Latex Allergy and Occupational Asthma in Health Care Workers: Adverse Outcomes

Sania Amr; Mary E. Bollinger

Disclosures

Environ Health Perspect. 2004;112(3) 

In This Article

Discussion

Two nurses, who worked at the same community hospital, developed severe latex allergy with dermatologic and respiratory symptoms, including urticaria and occupationally induced asthma and anaphylaxis. They also became sensitized to various chemicals and other environmental and food allergens. These nurses continued to experience respiratory symptoms that became severe, despite the fact that they were not using latex. Once the diagnosis of latex allergy was established, efforts were made to minimize the employees' direct skin contact with latex, but little attention was given to their work environment. These sensitized workers remained in environments where powdered NRL gloves and other respiratory irritants and potential sensitizers (e.g., glutaraldehyde and other disinfectants) were commonly used and where latex balloons were brought in occasionally.

Occupational asthma caused by NRL has been reported in health care workers (Liss et al.1997; Vandenplas et al. 1995). Most patients with latex allergy develop dermatologic symptoms as the first manifestation, with the most typical skin reaction being contact urticaria (Sussman et al. 1991). With continued exposure they may develop upper and lower respiratory symptoms, angioedema, and even anaphylaxis (Sussman et al. 1991).

Allergic reactions to latex consist of immediate-type hypersensitivity reaction and delayed-type hypersensitivity reaction. The latter is a cell-mediated immune reaction in the skin that usually results from a hypersensitivity to one of the numerous chemicals added during processing (von Hintzenstern et al. 1991; Wyss et al. 1993), and it is rarely associated with systemic manifestations. However, patients with delayed-type hypersensitivity reactions are at greater risk of developing immediate reactions due to skin breakdown and resultant increased exposure to NRL (Charous et al. 1994; Turjanmaa 1994). Immediate-type hypersensitivity reactions occur within minutes of exposure to latex products and are mediated by IgE to various latex proteins. Contact urticaria may develop in skin exposed to latex. If the latex proteins are aerosolized, wheezing, rhinitis, and conjunctivitis may occur. In severely allergic persons, reactions can progress to anaphylaxis. Delayed-type reactions and immediate-type reactions can also occur concurrently (Fuchs and Wahl 1992). The clinical manifestations of the present cases are consistent with immediate-type hypersensitivity that is IgE mediated.

The diagnosis of latex allergy is based on a comprehensive medical history and diagnostic tests. The skin-prick test is the preferred and most useful test in diagnosing type I latex hypersensitivity (Taylor and Praditsuwan 1996). However, there is a risk of causing anaphylaxis in highly allergic individuals (Kelly et al. 1993). The skin-prick test is the best predictor of latex allergy with 97% sensitivity and 100% specificity (Ebo et al. 1997), but the U.S. Food and Drug Administration (FDA) has not approved standardized latex solution to be used in the in vivo tests. A skin-prick test may show negative findings if the serum used did not contain the specific latex allergens responsible for the reaction in the individual being tested. Therefore, it is important that testing occur with more than one type of latex product, as well as with raw latex (Hamilton and Adkinson 1996).

The RAST identifies specific IgE antibodies to latex in the blood. Current FDA-approved in vitro latex IgE assays have lower sensitivity and specificity than the skin-prick test (Ebo et al. 1997) and produce a substantial number (25-28%) of false-negative and false-positive IgE antibody results (Hamilton et al. 1999). The presence of allergen-specific IgE does not always correlate with clinical symptoms (Bollinger et al. 2002). The RAST can confirm an NRL allergy diagnosis, but it should not be used as a screening tool because only 50% of a group of individuals identified as latex allergic by the skin-prick test had IgE antibodies to latex by the RAST (Taylor and Praditsuwan 1996).

In the two cases described above, we were able to document a history of clinical symptoms and positive skin-prick and RAST tests; we were therefore able to confirm the diagnosis of NRL allergy.

The existence of underlying atopy increases the risk of sensitization from workplace exposure to environmental allergens (Petsonk 2002). Health care workers who are atopic develop latex hypersensitivity more frequently than those who are not atopic (Bubak et al. 1992; Hunt et al. 1995). Taylor and Praditsuwan (1996) reviewed 44 patients with latex hypersensitivity and found that 77% of them were atopic; all but 2 of these patients were health care workers.

Subjects with latex allergy are more likely to develop sensitivity to other allergens, particularly foods. The prevalence rates of food allergy can be as high as 50% in latex-sensitive individuals, whereas the prevalence rate in the general population is 2% (Beezhold et al. 1996; Blanco et al. 1994). Both of the nurses in our study had atopy, and they developed multiple food allergies.

Several studies (Heilman et al. 1996; Tarlo et al. 1994; Tomazic et al. 1994) have shown that the cornstarch powder used to lubricate gloves acts as a carrier for latex proteins; when the gloves are removed, latex proteins in dust particles become airborne and can be readily inhaled, even by those not wearing the gloves. Using powdered latex gloves can lead to measurable latex allergen in the environment on particles that are small enough to enter the airways and cause sensitization and symptoms (Swanson et al. 1994; Swanson and Ramalingam 2002).

Latex gloves contain various levels of latex allergens, depending on the brand and type of latex worn (Alenius et al. 1994). The amount of allergens aerosolized from the gloves correlates with the number of gloves used at the premises (Heilman et al. 1996; Sussman et al. 1998; Swanson et al. 1994). Latex aeroallergens are primarily generated by active glove use (Charous et al. 2000), and from balloons (Yunginger et al. 1994). High levels of latex aeroallergens have been detected in areas of heavy glove use, such as operating rooms, emergency rooms, and intensive care units (Heilman et al. 1996). Furthermore, airborne particles of powder and NRL proteins may remain suspended for up to 5 hr, contaminating the air and the ventilating system (Kelly et al. 1996). Therefore, for latex-sensitive health care workers with respiratory symptoms, the use of nonlatex gloves is only one of many steps required to reduce and eventually eliminate overall latex exposure.

A crucial step in the reduction or elimination of airborne NRL can be achieved by substituting nonlatex or powder-free NRL for powdered gloves. Such substitution has been found to be an effective prevention strategy that reduces the incidence of suspected latex allergy and specifically latex-related occupational asthma (Allmers et al. 2002; Tarlo et al. 2001; Vanderplas et al. 2002). After occupational exposure, the rates of sensitization and NRL-induced asthma rise dramatically in individuals using powdered NRL gloves but not in individuals using powder-free gloves (Charous et al. 2002). The Occupational Health Surveillance Program of the Massachusetts Department of Public Health (Boston, MA) conducted a survey of all acute care and several chronic care hospitals across the state. Of the hospitals with a program or policy to reduce employee exposure to latex, 40% reported a decrease in latex-related symptoms after the implementation of their program. Those hospitals with a program in place for > 2 years were more likely to see decreases in symptoms than hospitals with a more recently established program. Most programs included the use of nonlatex or latex powder-free gloves (SENSOR 2002).

Some health care centers and professional offices have implemented a nonlatex glove policy throughout the workplace. Others have converted to powder-free latex in order to decrease the risk of airborne allergens. However, most of the health care settings, including dental offices, also use a number of detergents, germicides, and other chemicals that can also induce and exacerbate allergenic conditions and play a role in the development of occupational asthma (Petsonk 2002; Preller et al. 1996). For example, Cidex, a widely used cold sterilization solution for endoscopic equipment, is a well-known respiratory irritant and sensitizer (DiStefano et al. 1998; Petsonk 2002). In a study that was based on 9 years of surveillance of work-related and occupational respiratory disease, McDonald et al. (2000) reported evidence for an increase in cases of occupational asthma due to latex and glutaraldehyde. The prevalence of work-related lower respiratory tract symptoms in hospital endoscopy nurses has been reported to be 8.5% and 66.6% in current employees and ex-employees, respectively (Vyas et al. 2000).

It is likely that patient 1's continuous exposure to Cidex, even after she was diagnosed with occupational asthma, contributed to her persistent clinical symptoms and her developing reactions to all sorts of environmental irritants.

In long-term follow-up studies of workers with sensitizer-induced occupational asthma, the clinical symptoms have been reported to persist in approximately 70% of affected workers who were no longer exposed to the sensitizing agent (Chan-Yeung and Malo 1999; Malo et al. 1992). It has been postulated that once a person is sensitized to an allergen or chemical, he or she may develop asthma, which may be "driven and maintained by the persistence of a specialized subset of chronically activated T-memory cells sensitized against an array of allergenic, occupational, or viral antigens" (Kay 1997). This can explain the fact that asthma can be aggravated in a nonspecific manner by exposure to dust, smoke, fumes, and low levels of irritant chemicals. Persistence of exposure to the sensitizing agent leads to worsening of asthma (Chan-Yeung and Malo 1999), especially in health care workers with latex allergy (Charous et al. 1994), and early removal has been consistently found to be associated with a better outcome.

To establish a latex-safer environment, an effective program or policy would include provision of screening for and surveillance of workers at risk of becoming sensitized to latex. Such screening should be based not only on a positive latex-specific IgE test but also on a clinical history elicited through a questionnaire. Indeed, such a program was implemented at the University of Maryland Hospital in 1997 (Bollinger et al. 2002). A latex sensitization rate of 8.2% was found in the subjects screened. Of note, 45% of the latex IgE positive employees were asymptomatic and 21% of the latex specific IgE negative employees were symptomatic with latex exposure. All employees with either latex-associated symptoms and/or latex-specific IgE were advised to avoid latex products. The hospital gradually converted all gloves to powder-free low protein. Since the program's inception, there have been no further latex-related workers' compensation claims. Similar decreases in latex-related workers' compensation claims have been described by Tarlo et al. (1994, 2001) in Canada after conversion to powder-free gloves.

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