Latex has been documented as causing immediate hypersensitivity reactions ranging from contact urticaria to severe anaphylaxis. Latex proteins may also act as airborne allergens causing rhinitis and asthma. The prevalence of occupational asthma due to latex gloves among health care workers is unknown. We surveyed the employees of a primary care hospital including nurses (n = 201), members of the cleaning staff (n = 50), and laboratory technologists (n = 38). In the initial part of the study, a questionnaire and skin-prick tests with latex and common inhalant allergens were administered to 273 of 289 (94%) members of the target population. Thirteen of the 273 subjects (4.7%; 95% CI: 2.6 to 8.1%) showed skin reactivity to latex. All latex-sensitive subjects reported glove-related urticaria, which was associated with rhinoconjunctivitis in 12 subjects and asthma in five subjects. No subject had a history suggestive of occupational asthma among those who had negative skin tests to latex. In the second part of the study, a histamine inhalation challenge was performed on 12 of 13 latex-sensitive subjects, including the five subjects with a history of occupational asthma. These 12 subjects demonstrated significant bronchial hyperresponsiveness. All underwent specific inhalation challenges with latex gloves in the laboratory. Seven subjects developed a significant bronchial response (four immediate and three dual reactions) to latex glove exposure. We conclude that occupational asthma due to latex occurred in 2.5% (95% CI: 1.0 to 5.2%) of hospital employees. Widespread use of latex gloves should therefore be considered a significant risk to the respiratory health of hospital employees.

The aim of this study was to investigate the socioeconomic outcomes of subjects who experienced work-related asthma symptoms in the absence of demonstrable occupational asthma (OA) and to compare these outcomes with those found in subjects with documented OA.Subjects (n=157) who were being investigated for work-related asthma, were surveyed. Of these 86 had OA, ascertained by a positive specific inhalation challenge (SIC), and 71 subjects had a negative SIC response. After a median interval of 43 months (range 12-85 months), the subjects were interviewed to collect information on employment status, income changes, and asthma-related work disability.Rates of work disruption and income loss at follow-up were similar in subjects with negative SIC (46% and 59%, respectively) and in those with OA (38% and 62%). The median loss as a percentage of initial income was 23% in subjects with negative SIC and 22% in subjects with OA. Asthma-related work disability, defined as any job change or work loss due to asthma, was slightly more common in subjects with OA (72%) than in those with negative SIC (54%).This study shows that, even in the absence of demonstrable occupational asthma, work-related asthma symptoms are associated with considerable socioeconomic consequences.

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Background-Specific bronchial reactivity to occupational agents may decline after exposure in the workplace ceases leading to falsely negative specific inhalation challenges. A study was carried out to assess prospectively whether increases in nonspecific bronchial hyperresponsiveness could be useful in detecting the bronchial response to occupational agents during specific inhalation challenges. Methods -Specific inhalation challenges were performed in 66 subjects with possible occupational asthma due to various agents. After a control day the subjects were challenged with the suspected agent for up to two hours on the first test day. Those subjects who did not show an asthmatic reaction were rechallenged on the next day for 2-3 hours. The provocative concentration of histamine causing a 20% fall (PC20) in the forced expiratory volume

Occupational asthma has been documented in workers exposed to various metals, including platinum, chromium, cobalt, nickel and zinc [1,2]. Work-related asthma has been described in aluminium smelters [3,4] and in workers exposed to aluminium salts [5,6], although the exact aetiological agent has not yet been identified.We investigated a subject experiencing asthma on exposure to aluminium welding, whose inhalation challenges and environmental assessments provided evidence that aluminium was the most likely causal agent. Case reportA 32 yr old man had been employed as a maintenance worker in a leather plant. He had to perform electric arc welding on mild steel, using manual metal arc and inert gas metal arc techniques. Approximately once a month, he welded aluminium pieces using a manual metal arc process with a flux-coated electrode. After 4 yrs of intermittent exposure to these various welding processes, he developed chest tightness and wheezing that occurred specifically on days he welded on aluminium. Asthmatic symptoms started 1-4 h after the end of exposure to aluminium welding and persisted for several hours. The subject never experienced myalgia, chills or fever. He was treated with inhaled budesonide (400 µg daily) and salbutamol when necessary.The subject was referred for investigation 18 months after the onset of work-related asthmatic symptoms. At that time, he was experiencing asthma on exercise. He had smoked five cigarettes·day -1 for 12 yrs and reported a history of allergic rhinitis since childhood. Skin-prick tests with a battery of common inhalant allergens elicited a positive reaction to mixtures of tree, grass and weed pollens. Skintesting with Al(SO 4 ) 3 , Al(NO 3 ) 3 , Cr 2 (SO 4 ) 3 and NiSO 4 yielded negative results using concentrations of 0.01, 0.1, 1 and 10 mg·mL -1 in saline. Inhalation challengesInhalation challenges were performed in the hospital workshop, according to recent guidelines [7]. Baseline spirometric measurements showed a forced expiratory volume in one second (FEV1) of 4.38 L (100% predicted value) and a FEV1/forced vital capacity (FVC) ratio of 73% (89% pred). On a control day without exposure to occupational agents, spontaneous fluctuations of FEV1 were <10% ( fig. 1a). At the end of the control day, the provocative concentration of histamine causing a 20% fall in FEV1 (PC20) was 0.07 mg·mL -1 [8]. The next day, manual metal arc welding on aluminium for 1 h with the fluxcoated electrodes used at work resulted in a transient fall in FEV1, with a maximum of 17% that was recorded 7 h after the end of exposure. On the following day, exposure to aluminium welding for 2 h provoked an asthmatic reaction with a progressive fall in FEV1, reaching 52% at 2 h postexposure. The subject was given inhaled salbutamol (200 µg) at that time and again 4 h later. On the next morning, FEV1 was still 20% lower than pre-exposure value, so that histamine PC20 was not reassessed.The subject gave informed consent for additional inhalation challenges. One month after the first set of tests, h...