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A cross-sectional medical evaluation was conducted to determine respiratory and dermatological effects of platinum salts sensitization among workers in a secondary refinery of precious metals. Fifteen of 107 current employees and eight (28%) of 29 former employees, who had been terminated from employment on average for 5 years because of respiratory symptoms, had positive skin reactivity to platinum salts. Platinum salts skin reactivity was significantly associated with average air concentrations of platinum salts in employees' present work area. Workers with positive platinum salts skin tests had significantly higher prevalences of reported rhinitis, asthma, and dermatitis than negative skin test workers. They also had increased bronchial response to cold air challenge and elevated levels of total serum IgE. Platinum salts sensitization was not associated with atopic tendency as measured by sensitivity to common aeroallergens, but was strongly associated with cigarette smoking status. The findings indicate that cigarette smoking may be a risk factor for the development of platinum salts allergy. The persistence of platinum salts sensitization and high prevalence of adverse health outcomes among former workers demonstrate the importance of regular medical monitoring so that sensitized workers can be removed from exposure before they develop long-term health problems.

Occupational asthma is reversible airways obstruction induced by inhaled dusts, vapors, fumes, and gases encountered in the workplace, and should be distinguished from preexisting asthma that is exacerbated by exposure to industrial irritants. There is usually a latent or “sensitizing” period-sometimes years-before the disease develops. Bronchoprovocation studies have demonstrated that occupational asthma may manifest as an immediate (usually occurring within minutes of exposure), late (beginning hours after exposure) or dual response.’ Late responses may demonstrate a circadian rhythm, lasting for weeks after initial exposure.* Overall prevalence of occupational asthma is difficult to determine. A confounding factor in the attempt to determine prevalence is that, in many instances, there may be “self-selection” by workers who leave the industry once they become affected.3 Surveys suggest that 2% to 6% of the general adult population have asthma: it is estimated that 2% to 15% of this asthma may be of occupational origin.4 This figure varies widely depending on the country, the particular industry, and the type of agent to which workers are exposed.

Acid anhydride compounds are reactive chemicals that have been previously associated with immunoglobulin E (IgE) mediated occupational asthma. Twenty workers with exposure to himic anhydride powder used for the manufacture of a synthetic flame retardant were questioned about respiratory symptoms. The study was initiated after one individual from the plant developed asthma. A test for serum-specific IgE to human serum albumin conjugates of himic anhydride, phthalic anhydride, hexahydrophthalic anhydride and trimellitic anhydride was performed for seven workers with respiratory symptoms associated with himic anhydride exposure. Three of the seven symptomatic workers who reported wheezing at work exhibited elevated specific IgE to two or more acid anhydride-human serum albumin conjugates. Radioallergosorbent inhibition studies performed with sera containing high levels of himic anhydride-human serum albumin specific IgE from a symptomatic worker demonstrated cross-allergenicity between himic anhydride-human serum albumin and hexahydrophthalic anhydride-human serum albumin allergenic determinants. This study demonstrated that himic anhydride can elicit IgE-mediated sensitization in the workplace.

Possible immunoreactivity to chemically well-characterized mono- and diisocyanate protein conjugates was reevaluated in 15 workers with TDI asthma and 17 normal (nonexposed) volunteers. Lymphocytes of nine sensitive workers were incubated with TDI human serum albumin (HSA) conjugates. Leucocyte inhibitory factor (LIF) was produced. Leucocyte inhibitory factor was also induced by hexamethylene diisocyanate (HDI) protein conjugates in four of these workers who had no prior history of exposure to HDI. Disappearance of TDI- and HDI-induced LIF was noted in several sensitive workers who were removed from further TDI exposure. Three LIF-positive workers also demonstrated positive intracutaneous reactivity to TDI-HSA. One workers had a markedly positive RAST (25.5% binding) to a monofunctional (p-tolyl isocyanate) protein reagent. These studies suggest that isocyanates have the potential for eliciting heterogeneous immune responses in certain subpopulations of exposed workers. Continued contact with isocyanates may be necessary for maintenance of specific immunity. Possible cross reactivity between TDI and HDI may be determined by new antigenic sites created by isocyanate protein interactions.

A worker with occupational asthma due to toluene diisocyanate (TDI) was studied. Detailed immunologic studies, including those for p-tolyl isocyanate IgE antibodies and the presence of leukocyte inhibition factor for isocyanate antigen, were negative. Clinically, the subject noted more pronounced symptoms beginning on Monday morning, followed by weekend off work, and lessening of her symptoms over the working week. Methacholine challenges were negative when performed on three separate occasions, including the time when maximum symptoms were present, and again six months later, before and after bronchial challenge testing. A dose-related response to TDI was observed on bronchial provocation testing using nonirritating concentrations of TDI of 0.0165 and 0.030 ppm. This case provides evidence that the response of the airway to TDI may not always be accompanied by hyperreactivity to methacholine. Screening programs utilizing methacholine challenges may not always identify sensitized workers, since a negative methacholine challenge test does not exclude TDI sensitization.

Sensitization to HMW allergens is a relatively common immunopathogenic factor in occupational asthma. The mechanism of sensitization is an IgE-mediated, type I reaction. High molecular weight allergen refers to proteins and polymers of organic compounds over 5 kd and usually in the 20 to 50 kd range. In most cases diagnosis requires: 1.1. A high index of suspicion of job-related asthma. 2.2. Exposure to HMW compounds and clinical findings associated with such an exposure. 3.3. Confirmation of sensitization by appropriate in vitro or in vivo tests. 4.4. Confirmation of a pathogenic role by physiologic measurements in either a natural setting or during laboratory-controlled challenges.

This study of 183 ambulatory patients with steroid-dependent asthma was conducted to evaluate the efficacy and safety of nebulized bitolterol mesylate solution (0.2%) compared to isoproterenol hydrochloride solution (0.3%). A double-blind, randomized, parallel-group, repetitive-dose design was followed at nine centers for 3 months. Patients received either 1.0 mg of bitolterol or 1.5 mg of isoproterenol three times a day with a closed, intermittent-flow nebulization system. Pulmonary function was evaluated on four 8-hour office visits at approximately 30-day intervals. Efficacy was based on a 15% increase in FEV1 over baseline. Both medications resulted in bronchodilatation within 5 minutes, whereas nebulized bitolterol was statistically superior (p less than 0.05) to nebulized isoproterenol in terms of duration of action and area under the curve. The mean FEV1 response to bitolterol therapy remained greater than 15% over baseline for 5 to 8 hours on the four test days compared to 2 to 4.75 hours for isoproterenol therapy. Both medications were well tolerated. Adverse reactions were transient, and most were mild to moderate. Tremor was the most frequent side effect occurring in approximately 30% of the patients in both groups. There were no clinically significant laboratory changes or electrocardiographic findings. Nebulized bitolterol mesylate was found to be a safe and effective bronchodilator in steroid-dependent patients with asthma.

Approximately one year after enzymes were incorporated into the manufacturing process of one detergent plant in this country, some employees who were exposed to high concentrations of enzyme dust developed both upper and lower respiratory symptoms. These symptoms ranged from nasal stuffiness, rhinorrhea, lacrimation, and throat irritation to chest tightness, cough, and breathlessness. The chest symptoms characteristically occurred 3 to 8 hours after leaving work. Chest x-rays revealed no abnormalities. The prevalence of atopy as determined by personal history was approximately equal to the prevalence in the general population. Intracutaneous skin tests with appropriate enzyme antigens were positive in the majority of affected individuals. Passive-transfer studies with sera from 5 symptomatic employees were positive. Serum precipitins were demonstrated in skin test-negative and skin test-positive employees as well as in persons who had never been exposed to enzyme-containing dust. Complete pulmonary function studies in skin test-negative workers revealed an occasional abnormality. Seventy per cent of the skin test-positive group initially showed disturbances in ventilatory function and/or reduction in the carbon monoxide gas-transfer test. Bronchial challenge tests were positive in 9 of 10 employees with preceding symptoms and positive skin tests. A typical biphasic response pattern was observed in all cases. As stringent dust control measures have been instituted and employees have been instructed in protective measures, the number of respiratory complaints has fallen drastically in this plant.

Excerpt INTRODUCTION It is generally recognized that steroid therapy is very effective in the management of allergic states, but, on the other hand, the delayed responses of these substances at loc...

Although minor manifestations of sensitivity to heparin sodium have been encountered in the early clinical usage of heparin therapy, reports of heparin anaphylaxis did not appear until 1946. The present report deals with another instance of anaphylaxis to heparin in a patient with allergies to multiple inhalants. It is the eighth such case in the available literature and the fourth to be supported by skin and passive transfer tests. It is presented in order to alert the profession to the possibility of such a catastrophic event when heparin is employed. A 71-year-old man was admitted to the hospital on May 5, 1955, with a history of substernal chest pain of 10 days' duration. The pain was oppressive in nature and radiated down both arms. Review of his history revealed the existence of long-standing seasonal rhinitis and asthma, for which he had received desensitization therapy at different periods. Physical examination dis