Development Of Occupational Asthma Research Articles

Incidence of Immunological Occupational Asthma in 2015–2022 by Occupation: Macedonian Experience

BACKGROUND: Immunologic occupational asthma (OA), a more prevalent OA type than non-immunologic OA, became an important public health problem in the last decades worldwide. AIM: To present the distribution of new diagnosed cases of immunologic OA in the RN Macedonia in the period 2015–2022 by occupation. METHODS: Immunologic OA was diagnosed by the serial measurement of peak expiratory flow rate (PEFR) at and away from work or by combination of serial PEFR measurement at and away from work and non-specific bronchial provocation at and away from work in workers with diagnosed asthma and work-relatedness of the symptoms. Sensitization to common inhalant and occupational allergens was evaluated by skin prick test. RESULTS: The annual incidence rate of the diagnosed immunologic OA in this period varied from 1.9 / 100,000 working population in 2015–2.6 / 100,000 in 2022 with a drop in 2020 and 2021, i.e. in the period of COVID-19 pandemic (0.6 and 0.5, respectively). Cleaning, bakery, cleaning, textile manufacture, wood industry, agriculture, and metal-parts manufacture were the most important occupations for the development of immunologic OA. More than a half of the new diagnosed immunologic OA cases were atopics. CONCLUSION: Our findings indicated the occupations with the highest incidence of immunologic OA that could enable targeting of preventive measures and activities to reduce the occurrence of immunologic OA as well as its adverse health outcomes.

Genotypes and frequencies of the TSLP gene variant rs1837253 in different occupational asthma phenotypes

Introduction. Currently, despite the fact that occupational asthma has long been considered as a separate, independent disease, recent studies pay more and more attention to its heterogeneity. Occupational asthma phenotyping was originally based on the identification of combinations of clinical characteristics of the disease, but now more and more data that allow understanding the cause of clinical differences at the molecular genetic level are emerging. Thus, molecular genotyping opens up new opportunities in the search for a more targeted and personalized approach to the treatment of occupational asthma, as well as in the development of an individual strategy for its prevention. The aim of the study was to determine the genetic risk markers for the development of oc cupational asthma under the influence of sensitizers by assessing the TSLP gene polymor phism rs1837253. Materials and methods. The study was conducted on the basis of the Department of Occupational Diseases and Clinical Pharmacology named after honored scientist of the Russian Federation professor V. V. Kosarev, FSBEI HE Samara State Medical University of the Ministry of Health of the Russian Federation, and the Department of Occupational Pathology, SBHI SR Samara Medical and Sanitary Unit No. 5 of the Kirovsky District. The study involved 170 patients with various phenotypes of occupational bronchial asthma (OBA) and 50 people in the control group: group 1 (42 people) — the phenotype «allergic occupational bronchial asthma», group 2 (36 people) — the phenotype «non-allergic occupational bronchial asthma», group 3 (58 people) — the phenotype «occupational bronchial asthma — occupational chronic obstructive pulmonary disease», group 4 (34 people) — the phenotype «occupational bronchial asthma — metabolic syndrome», group 5 (50 people) — the control group (healthy). As part of the study of genetic predisposition to occupational bronchial asthma,genetic polymorphisms of the rs1837253 TSLP gene were determined. DNA samples were isolated from peripheral venous blood lymphocytes by phenol-chloroform extraction. Genotyping was performed by real-time polymerase chain reaction using primers and probes developed with the PrimerQuest tool (Integrated DNA Technologies, Inc.). Results. Thus, for the first time, genetic risk markers for the development of occupational asthma under the influence of sensitizers have been identified: the TSLP gene polymorphisms rs1837253, which makes it possible to recommend determining these genetic markers during in-depth periodic medical examinations in persons working under exposure to sensitizing and irritating substances in the presence of clinical, functional, and immunological changes. Conclusion. The identified marker profiles of OBA genotypes can optimize the approach to the diagnosis, treatment and prevention of this pathology, as well as expand the range of criteria for predicting the course of the disease. If polymorphisms of the TSLP gene are detected during molecular genetic studies, patients need to be registered with a dispensary and require repeated examinations of the function of external respiration once every 6 months and in-depth periodic medical examinations in a specialized center of occupational pathology with the obligatory participation of a pulmonologist, an allergist-immunologist, an occupational pathologist, as well as conducting extended functional and immunological studies once every 2 years.

Occupational rhinitis.

Occupational rhinitis (OR) has so far received little attention even though it shares common pathophysiological features and trigger factors and is closely associated with occupational asthma (OA). Work-related exposure to certain substances, such as animal dander, is considered to be the main factor for the development of OR. The new EAACI definition of OR stresses the causal relationship between workplace exposure and onset of rhinitis symptoms as opposed to previous definitions that mainly focused on a temporal relationship between workplace exposure and occurrence of nasal symptoms. Also, it has been suggested to use the term “work-related rhinitis” for classifying the different forms of rhinitis associated with the workplace. These forms can be subdivided into allergic or non-allergic OR, which is due to causes and conditions related to a particular work environment, as well as work-exacerbated rhinitis, which is defined as a pre-existing rhinitis exacerbated by exposure at the workplace. Even though taking a detailed patient history is especially important when it comes to diagnosing OR, the gold standard for confirming the diagnosis is nasal provocation testing. Best possible symptomatic relief and prevention of development of OA constitute the main therapeutic objectives in OR. Treatment options consist of total avoidance of trigger substances (main goal), reduction of exposure to certain substances, and pharmacotherapy. Furthermore, it is important to note that allergic OR is an occupational disease in Germany (Berufskrankheit No 4301) and needs to be reported to health authorities.

Occupational Rhinitis

There is convincing evidence that tight relationships between the upper and lower airways also apply to the workplace context. Most patients with occupational asthma (OA) also suffer from occupational rhinitis (OR), although OR is 2 to 3 times more common than OA. OR most often precedes the development of OA, especially when high-molecular-weight protein agents are involved, and longitudinal cohort studies have confirmed that OR is associated with an increased risk for the development of OA. The level of exposure to sensitizing agents at the workplace is the most important determinant for the development of IgE-mediated sensitization and OR. Atopy is a risk factor for the development of IgE-mediated sensitization only to high-molecular-weight agents. In workers with work-related rhinitis symptoms, documentation of IgE-mediated sensitization to a workplace agent via skin prick testing or serum specific IgE confirms a diagnosis of probable OR, whereas specific nasal provocation testing in the laboratory remains the reference method to establish a definite diagnosis of OR. Complete avoidance of exposure to the causal agent is the most effective therapeutic option for controlling work-related nasal symptoms and preventing the development of OA. If complete elimination of exposure is expected to induce meaningful adverse socioeconomic consequences, reduction of exposure can be considered as an alternative approach, but it is important to consider the individual risk factors for the development of OA to implement a more personalized management of OR.

Cross-reactivity between halogenated platinum salts in an immediate-type respiratory hypersensitivity model

Halogenated platinum salts can trigger the development of occupational asthma. Until recently, laboratory research into the development and manifestation of platinum hypersensitivity responses were hindered by the lack of an animal model suitable for assessing the functional consequences of allergic sensitization. We employed a newly developed mouse model to assess the potential allergenicity of ammonium tetrachloroplatinate (ATCP), compare the relative potency of ATCP and another platinum salt, ammonium hexachloroplatinate (AHCP) and assess potential cross-reactivity. Mice were topically sensitized with ATCP before being challenged by intratracheal aspiration (IA) with ATCP. Ventilatory responses were assessed using whole-body plethysmography (WBP). An immediate response (IR) was observed in ATCP-sensitized and challenged mice. Two days later, responsiveness to the nonspecific stimuli methacholine (Mch) was detected in ATCP-sensitized mice using WBP. Bronchoalveolar lavage fluid collected from sensitized mice contained an average of 3.3% eosinophils compared to less than 0.5% in non-sensitized mice (p<.05). Serum harvested from sensitized mice also contained increased total serum immunoglobulin E (p<.05). These data are the first to demonstrate that topical exposure to ATCP is sufficient to develop immediate type hypersensitivity and that a single intra-airway challenge is capable of triggering pulmonary responses. To investigate potential cross-reactivity, mice were sensitized to AHCP and, challenged by a single IA with a second platinum compound, ATCP. Compared to non-sensitized mice challenged with ATCP, these mice exhibited an IR, responsiveness to Mch, and eosinophilic infiltration in the lungs similar to that achieved with AHCP challenge, thus demonstrating cross-reactivity.

ROLE OF POLYMORPHIC VARIANTS OF THE GENES TNFA, TSLP IN THE OCCUPATIONAL ASTHMA DEVELOPMENT

The aim of the study was to find possible associations of polymorphic variants rs1800629 of gene TNFA and rs1837253 of gene TSLP with the development of occupational asthma. The analysis of polymorphism of cytokine genes was carried out by means of polymerase chain reaction of DNA synthesis in 83 patients and 195 control subjects. Genomic DNA was isolated from whole blood samples using standard phenol/chloroform extraction techniques. Statistical analysis was performed using χ test as amended by Yeats and odds ratios with 95 % confidence intervals. As a result, it found that in patients with occupational asthma allele C and genotype CC polymorphic locus rs1837253 TSLP gene occurs more frequently (OR = 1.91, 95 % CI 1.11-3.28; p = 0,026 и OR = 2.48, 95 % CI 1.29-4.77; p = 0.010 respectively) than in the control group. The analysis of the association of polymorphic locus rs1800629 TNFA gene with occupational asthma did not reveal statistically significant results. The received data suggest the possible involvement of rs1837253 polymorphism TSLP gene in the formation of occupational asthma.

Asthma control in the workplace

Workplace exposures may result, in susceptible workers, in the development of occupational asthma from sensitising or toxic/irritant exposure, or in the worsening of a pre-existing asthmatic condition, so-called “work-exacerbated asthma” [1–3]. Occupational asthma is a relatively common condition, although it is often unrecognised [1, 4]. Exposure to the sensitising agents can lead to permanent airway changes, so that even when stopped, the majority of workers will still experience persistent asthma symptoms and show residual airway hyperresponsiveness [2–5]. Early cessation from exposure to the offending agent, however, results in a better prognosis, while persistent exposure can lead to more severe asthma and more frequent acute asthma events [5, 6]. It has become evident from recent studies of work-exacerbated asthma that exposure to “asthmagens” and irritants at the workplace can lead to troublesome symptoms and trigger exacerbations of asthma [1, 6, 7]. As for non-work-related asthma, poor asthma control can result from common environmental exposures, such as allergens or pollutants in susceptible subjects, or from insufficient controller therapy or non-adherence to it. Such poor “baseline” airway control may render the worker more susceptible to the effects of various dusts, aerosols and other contaminants at work, and predispose to asthma exacerbations [1, 8, 9]. However, the contribution of various exposures at work to asthma control and exacerbations remains to be better documented. The European Community Respiratory Health Survey (ECRHS) I and II have been a rather useful source of information on asthma and these data are certainly still currently relevant. In this issue of the European Respiratory Journal , Le Moual et al . [10] looked at the relationship between occupational exposures and asthma control, as defined …

291 Occupational exposure to isocyanates; a baseline exposure assessment as basis for an intervention strategy

ObjectivesOccupational exposure to isocyanates has been associated with the development of occupational asthma. This study serves as baseline measurement within an intervention study, aimed at 1) conducting a detailed exposure...

S5 The prevalence of asthma among cleaners in the UK

BackgroundA number of epidemiological studies have shown a significant association between asthma and working as cleaner but reporting schemes and workforce surveys have identified typical features of occupational asthma in...

Prevalence of Possible Occupational Asthma in Hairdressers Working in Hair Salons for Women

Background: The aim of this study was to determine the prevalence of possible occupational asthma (OA) in hairdressers. Methods: A telephone questionnaire (Q1) was administered to 1,334 individuals from a total of 1,875 hairdressers working in hair salons for women in Barcelona (response rate 71%) to identify those with respiratory symptoms. Multiple correspondence analysis showed 5 specific questions for assessing symptoms of asthma. Individuals who gave a positive response to 1 of these questions (n = 251) were given a second validated questionnaire (Q2) to identify those with suspected OA. OA was defined according to a classification tree based on the response to queries on nasal itching, daily symptoms throughout the week at work, nasal secretions, voice loss, wheezing, and sputum production as reported previously. Moreover, we calculated the prevalence of OA according to the conventional criteria of improvement and/or worsening of symptoms in relation to exposure at work and during off-work time on weekends and during vacations. Results: Asthma was present in 9.5% of hairdressers. From Q2 data, 72 were classified as having possible OA, yielding a prevalence of OA from 5.4 (72/1,334) to 7.8% according to the classification tree previously described. A prevalence from 4.6 (62/1,334) to 6.7% was obtained using conventional criteria. Rhinitis or dermatitis (OR 7.80), as well as exacerbation of symptoms at work and persistence of symptoms on weekends (OR 2.99) were associated with the development of OA. Conclusions: Hairdressing employment can induce asthma. Episodes of rhinitis or dermatitis seem to be risk factors for the development of OA in this population.

Choice of Mouse Strain Influences the Outcome in a Mouse Model of Chemical-Induced Asthma

BackgroundThe development of occupational asthma is the result of interactions between environmental factors and individual susceptibility. We assessed how our model of chemical-induced asthma is influenced by using different mouse strains.Methodology/Principal FindingsOn days 1 and 8, male mice of 7 different strains (BALB/c, BP/2, A/J, C57Bl/6, DBA/2, CBA and AKR) were dermally treated with toluene-2,4-diisocyanate (TDI) (0.3%) or vehicle (acetone/olive oil, AOO, 2∶3) on each ear (20 µl). On day 15, they received an oropharyngeal instillation of TDI (0.01%) or AOO (1∶4). Airway reactivity to methacholine, total and differential cell counts in bronchoalveolar lavage (BAL) and total serum IgE and IgG2a levels were measured. Lymphocyte subpopulations in auricular lymph nodes and in vitro release of cytokines by ConA stimulated lymphocytes were assessed. In TDI-sensitized and challenged mice, airway hyper-reactivity was only observed in BALB/c, BP/2, A/J and AKR mice; airway inflammation was most pronounced in BALB/c mice; numbers of T-helper (CD4+), T-activated (CD4+CD25+), T-cytotoxic (CD8+) and B- lymphocytes (CD19+) were increased in the auricular lymph nodes of BALB/c, BP/2, A/J and CBA mice; elevated concentrations of IL-4, IL-10, IL-13 and IFN-γ were detected in supernatant of lymphocytes from BALB/c, BP/2, A/J, C57Bl/6 and CBA mice cultured with concanavaline A, along with an increase in total serum IgE.ConclusionThe used mouse strain has considerable and variable impacts on different aspects of the asthma phenotype. The human phenotypical characteristics of chemically-induced occupational asthma were best reproduced in Th2-biased mice and in particular in BALB/c mice.

Seafood workers and respiratory disease: an update

This review focuses on seafood workers engaged in harvesting, processing and food preparation. These groups are increasingly at risk of developing occupational allergy and respiratory disease as a result of seafood handling and processing activities. This review provides an update of a previous review conducted a decade ago. Exposure characterization studies have demonstrated that aerosolization of seafood (muscle, visceral organs, skin/mucin) during canning and fishmeal operations result in highly variable levels of airborne particulate (0.001-11.293 mg/m3) and allergens (0.001-75.748 ug/m3). Occupational asthma is more commonly associated with shellfish (4-36%) than with bony fish (2-8%). Other seafood-associated biological (Anisakis) and chemical agents (protease enzymes, toxins and preservatives) have also been implicated. Atopy, smoking and level of exposure to allergens are significant risk factors for sensitization and the development of occupational asthma. Molecular studies of the allergens suggest that aside from tropomyosin and parvalbumin, other as yet uncharacterized allergens are important. Future research needs to focus on detailed characterization of allergens in order to standardize exposure assessment techniques, which are key to assessing the impact of interventions. The clinical relevance of agents such as serine proteases and endotoxins in causing asthma through nonallergic mechanisms needs further epidemiological investigation.

Characterization of exposures among cemented tungsten carbide workers. Part II: Assessment of surface contamination and skin exposures to cobalt, chromium and nickel

Cobalt, chromium and nickel are among the most commonly encountered contact allergens in the workplace, all used in the production of cemented tungsten carbides (CTC). Exposures to these metal-containing dusts are frequently associated with skin sensitization and/or development of occupational asthma. The objectives of this study were to assess the levels of cobalt, chromium and nickel on work surfaces and on workers' skin in three CTC production facilities. At least one worker in each of 26 work areas (among all facilities) provided hand and neck wipe samples. Wipe samples were also collected from work surfaces frequently contacted by the 41 participating workers. Results indicated that all surfaces in all work areas were contaminated with cobalt and nickel, with geometric means (GMs) ranging from 4.1 to 3057 microg/100 cm(2) and 1.1-185 microg/100 cm(2), respectively; most surfaces were contaminated with chromium (GM=0.36-67 microg/100 cm(2)). The highest GM levels of all metals were found on control panels, containers and hand tools, whereas lowest levels were on office and telecommunication equipment. The highest GM levels of cobalt and nickel on skin were observed among workers in the powder-handling facility (hands: 388 and 24 microg; necks: 55 and 6 microg, respectively). Levels of chromium on workers' skin were generally low among all facilities. Geometric standard deviations associated with surface and skin wipe measurements among work areas were highly variable. Exposure assessment indicated widespread contamination of multiple sensitizing metals in these three facilities, suggesting potential transfer of contaminants from surfaces to skin. Specific action, including improved housekeeping and training workers on appropriate use and care of personal protective equipment, should be implemented to reduce pathways of skin exposure. Epidemiologic studies of associated adverse health effects will likely require more biologically relevant exposure metrics to improve the ability to detect exposure-response relationships.

10. Occupational asthma

A diversity of airborne dusts, gases, fumes, and vapors can induce dose-related respiratory symptoms in individuals exposed in the workplace. These agents can cause annoyance reactions, irritational effects, sensitization, or the induction of corrosive changes in the respiratory tract, depending on their composition, concentration, and duration of exposure. The prevalence of occupational asthma (OA) ranges from 9% to 15% of the asthmatic population. Factors that might influence the development of OA include the work environment, climatic conditions, genetic proclivities, tobacco and recreational drug use, respiratory infection, bronchial hyperresponsiveness, and endotoxin exposure. Pathogenetically, new-onset OA can be allergic or nonallergic in origin. The allergic variants are usually caused by high-molecular-weight allergens, such as grain dust and animal or fish protein. Selected low-molecular-weight agents are also capable of inducing allergic OA. Symptoms ensue after a latent period of months to years. Nonallergic OA can be precipitated by a brief high-level exposure to a potent irritant. Symptoms occur immediately or within a few hours of the exposure. Once the diagnosis of allergic OA is established, the worker should be removed from further exposure in the workplace. In nonallergic OA the worker can return to work if the exposure was clearly a nonrecurring event. If the diagnosis is made in a timely fashion, most workers experience improvement. Prevention is the best therapeutic intervention.

Pre-employment assessment and health surveillance for employees exposed to occupational asthmagens: overview

The recent publication of an evidence-based review of occupational asthma [1] has highlighted the areas for which there is little evidence to guide the practising occupational physician dealing with workers exposed to occupational asthmagens. In particular, there is little or no evidence for effective management of prospective employees with a pre-existing or current history of asthma. There are few studies of efficacy of health surveillance programmes and an absence of guidance regarding important components and recommended frequency of assessment. This in-depth review sets out to review these important practical subjects for occupational physicians and where there is little evidence gives example of good practice from major employers in a number of different industries. The final paper looks to the future and the emerging areas of knowledge. The paper by Tarlo and Liss [2] sets out areas where good evidence exists for prevention of occupational asthma now thought to account for 10% of adult-onset asthma. Early diagnosis and early removal from exposure are essential to minimize the impact of occupational asthma once it has developed. Following diagnosis, the management of choice is complete removal from exposure, but even with early intervention there will be socio-economic consequences. The evidence for health surveillance is less certain, but one of the major studies [3] in Ontario is discussed in detail. Although there was some evidence of benefit, improvements in incidence were temporarily related to other hygiene changes in the workplace, which may have impacted on the development of occupational asthma. Areas which still need to be addressed include the important components and the optimum frequency of health surveillance assessments. In the paper by Linnet [4] the practice of a major platinum refiner is described. Platinum is a potent sensitizer with between 25–90% of employee populations becoming sensitized. Its refining also involves exposure to a number of irritants. The current practice is to exclude smokers and current active asthmatics on treatment. A previous history of asthma would exclude an employee if he/she were young and had not been tested in an industrial environment. Skin-prick testing with platinum salts is the mainstay of health surveillance and is conducted on a 3-monthly basis in areas of high exposure. The platinum industry does not exclude atopics because it is now recognized that exclusion of this group, prevalent in the general population, would exclude a large proportion of potential employees who would never go on to develop occupational asthma. The paper by Gannon [5] describes a global integrated programme for the prevention, early detection and mitigation of occupational asthma in an industry where employees work with isocyanates. The reason isocyanates cannot often be substituted are discussed. The practical issues of a global company policy which has to integrate with local legal and accepted professional practice are described. The authors suggest that this approach could be a model for other industries.

Small nonspecialized farming as a protective factor against immediate‐type occupational respiratory allergy?

In Poland small, nonspecialized farms, growing different crops and raising usually a few animals of various species constitute the majority. The aim of the case-control study was to evaluate the risk factors of work-related respiratory symptoms and occupational asthma and/or rhinitis in Polish farmers and investigate whether the farming characteristics may have influence on the prevalence of atopy and allergic diseases. The study groups comprised 100 cases who were farmers reporting work-related asthmatic and/or rhinitis symptoms from randomly selected family doctors practices (80 of 353) and 102 healthy controls. All subjects were examined by means of a questionnaire, skin prick tests (SPT) to common and occupational allergens, total serum immunoglobulin (Ig)E level and the presence of specific IgE and allergen-specific inhalation challenge tests were performed. The provocation tests were monitored with the spirometry, histamine challenge test and evaluation of nasal symptoms score and nasal washings. Respiratory allergic disease was recognized in 68 symptomatic patients, including 41 cases because of occupational allergens (asthma n=38, rhinitis n=41). Step-wise logistic regression analysis confirmed the protective role of small farms against the development of work-related symptoms (OR 0.23; 95% CI 0.11, 0.47) as well as the significance of positive SPT to cereals (OR 5.55; 95% CI 1.6, 19.21) and storage mites (OR 3.73; 95% CI 1.27, 10.96) as a risk factor of these symptoms. Cereal farming (OR 13.75; 95% CI 2.39, 78.83) and positive SPT to cereals (OR 26.92; 95% CI 5.33, 135.9) and storage mites (OR 44.07; 95% CI 8.40, 231.1) were found to be significant risk factors of occupational asthma and/or rhinitis. Cereal farming and hypersensitivity to cereals plays the significant role in the development of occupational asthma among Polish farmers. It also seems that working on small farms may protect farmers against work-related respiratory symptoms that are mostly because of allergy.

Pathogenesis of occupational asthma.

The development of occupational asthma (OA) is likely to result from the complex interaction of environmental and host factors. This article addresses a series of issues relating to the multiple environmental factors that could affect the initiation of OA, including the intrinsic characteristics of causative agents, as well as the influence of the level, mode and route of exposure. Although the clinical and pathological features of OA caused by low molecular weight agents resemble those of immunoglobulin (Ig)E-mediated asthma, the failure to detect specific IgE antibodies against most of these agents and/or poor association with disease status have resulted in intense speculation about alternative or complementary physiopathological mechanisms leading to airway sensitisation. In this contribution, the roles of specific immunoglobulin E and G antibodies, cell-mediated immunity and inflammatory effector cells are critically reviewed. Recent advances in the characterisation of the molecular interactions between chemical sensitisers and human airway proteins provide promising avenues for elucidating the immunological basis of occupational asthma caused by low molecular weight agents.

HLA phenotype and exposure in development of occupational asthma

To review relevant scientific literature to understand the contribution of exposure to the risk of developing occupational asthma and whether HLA class 2 molecules contribute to individual susceptibility to sensitization and asthma caused by low-molecular-weight chemicals. The author's expert opinion was used to select relevant articles based on systematic reviews of relevant literature. Studies during the past decade have shown that intensity of exposure is an important determinant of asthma induced by inhaled respiratory sensitizers, both proteins and low-molecular-weight chemicals. There is evidence that HLA class 2 alleles contribute to the risk of sensitization and asthma caused by low-molecular-weight chemical sensitizers. HLA-DR3 is associated with an increased risk of developing specific IgE to trimellic anhydride (TMA) and complex platinum salts such as ammonium hexachloroplate (ACP). In those exposed to ACP and possibly also to TMA, risk is greater in those who have experienced lower intensity of exposure. Exposure intensity is an important determinant of sensitization and asthma caused by respiratory sensitizers. HLA class 2 alleles contribute to individual susceptibility to low-molecular-weight chemicals. For some chemicals, the contribution of HLA class 2 alleles is greater in those less exposed at work to the relevant chemical.

8. Occupational asthma and allergies

A diversity of airborne dusts, gases, fumes, and vapors can cause dose-related symptoms in individuals exposed in the workplace. More than 250 chemicals have been incriminated as a cause of occupational asthma (OA). The prevalence of OA ranges from 2% to 6% of the asthmatic population. Predisposing factors facilitating the development of OA include the work environment, climatic conditions, genetic proclivities, tobacco and recreational drug use, respiratory infection, and bronchial hyperresponsiveness. Pathogenetically, new-onset OA may be immunologic or nonimmunologic in origin. The immunologic variants are usually caused by high molecular-weight allergens such as grain dust and animal or fish protein. Symptoms ensue after a latent period of months to years. Nonimmunologic OA can be precipitated by a brief, high-level exposure to a potent irritant. Symptoms occur immediately or within a few hours of the exposure. In either instance, once the diagnosis is established, the worker should be removed from the workplace. If the diagnosis is made in a timely fashion, most workers experience improvement. Prevention is the best therapeutic intervention. (J Allergy Clin Immunol 2003;111:S530-9.)

Primary prevention of natural rubber latex allergy in the German health care system through education and intervention.

The development of occupational asthma and allergic skin reactions caused by natural rubber latex (NRL) allergy are risks for health care workers. There are few published studies to suggest that intervention programs to reduce exposure will lead to primary prevention of sensitization. This study assesses the effects of intervention to reduce the incidence of NRL allergy in personnel working in health care facilities insured by the German statutory accident insurance company for health care workers, Berufsgenossenschaft für Gesundheitsdienst und Wohlfahrtspflege, with approximately 3 million insured employees, by switching to powder-free NRL gloves. The timing of introduction of intervention strategies, such as education of both physicians and administrators, together with regulations demanding that health care facilities only purchase low-protein, powder-free NRL gloves are reported. We reviewed the annual numbers of reported suspected cases of NRL-caused occupational allergies and the amount and type of gloves used in German acute-care hospitals since 1986. The purchase of powder-free NRL examination gloves exceeded that of powdered gloves for the first time in 1998. This only became true for powder-free NRL sterile gloves 2 years later in 2000. The incidence of suspected occupational NRL allergy cases rose until 1998 and has declined steadily since. There was a 2-year lag between the beginning of the decline in the purchase of powdered NRL examination gloves and the beginning of a decline in suspected NRL-caused occupational asthma cases. Despite the effect of increased recognition of NRL allergies, education about NRL allergies in health care facilities combined with the introduction of powder-free gloves with reduced protein levels has been associated with a decline in the number of suspected cases of occupational allergies caused by NRL in Germany on a nationwide scale. These results clearly indicate that primary prevention of occupational NRL allergies can be achieved if these straightforward and practical interventions are properly carried out and maintained.