Jean-Luc Malo

An Official ATS Proceedings: Asthma in the Workplace The Third Jack Pepys Workshop on Asthma in the Workplace: Answered and Unanswered Questions

The Third Jack Pepys Workshop on Asthma in the Workplace held in Montreal, Canada in May 2007 focused on emerging data, including progress over the previous three years touching on questions identified at a previous Workshop (2004). The format, based on that used in previous workshops, consisted primarily of short, thematic, structured slide presentations followed by extensive, open-ended discussion periods. The key summary content of the workshops discussions has been distilled for this account. (Expanded details of the prepared presentations in PowerPoint format can be found at: www.asthma-workplace.com.) The topics reflect an expanded scope of interest including consideration of: (1) work-related asthma (WRA), subsuming both occupational asthma (OA) and work-exacerbated asthma (WEA); although the latter condition is commoner than OA, discussion mainly focused on OA because the corpus of scientific literature is larger; (2) other related occupational airway pathologic processes, beyond WRA, including rhinitis and eosinophilic bronchitis, with focus on various methods that improve objective confirmation of these conditions; (3) the psycho-socioeconomic impact of WRA with presentation of questionnaires that assess disability due to OA; (4) development of a world-wide perspective on work-related airway disease, including the situation in countries with emerging economies where the frequency of WRA is likely similar to or even greater than that in developed countries. The overarching conclusion was that WRA and related airway conditions are underrecognized and underdiagnosed both in developed and developing countries, with a great many aspects related to personal and environmental risk, exposure, mechanisms, and assessment of impairment/disability remaining to explore to better inform primary, secondary, and tertiary disease prevention.

Frequency of work-related respiratory symptoms in workers without asthma.

BACKGROUND Clinicians are faced with subjects complaining of work-related respiratory symptoms (WRS) without any evidence of asthma. We sought to assess the prevalence of subjects with WRS without asthma in a cohort of workers referred for possible work-related asthma (WRA) as well as compare the characteristics and the work environment of subjects with WRS to subjects with WRA. METHODS A prospective observational study of workers referred for possible WRA over a 1-year period. Detailed medical and occupational questionnaires were administered. Pulmonary function tests as well as specific-inhalation challenges were performed. RESULTS One hundred twenty workers were investigated. Fifty-one had WRA while 69 had WRS. The type and the severity of the respiratory symptoms were similar in both groups, except for wheezing which was more frequently reported in subjects with WRA (32 (62.7%)) than in subjects with WRS (16 (23.2%)) (P < 0.01). Both the workers with WRS and WRA were mainly employed in the manufacturing sector (64.7% (WRA) and 71% (WRS)). At the time of the first assessment 64.7% of subjects with WRA and 56.5% with WRS had left their workplace because of their bothersome respiratory symptoms. CONCLUSIONS Subjects with WRS without asthma represent a large proportion of the subjects assessed in clinics specialized in the field of WRA. Like subjects with WRA, the population with WRS is likely to represent a significant medical burden. The similarity of the symptoms between the WRA and the WRS groups emphasizes the need to perform a thorough and objective investigation to diagnose WRA.

Asthma and the Workplace

The workplace is, apart from smoking, a clearly identified cause for the development of chronic obstructive lung diseases, including asthma (Trupin et al. 2003). Many asthmatic subjects complain that their symptoms are worse at work as related to exposure to their workplace physical and psychological environmental stimuli. Epidemiological studies in the general population show that from 5% to one-third of all asthmatic subjects answer “yes” to the question: “Are your asthmatic symptoms worse at work?” (Blanc and Toren 1999; Johnson et al. 2000). Asthma in the workplace (AWP) encompasses several entities (Fig. 18.1) (Vandenplas and Malo 2003; Bernstein et al. 2006). First, some workplaces can cause asthma, mostly in subjects who, before starting to work, reported no respiratory symptoms. This condition is labelled “occupational asthma” (OA). Two causal mechanisms are implicated. Workers may develop an “allergy” to a product present at work or develop asthmatic symptoms after accidental inhalation of a product generated at abnormally high concentrations. Second, asthmatic subjects may report that their symptoms are aggravated or exacerbated at work although the workplace is not the cause of asthma. Third, several variants of asthma related to the workplace have been described. For instance, some workers in aluminium potrooms develop symptoms that share features of symptoms experienced by asthmatic subjects. Also, a condition that is called occupational eosinophilic bronchitis reproduces the pathologic but not the lung function features of OA.

Asthma in apprentice workers The birth cohort parallel: Using apprentices as a powerful cohort design for studying occupational asthma

This chapter presents a review of longitudinal studies of apprentices in trades and professions entailing substantial risks for the development of occupational asthma (OA). Prospective studies of OA enable the assessment of host characteristics before apprentices/workers enter a particular workforce, thus before being exposed to a suspected etiological agent, as well as the early detection of sensitization to a specific work-related antigen and the evaluation of bronchial responsiveness before onset of symptoms of asthma. Since 1973, several cohort studies have been conducted in Europe and Canada among apprentices exposed to high- and low-molecular-weight agents. The investigated outcomes were, apart from OA, work-aggravated asthma, bronchial hyperresponsiveness, work-related symptoms and specific sensitization. The rate of onset of the relevant outcomes was high even after 1 year of training; the implications for setting timing of surveillance programs would be to screen for sensitization and symptoms in the first 2–3 years of apprenticeship. Several host factors assessed at baseline were identified as risk factors for the incidence of work-related outcomes. However, more investigations are needed to explore the extent to which the risk of work-related allergy and asthma increases with exposure characteristics during apprenticeship. Directions for research in the existing cohorts and in future ones are suggested.

Chapter 36 – Occupational Agents

Publisher Summary Occupational agents (OA) is a disease characterized by variable airflow limitation and/or airway hyperresponsiveness and/or inflammation due to causes and conditions attributable to a particular occupational environment and not to stimuli encountered outside the workplace. Over 300 agents in the workplace have been implicated in causing asthma. The agents can be divided into two groups according to the pathogenic mechanisms: those that give rise to asthma by immunological mechanisms and those by nonimmunological mechanisms. Agents in the former group can cause asthma by immunoglobulin (Ig)E-dependent or IgE-independent mechanisms. Irritant-induced asthma (IIA) is a type of OA caused by an apparently nonimmunological mechanism. Many patients may have been exposed to multiple sources, and the relative contributions of each may be impossible to disentangle. COPD is the symptomatic and functional consequence of chronic exposure to these polluted air sources. Therefore, it seems appropriate to pose a definition for occupational COPD that allows it to coexist with “smoking-induced COPD” or “urban air pollution-induced COPD.” Asthma is a common respiratory occupational ailment. Whereas improvement in diagnostic tools and pathophysiological mechanisms still need to be considered, emphasis should be put on prevention programs through identification and application of permissible respirable levels and of affected subjects at an early stage of sensitization or disease to prevent long-term sequelae of permanent asthma.