Platinum Salt Asthma

Abstract

Platinum salt allergies have been almost exclusively restricted to workers in platinum refineries in the past. A more recent source of platinum salt exposure is the increasing number of catalyst factories. There has been some concern about allergic diseases in the general population due the increasing use of platinum catalysts in cars to reduce air pollution. However, there have been no convincing data to prove this assumption. Allergic reactions to metallic platinum (e.g., jewellery) are unknown. Subjects exposed to platinum salts develop symptoms of an immediate type allergy, including rhinitis, conjunctivitis, and/or asthma, often associated with dermatitis/urticaria, varying between 15 days and several years after exposure. The sensitization index (i.e., the rate of subjects with symptoms) may exceed 50%. The high prevalence of respiratory symptoms in platinum refineries demands preventive measures. The legal concentration limits do not prevent an unacceptable rate of asthma cases. Medical history is unequivocal in most cases. To confirm the anamnestic data, skin prick tests, which are a simple and reliable tool, may be performed. Stepwise testing from an initial dilution of 10-8 M (PtCl6)2- is employed in order to avoid anaphylactic side effects. Bronchial provocation tests with platinum salts may cause severe side effects by overdose of the agent. An initial dilution until 10-10 M (PtCl6)2- may be necessary. The reactions may be of the immediate or dual type. The sensitivity of bronchial provocation tests is higher than that of skin prick tests. They are specific; atopic or normal controls do not react to platinum salt inhalation. The immune mechanism is not yet fully understood. It is postulated that platinum salts act as haptens by changing the molecular structures of certain human proteins, rendering them im-munogens or allergens, and also by changing nonimmunogenic surface structures of cell membranes into allergenic epitopes. The excessive allergen-inducing activity of (PtCl6)2- might be due to the reaction with free carbonyl or amino groups and/or particularly with sulphhydryl or methionine side chains. The “immunogenic” activity of platinum salts is related to the number of chlorine ligands of the compounds. An allergic mechanism is suggested by a number of observations: (a) latency between first exposure and first symptoms, (b) no reactions in a proportion of exposed subjects, (c) reactions to minimum amounts of (PtCl6)2- after “sensitization”, (d) experimentally induced sensitization in monkeys, (e) specific skin test in exposed symptomatic subjects. Passive transfer of skin test reactivity from “sensitized” subject to primates and nontoxic histamine release from basophils was demonstrated by several groups including our own. Several investigators demonstrated higher “platinum salt-specific” IgE by modified RAST in exposed asthmatic subjects compared with exposed healthy subjects or nonexposed controls. However, in vitro techniques are of a relatively poor specificity; results can be correlated to total IgE concentrations.