a new medicated bandage: The Aparaben paradox.@ Contact Dermatitis 5(4):273-4, July 1979. 149. Dahl MV, Jordan WP Jr: Hearing aid dermatitis. Arch Dermatol 115(6):676, June 1979. 150. Mazal S: Migraine attacks and increased platelet aggregability induced by oral contraceptives. Aust NZJ Med 8(6):646-8, Dec 1978.

151. Johnson ES: A basis for migraine therapyCthe automatic theory reappraised. Postgrad Med J 54(630):231-43, Apr 1978.

152. Sicuteri F, Fanciullacci M, Michelacci S: Decentralization supersensitivity in headache and central panalgesia. Res Clin Stud Headache 6:19-33, 1978.

153. Stavorovsky M, Lichtenstein D, Nissim F: Skin petechiae and ecchymoses (vasculitis) due to anticoagulant therapy. Dermatologica 158(6):451-61, 1979.

154. Kiefaber RW: Letters to the Editor. N Engl J Med 305(4):225, July 1981. 155. Monroe EW, Schulz CI, Maize JC, Jordon RE: Vasculitis in chronic urticaria: An immunopathologic study. J Invest Dermatol 76(2):103-7, Feb 1981.

156. Ignoffo RJ, Friedman MA: Therapy of local toxicities caused by extravasation of cancer chemotherapeutic drugs. Cancer Treatment Review 7:17-27, 1980.

157. Heazlewood VJ, Bochner F, Craswell PW: Hallucinogenic drug induced vasculitis. Med J Aust 1(7):359-60, Apr 4, 1981.

158. Svedhem A, Alestis K, Jertborn M: Phlebitis induced by parenteral treatment with flucloxacillin and cloxacillin: A double-blind study. Antimicrob Agents Chemother 18(2):349-52, Aug 1980.

159. Brandstetter RD: Exacerbation of diazepam-induced phlebitis by oral penicillamine. Br Med J 283(6290):525, Aug 1981.

160. Hunter AR: Letters to the Editor, Phlebitis vs cutaneous vasodilation. Anesthesiology 52(2):188, Feb 1980.

161. Heupler FA Jr: Syndrome of symptomatic coronary arterial spasm with nearly normal coronary arteriograms. Am J Cardiol 45:873-81, Apr 1980.

162. Harvey HA, Lipton A, Lawrence BV: Raynaud=s phenomenon with vinblastine and bleomycin. Ann Intern Med 94(4 pt 1):542-3, Apr 1981.

163. Reid H, Holt S, Housley E, Sneddon DR: Raynaud=s phenomenon induced by sulphasalazine. Postgrad Med 56(652):106-7, Feb 1980.

164. Nurse DD: Nickel sensitivity induced by skin cliips. Contact Dermatitis 6(7):497, Dec 1980. 165. Brandao FM, Pinto J: Allergic contact dermatitis to epoxy resin in hemodialysis needles. Contact Dermatitis 6(3):218-9, Apr 1980.

166. Bommer J, Ritz E, Andrassy K: Necrotizing dermatitis resulting from hemodialysis with polyvinylchloride tubing. Ann Intern Med 91(6):869-70, Dec 1979.

167. Holland Moritz R, Rimpler M, Rudolph PO: Allergy to gold in the oral cavity? Dtsch Zahnaerztl Z 35(10):963-7, 1980.

168. Gill C, Michaelides PD: Dental drugs anaphylactic reactions. Report of a case. Oral Surg 50(1):30-2, July 1980.

169. Kubba R, Taylor JS, Marks KE: Cutaneous complications of orthopedic implants, A two year prospective study. Arch Dermatol 117(9):554-60, Sept 1981.

170. Crimalt F, Romaguera C: Acute nickel dermatitis from a metal implant. Contact Dermatitis 6(6):441, Oct 1980.

171. Christiansen K, Homes K, Zxilko PJ: Metal sensitivity causing loosened joint prostheses. Ann Rheum Dis 39(5):476, Oct 1980.


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