Susan M. Tarlo

Diagnosis and management of cough executive summary: ACCP evidence-based clinical practice guidelines

Recognition of the importance of cough in clinical medicine was the impetus for the original evidence-based consensus panel report on “Managing Cough as a Defense Mechanism and as a Symptom,” published in 1998,1 and this updated revision. Compared to the original cough consensus statement, this revision (1) more narrowly focuses the guidelines on the diagnosis and treatment of cough, the symptom, in adult and pediatric populations, and minimizes the discussion of cough as a defense mechanism; (2) improves on the rigor of the evidence-based review and describes the methodology in a separate section; (3) updates and expands, when appropriate, all previous sections; and (4) adds new sections with topics that were not previously covered. These new sections include nonasthmatic eosinophilic bronchitis (NAEB); acute bronchitis; nonbronchiectatic suppurative airway diseases; cough due to aspiration secondary to oral/pharyngeal dysphagia; environmental/occupational causes of cough; tuberculosis (TB) and other infections; cough in the dialysis patient; uncommon causes of cough; unexplained cough, previously referred to as idiopathic cough; an empiric integrative approach to the management of cough; assessing cough severity and efficacy of therapy in clinical research; potential future therapies; and future directions for research.

Diagnosis and Management of Work-Related Asthma: American College of Chest Physicians Consensus Statement

BACKGROUND A previous American College of Chest Physicians Consensus Statement on asthma in the workplace was published in 1995. The current Consensus Statement updates the previous one based on additional research that has been published since then, including findings relevant to preventive measures and work-exacerbated asthma (WEA). METHODS A panel of experts, including allergists, pulmonologists, and occupational medicine physicians, was convened to develop this Consensus Document on the diagnosis and management of work-related asthma (WRA), based in part on a systematic review, that was performed by the University of Alberta/Capital Health Evidence-Based Practice and was supplemented by additional published studies to 2007. RESULTS The Consensus Document defined WRA to include occupational asthma (ie, asthma induced by sensitizer or irritant work exposures) and WEA (ie, preexisting or concurrent asthma worsened by work factors). The Consensus Document focuses on the diagnosis and management of WRA (including diagnostic tests, and work and compensation issues), as well as preventive measures. WRA should be considered in all individuals with new-onset or worsening asthma, and a careful occupational history should be obtained. Diagnostic tests such as serial peak flow recordings, methacholine challenge tests, immunologic tests, and specific inhalation challenge tests (if available), can increase diagnostic certainty. Since the prognosis is better with early diagnosis and appropriate intervention, effective preventive measures for other workers with exposure should be addressed. CONCLUSIONS The substantial prevalence of WRA supports consideration of the diagnosis in all who present with new-onset or worsening asthma, followed by appropriate investigations and intervention including consideration of other exposed workers.

Effect of low concentrations of ozone on inhaled allergen responses in asthmatic subjects

The relation between inhalation of ambient concentrations of ozone and airway reactivity to inhaled allergens may be important in asthma, since both agents can produce inflammatory changes in the airways. Seven asthmatic patients (mean age 40 [SD 13] years), with seasonal symptoms of asthma and positive skin tests for ragweed or grass, took part in a study to investigate whether exposure to low concentrations of ozone potentiates the airway allergic response. The patients were studied during 4 separate weeks in the winter. In each week there were 3 study days: on days 1 and 3 methacholine challenges were carried out; and on day 2 the subject received one of four combined challenges in a single-blind design--air breathing followed by inhalation of allergen diluent (placebo); ozone followed by inhalation of allergen diluent; air followed by allergen; or ozone followed by allergen. The ozone concentration was 0.12 ppm during 1 h of tidal breathing at rest, and allergens were inhaled until the forced expiratory volume in 1 s (FEV1) had fallen by 15% (PC15). There were no significant differences in baseline FEV1 after exposure to ozone but PC15 was significantly reduced when allergen was preceded by ozone inhalation: the mean PC15 after air was 0.013 (SD 0.017) mg/ml compared with 0.0056 (0.0062) mg/ml after ozone (p = 0.042). Thus, low ozone concentrations, similar to those commonly occurring in urban areas, can increase the bronchial responsiveness to allergen in atopic asthmatic subjects. This effect does not seem to be the result of changes in baseline airway function.

Latex sensitivity in dental students and staff: A cross-sectional study

BACKGROUND Dental practitioners, like other health care providers who regularly use latex gloves, are at increased risk for latex sensitivity. They are also at risk for irritant or allergic contact dermatitis. OBJECTIVE This study was carried out to determine the prevalence of latex sensitivity and possible risk factors in staff and students of a Faculty of Dentistry. METHODS A cross-sectional study was performed by using a questionnaire and allergy skin prick testing. RESULTS Two hundred three students and staff members completed the questionnaire. Five percent reported asthma symptoms on exposure to rubber products, 13% reported symptoms of rhinitis or conjunctivitis, and 17% reported pruritus or urticaria within minutes of exposure to rubber. Overall, 10% of 131 subjects who underwent skin prick tests had a positive response to natural rubber latex. Among the students tested, there were increasing percentages of positive skin test responses to latex with increasing years of study (0% of Year 1 and 2 students tested; 6% of Year 3; and 10% of Year 4). Positive responses were seen as early as Year 3 in students (in their second year of clinical activity and glove use). Positive skin prick test responses to latex were related to a personal history of atopy (p = 0.005), positive prick test responses to common allergens (p < 0.005), latex-attributed immediate pruritus or urticaria (p < 0.05), rhinoconjunctivitis (p < 0.001), and asthma symptoms (p < 0.001). CONCLUSION Dental school students and faculty are at high risk for latex sensitization. This occurs as early as the second year of glove use. Overall prevalence of skin sensitization was 10% of those tested. Preventive strategies in this group merit further investigation.

An Official American Thoracic Society Statement: Work-Exacerbated Asthma

RATIONALE Occupational exposures can contribute to the exacerbation as well as the onset of asthma. However, work-exacerbated asthma (WEA) has received less attention than occupational asthma (OA) that is caused by work. OBJECTIVES The purpose of this Statement is to summarize current knowledge about the descriptive epidemiology, clinical characteristics, and management and treatment of WEA; propose a case definition for WEA; and discuss needs for prevention and research. METHODS Information about WEA was identified primarily by systematic searches of the medical literature. Statements about prevention and research needs were reached by consensus. MEASUREMENTS AND MAIN RESULTS WEA is defined as the worsening of asthma due to conditions at work. WEA is common, with a median prevalence of 21.5% among adults with asthma. Different types of agents or conditions at work may exacerbate asthma. WEA cases with persistent work-related symptoms can have clinical characteristics (level of severity, medication needs) and adverse socioeconomic outcomes (unemployment, reduction in income) similar to those of OA cases. Compared with adults with asthma unrelated to work, WEA cases report more days with symptoms, seek more medical care, and have a lower quality of life. WEA should be considered in any patient with asthma that is getting worse or who has work-related symptoms. Management of WEA should focus on reducing work exposures and optimizing standard medical management, with a change in jobs only if these measures are not successful. CONCLUSIONS WEA is a common and underrecognized adverse outcome resulting from conditions at work. Additional research is needed to improve the understanding of the risk factors for, and mechanisms and outcomes of, WEA, and to inform and evaluate preventive interventions.

Hypersensitivity to natural latex

Rubber hypersensitivity is well described but usually as a contact dermatitis caused by chemicals added during the process of making natural latex or synthetic rubber. IgE-mediated reactions, mainly contact urticaria, have rarely been reported in Europe. We report a case of immediate hypersensitivity to latex. A 34-year-old female operating room nurse developed hand eczema to natural latex. On two occasions, while she was gloving for surgery, she had the following reactions: flushing, tachycardia, urticaria, angioedema, wheezing, and light-headedness. Prick and patch testing to thiuram mix, mercaptobenzothiazole, phenylenediamine mix, and carbamate mix (common rubber additives) were negative. Prick tests to natural latex elicited a 4+ reaction associated with immediate flushing, tachycardia, urticaria, and light-headedness. Five control subjects did not react. IgE antibodies to latex by RAST demonstrated 17.7% binding (control, 4%). This case demonstrates that natural latex can cause IgE-mediated symptoms. The route of exposure was cutaneous absorption of relevant latex allergens. As the use of latex rubber products continues to escalate, more cases are likely to occur.

Canadian Thoracic Society Guidelines for Occupational Asthma

OBJECTIVE To provide broad guidelines and principles to help primary care physicians, occupational physicians, allergists and respirologists with the recognition, diagnosis and management of patients with occupational asthma (OA). OPTIONS These guidelines are mainly directed towards OA induced by a workplace sensitizing agent. However, irritant-induced asthma and workplace aggravation of underlying asthma are also addressed, and some consideration is given to other differential diagnoses. OUTCOMES To enable the assessing physician to investigate patients with possible OA appropriately and to provide guidelines for appropriate early referral when specialized investigations are required. To provide an understanding of the appropriate management strategies following objective diagnosis. EVIDENCE The key diagnostic and management recommendations were based on a critical review of the literature and by specialist consensus meetings. VALUES Evidence was categorized as follows. Level 1: Evidence from at least one randomized, controlled trial. Level 2: Evidence from at least one well-designed clinical trial without randomization, from cohort or case-control analytical studies, preferably from more than one centre, from multiple time series or from dramatic results in uncontrolled experiments. Level 3: Evidence from the opinions of respected authorities based on clinical experience, descriptive studies or reports of expert committees. Evidence was further subdivided as follows: A. Good evidence to support a recommendation for use; B. Moderate evidence to support a recommendation for use; C. Poor evidence to support a recommendation for or against use; D. Moderate evidence to support a recommendation against use; E. Good evidence to support a recommendation against use. BENEFITS, HARM AND COSTS The medical and socioeconomic risks and benefits of an incorrect diagnosis of OA and of failure to diagnose true OA were considered in the recommendations. VALIDATION The document has been reviewed and endorsed by the Canadian Thoracic Society, the Canadian Society of Allergy and Clinical Immunology, and The College of Family Physicians of Canada. CONCLUSIONS There is good evidence for rapid investigation and objective categorization of presented symptoms into OA, aggravation of underlying asthma, unrelated asthma or other diagnoses. OA should be suspected in all adult onset asthmatics whose asthma begins or worsens while they are working. Investigations should be directed to an objective assessment of asthma and then to an assessment of the work relationship, using a combination of investigations as feasible, which may include immunological tests, pulmonary function assessed during work periods and away from work, and specific challenge tests. Early specialist referral is recommended for diagnosis. Management strategies include general asthma management in addition to measures to avoid further exposure to a relevant workplace sensitizer. Compensation issues and other workers at risk of developing OA also need to be considered when the diagnosis is made.

Outcome determinants for isocyanate induced occupational asthma among compensation claimants

OBJECTIVES: To compare the outcome of occupational asthma (OA) induced by isocyanates in Ontario (where a surveillance programme for exposed workers has been in place for over 15 years), with the outcome of OA induced by other work agents. METHODS: Compensated OA claims during the period 1984-88 in Ontario were retrospectively reviewed in a standardised way. RESULTS: 136/235 compensated claims were attributed to isocyanates. Compared with other causes of OA, those attributed to isocyanates had a shorter latent period before onset (5.9 v 7.9 years, P < 0.05), shorter duration of symptoms before diagnosis (2.0 v 3.0 years, P < 0.05), and less associated atopy (43% v 58%, P < 0.05). Outcome at a mean of 1.9 years after initial assessment was significantly better in those with OA induced by isocyanates; 73% cleared or improved v 56% with other causes of OA (P < 0.05). Ten subjects with OA induced by isocyanates stayed at the same work; none cleared and four had worsened at follow up. A better outcome in OA induced by isocyanates was associated with early diagnosis (P < 0.05), and early removal from isocyanates after the onset of asthma. CONCLUSIONS: The outcome in the group with OA induced by isocyanates is similar to previous follow up studies. However, it is better than the outcome in our comparison group with OA due to other causes, perhaps because of earlier diagnosis in the group with OA induced by isocyanates. This may be attributable to the medical surveillance of workers exposed to isocyanates in Ontario, either directly from the surveillance assessments, or indirectly by increasing awareness of the condition.

Asthma and exposure to cleaning products – a European Academy of Allergy and Clinical Immunology task force consensus statement

Professional and domestic cleaning is associated with work‐related asthma (WRA). This position paper reviews the literature linking exposure to cleaning products and the risk of asthma and focuses on prevention. Increased risk of asthma has been shown in many epidemiological and surveillance studies, and several case reports describe the relationship between exposure to one or more cleaning agents and WRA. Cleaning sprays, bleach, ammonia, disinfectants, mixing products, and specific job tasks have been identified as specific causes and/or triggers of asthma. Because research conclusions and policy suggestions have remained unheeded by manufactures, vendors, and commercial cleaning companies, it is time for a multifaceted intervention. Possible preventive measures encompass the following: substitution of cleaning sprays, bleach, and ammonia; minimizing the use of disinfectants; avoidance of mixing products; use of respiratory protective devices; and worker education. Moreover, we suggest the education of unions, consumer, and public interest groups to encourage safer products. In addition, information activities for the general population with the purpose of improving the knowledge of professional and domestic cleaners regarding risks and available preventive measures and to promote strict collaboration between scientific communities and safety and health agencies are urgently needed.

Assessment of the relationship between isocyanate exposure levels and occupational asthma.

As part of a previous study, we identified Ontario cases of isocyanate-induced occupational asthma (OA) and the companies at which they worked. The Ontario Ministry of Labour maintained a computerized database including isocyanate air sampling determinations conducted by the Ministry. Within this database, we compared levels of isocyanate concentrations measured at 20 case companies [with compensated isocyanate asthma (OA) claims] with 203 noncase companies, based on air samples collected during the same 4-year period during which the OA claims arose. The proportion of case companies that were ever recorded as having a measured ambient isocyanate concentration of > or = 0.005 ppm was greater than that for noncase companies, for TDI users (43% vs 22%), and for MDI users (40% vs 27%). This reached conventional significance when combined across companies and isocyanate types (50% vs 25%; P < 0.05). This provides some evidence that facilities having OA claims have higher isocyanate exposures than do those without claims.