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. 2017 Apr 20;2017(4):CD009674. doi: 10.1002/14651858.CD009674.pub2

Interventions for primary prevention of occupational asthma

Stefania Curti 1,✉, Stefano Mattioli 1, Alberto Baldasseroni 2, Andrea Farioli 3, Francesca Zanardi 3, Vittorio Lodi 4, Gerda J de Groene 5, David C Christiani 6, Francesco S Violante 3
PMCID: PMC6478241

Abstract

This is a protocol for a Cochrane Review (Intervention). The objectives are as follows:

To evaluate the effect of interventions aimed at preventing the onset of occupational asthma among workers exposed to asthmagens in occupational settings. We will compare the actual intervention with an alternative intervention, or no intervention. We will evaluate asthma symptoms, lung function and measures of exposure to asthmagens.

Background

Description of the condition

Occupational asthma refers to new‐onset asthma (or recurrence of previously quiescent asthma, i.e. asthma as a child or in the distant past that has been in remission) caused by workplace exposures (Tarlo 2008). This form of asthma is distinct from work‐exacerbated asthma, which refers to asthma triggered by various work‐related factors in workers who are known to have pre‐existing or concurrent asthma (i.e. asthma that is occurring at the same time but is not caused by workplace exposures) (Tarlo 2008).

Occupational asthma can be induced by sensitisation to a specific substance (sensitiser‐induced occupational asthma) or by exposure to an inhaled irritant at work (irritant‐induced occupational asthma, which includes reactive airways dysfunction syndrome) (Tarlo 2008). Among these two major patterns, a much higher incidence of sensitiser‐induced occupational asthma than irritant‐induced occupational asthma has been reported (Ameille 2003; Latza 2005; Vandenplas 2005).

Although occupational asthma is largely under‐recognised, especially in developing countries (Jeebhay 2007; Mbaye 2004), it is the most frequently reported occupational lung disease in industrialised countries (Elder 2004; McDonald 2000; Orriols 2006) and the second most common in developing countries (Hnizdo 2001; Syabbalo 1991). It was estimated that 38,000 deaths (23,000 men and 15,000 women) and 1.6 million DALYs (disability‐adjusted life years) result from occupational asthma each year (Driscoll 2005). Moreover, a recent systematic review estimates that 16.9% of all adult‐onset asthma is caused by occupational exposures (Toren 2009).

Causative agents (or 'asthmagens') of occupational asthma can be classified into high molecular weight agents (for example, cereal flours, grain dust, animal epithelia and latex proteins) and low molecular weight agents (for example, diisocyanates, welding fumes and aldehydes) (Malo 2009; Mapp 2005; Quint 2008).

Description of the intervention

Primary prevention of occupational asthma is aimed at avoiding the insurgence of new cases of asthma caused by agents present in the workplace.

The most straightforward way to achieve primary prevention is to remove or reduce exposure to asthmagens. There are different levels at which it is possible to act to modulate exposure, with different degrees in priority. In order to choose the most preferable way to prevent asthma, the hierarchy of controls should be followed. Briefly, the ways of controlling exposure can be summarised as follows (from the most preferred to the least preferred method).

  1. Elimination of the agent or compound.

  2. Substitution with a less sensitising agent.

  3. Engineering controls.

  4. Administrative controls.

  5. Personal protective equipment, training and education.

The elimination or substitution of asthmagens is the most preferred way to prevent occupational asthma, although it may not often be practical. This approach implies the possibility of changing production cycles. The feasibility of such a dramatic approach often relies on technological changes. An example of elimination is the adoption of digital imaging in radiology which made it possible to remove many chemical compounds from radiology units (Liss 2003). As regards substitution, the switch from glutaraldehyde to other chemicals less likely to sensitise (like ortho‐phthalaldehyde for the sterilisation of medical instruments), could be a suitable example (Fujita 2006).

If elimination or substitution are not feasible, engineering controls could be used to reduce (or virtually eliminate) exposure. For instance, it has been reported that encapsulation of enzymes reduced exposure among detergent production workers (Schweigert 2000). Moreover, the use of robots in enclosed settings, in addition to separated and ventilated areas, could be another method of reducing exposure to asthmagens (e.g. diisocyanates in foam‐making plants) (Tarlo 2005).

Administrative controls are often feasible but are less preferable than the previously cited measures. In practice, this control method consists of reducing the number of workers exposed, or the duration of exposure. Job rotation or adoption of rest periods could diminish cumulative exposure, while shift or location changes are more suitable for secondary prevention.

When it is not possible to control environmental exposure, personal protective equipment must be provided to workers in addition to specific training on their use (although this is at the bottom of the hierarchy of primary prevention measures). Unfortunately, the compliance of workers to the use of protective equipment often turns out to be quite low (Macfarlane 2008). Workers' training has been indicated as a possible determinant of risk of occupational asthma, as it could modulate the exposure of workers to asthmagens (Ricciuto 2006). Since an alarming level of misunderstanding or ignorance among managers has been reported on the knowledge of legislative requirements concerning employees’ exposure (Topping 1998; Topping 2001), the training and education of managers and employees might be effective in reducing the incidence of asthma (Cullinan 2003).

Apart from the hierarchy of controls, primary prevention of occupational asthma might also be achieved by excluding people with a high possibility of sensitisation from high risk jobs (obviously, in those countries where this is not considered illegal or unethical). In practice, pre‐employment physical examinations could be used to formulate a judgment on fitness to work based on an analysis of markers of susceptibility to occupational asthma. However, there is little empirical evidence supporting the goodness of criteria used to evaluate fitness for work (Serra 2007). In addition, ethical aspects should always be considered before adopting pre‐employment screening as a primary prevention strategy. On the other hand, a health examination before pupils enter professional training or education could lead to preventive measures. In fact, in performing an intervention at an early stage of a subject's working life, the balance between advantages (asthma prevention) and disadvantages (ethical implication) could be shifted in favour of screening.

Health monitoring during the working career could also play a role in primary prevention. Markers for early diagnosis of occupational asthma have been proposed (e.g. metalloproteinase‐9 for the early diagnosis of diisocyanate‐induced asthma) (Kim 2011) and they can be used to identify patients among exposed workers. However, early markers are probably still not appropriate for large scale populations, and they are only available for a few asthmagens. Typically, health monitoring is based on questionnaires, clinical examinations, routine blood tests and spirometries. In this scenario, health monitoring is a secondary prevention measure rather than a primary one, which is the focus of this review.

How the intervention might work

Elimination of an asthmagen from the workplace or its substitution with a non‐sensitizing (non‐irritant) or less‐sensitising agent are ideal approaches, as these methods should implicitly determine the disappearance of cases of occupational asthma due to this specific asthmagen. Unfortunately, elimination or substitution of an asthmagen is often not feasible. In addition, changing to a non‐sensitising agent may result in sensitisation to the newer agent (Woellner 1997). If complete removal is not possible, changes to reduce the exposure to a minimum are likely to reduce, if not completely eliminate, exposure to asthmagens.

Engineering controls might work by reducing, or virtually eliminating, the exposure to asthmagens (in the sense of their concentration), hence they should reduce the number and gravity of cases of occupational asthma (e.g. through encapsulation of enzymes in the detergent industry) (Schweigert 2000). Reducing the concentration of asthmagens, engineering controls consequently reduce the cumulative exposure as well.

The introduction of administrative controls might reduce the duration of exposure to asthmagens, hence reducing workers' cumulative exposure.

When environmental exposure cannot be reduced, improving workers’ personal protective equipment, as well as training and education are recommended. Wearing personal protective equipment will reduce workers' exposure to asthmagens (i.e. their concentration and consequently their cumulative exposure), and hence should reduce the number and gravity of cases of occupational asthma. The success of this intervention is strictly related to the compliance of workers, which often turns out to be quite low (Macfarlane 2008). However, training and education of managers and employees can increase the rate of compliance.

Why it is important to do this review

An overview on prevention of occupational asthma has been recently published by Tarlo and Liss (Tarlo 2010). This narrative article, in line with previous work by the same authors (Tarlo 2005), presented the different mechanisms that can be employed for primary, secondary and tertiary prevention.

In 2008, a review entitled Primary prevention of occupational asthma: identifying and controlling exposures to asthma‐causing agents was published in the American Journal of Industrial Medicine (Quint 2008). In contrast with the title, the review mainly dealt with the identification of possible asthma‐causing agents and did not report information on effectiveness of interventions.

In 2006, LaMontagne and colleagues presented a review on primary prevention of latex related sensitisation and occupational asthma (LaMontagne 2006). On the basis of the consistency of the findings (but without producing any quantitative assessment and also including studies not strictly referring to asthma (Jones 2004; Lee 2001)), the authors concluded that substitution of powdered latex gloves with low protein powder‐free natural rubber latex gloves or latex‐free gloves, greatly reduces asthma in healthcare workers. This article derived from a broader report available online (Sim 2005). In this text the authors presented a brief summary of intervention studies also for asthmagens other than latex.

Evidence based guidelines for the prevention, identification and management of occupational asthma were published in 2010, commissioned by the British Occupational Health Research Foundation (Nicholson 2010). In line with a previous review by the same authors (Nicholson 2005), there was no strong evidence for effectiveness of primary prevention interventions; the only moderate evidence was for reducing airborne exposure to sensitisers and for monitoring of specific IgE antibodies during health surveillance.

Recently, three Cochrane reviews related to occupational asthma have been published. Mahmud 2010 is a review on pre‐employment examinations for preventing occupational injury and disease in workers. In this review, the authors identified one study (De Looff 1992) showing a reduction in occupational asthma following the introduction of a bronchial challenge test in the pre‐employment examination.

The other two Cochrane reviews were published in 2011: one on workplace interventions for treatment of occupational asthma (De Groene 2011); the other on prevention of respiratory tract symptoms, infections and asthma by remediating buildings damaged by dampness and mould (Sauni 2011). In this last review, Sauni and colleagues identified two studies (Åhman 2000; Patovirta 2004) showing very low‐quality evidence that, after repairing a mould‐damaged school building, asthma‐related symptoms among teachers and school personnel decreased.

Despite the reviews mentioned above, a systematic review on interventions for primary prevention of occupational asthma, based on a sensitive search of high quality studies, within the framework of the Cochrane Collaboration is still lacking. We will exclude studies regarding pre‐employment examinations and building remediations from our review on primary prevention of occupational asthma, as this would constitute an overlap with the existing Cochrane reviews mentioned above (Mahmud 2010; Sauni 2011).

Objectives

To evaluate the effect of interventions aimed at preventing the onset of occupational asthma among workers exposed to asthmagens in occupational settings. We will compare the actual intervention with an alternative intervention, or no intervention. We will evaluate asthma symptoms, lung function and measures of exposure to asthmagens.

Methods

Criteria for considering studies for this review

Types of studies

We will include randomised controlled trials (RCTs) in this review. Since many intervention studies are conducted on a group level (often preventing a proper randomisation process), we will also consider controlled clinical trials (CCTs), controlled before‐and‐after (CBA) studies and interrupted time‐series (ITS) studies (according to the criteria of the Cochrane EPOC group) (EPOC).

Types of participants

Study participants will include male or female workers exposed to asthmagens. We will not apply any restrictions based on age or type of job activity. Hence, we will include studies conducted in all occupational sectors.

Types of interventions

We will include any type of intervention aimed at preventing occupational asthma among workers exposed to asthmagens.

Primary preventive interventions (excluding pre‐employment examinations) could be classified as follows.

  • Elimination or substitution of the asthmagens

  • Engineering controls

    • Process enclosure

    • Ventilation

    • Process or equipment modification

    • Other

  • Administrative controls

    • Job rotation

    • Rest periods

    • Shift or location changes

    • Other

  • Personal protective equipment (for the worker)

    • Personal respiratory protective devices

    • Other personal protective devices

  • Implementation of educational programmes and training (for the worker)

Types of outcome measures

Primary outcomes

We will include studies reporting data on asthma symptoms and lung function measurements as outcome measures.

For asthma symptoms, we will consider the following options as equally valid outcome measurements.

  • Physician’s diagnosis based on interview and clinical examination.

  • Physician’s diagnosis as reported by workers.

  • Asthma symptoms collected by validated questionnaire.

  • Prescription of medication for asthma.

For lung function measurements, we will consider the following tests as valid measures of asthma symptoms (Tarlo 2008).

  1. Specific inhalation challenge.

  2. Serial lung function testing.

  3. Non‐specific bronchial provocation testing.

We will also include studies that report data on measures of exposure to asthmagens (personal or environmental, or both) as an outcome measure, because if exposure is lower, the likelihood of asthma developing will also be reduced. We will consider all objective measurements as a valid measure of exposure.

Search methods for identification of studies

We will search different sources of research literature to locate intervention studies aimed at preventing occupational asthma among workers in occupational settings.

To identify potentially pertinent articles on occupational asthma, we will adopt the ‘more sensitive’ search strategy developed by Mattioli 2010, together with terms referring to asthma. Of note, having explored other possible terms (airflow limitation, airflow obstruction, reactive airway dysfunction syndrome, RADS, shortness of breath, whistling, “bronchial dilator”, sensitiz* and sensitis*) and having excluded them, we decided to include the following terms in our searches: asthm* (hence automatically including, among others, asthma and asthmatic), wheez*, bronchospas*, “airway hyperresponsiveness”, “airway responsiveness”, “bronchial hyperresponsiveness”, “bronchial responsiveness”, bronchodilator, “bronchial spasm” and bronchial spasm entered as a MeSH term.

To be more sensitive in locating studies of occupational health interventions, we will adopt the “intervention part” (i.e. the first part) of the ‘most sensitive’ search strategy proposed by the Occupational Safety and Health Review Group (Verbeek 2005).

To locate RCTs, we will use the most sensitive and precision‐maximising search strategy as recommended by the Cochrane Collaboration (Chapter 6 of the Cochrane Handbook for Systematic Reviews of Interventions) (Higgins 2011).

We will not restrict the searches by date, language or publication type. If necessary, we will organise translation of papers in languages other than English, French, Italian and Spanish.

See Appendix 1 for the search strategy to be used for MEDLINE. We will adapt this search strategy for other databases accordingly.

Electronic searches

We will search the following electronic databases.

  • Cochrane Occupational Safety and Health Group's Specialised Register

  • Cochrane Airways Group's Trials Register

  • Cochrane Central Register of Controlled Trials (CENTRAL)

  • MEDLINE through PubMed

  • EMBASE

  • PsycINFO

Through the Canadian Centre of Occupational Health and Safety (CCOHS), we will search the following OHS reference databases.

  • OSHLINE

  • NIOSHTIC

  • NIOSHTIC‐2

  • HSELINE

  • CISILO

  • Canadiana

We will search the following websites to identify additional studies.

  • DARE (Database of Abstracts of Reviews of Effects) produced by the Centre for Reviews and Dissemination, University of York. Available at http://www.crd.york.ac.uk

  • OpenSIGLE (System for Information on Grey Literature in Europe), which collects grey literature produced in the European Community. Available at http://opensigle.inist.fr

  • Health‐evidence.ca, which is an online registry of systematic reviews on the effectiveness of public health and health promotion interventions. Available at http://health‐evidence.ca

Searching other resources

We will look for additional studies by checking the reference lists of relevant articles. We will contact experts in the field to identify additional unpublished materials.

Data collection and analysis

Selection of studies

We will divide the identified studies between three pairs of authors (SC, SM; AB, AF; FZ, VL) in order to examine each reference twice.

Each author will independently screen titles and abstracts of the articles retrieved by the search strategy in order to identify the articles for potential inclusion. We will discuss disagreements within pairs until consensus is reached. We will obtain the full text of all articles potentially qualified for inclusion and the same pairs of authors who screened titles and abstracts will assess whether each full article meets the inclusion criteria. We will discuss disagreements within pairs until consensus is reached. If disagreement persists, another author (FSV) will make the final decision.

Data extraction and management

Two authors (SM and AF) will independently extract data based on methods, characteristics of the study participants, type of interventions, outcomes and main results of the included studies.

We will resolve disagreements by discussion. If disagreement persists, a third author (AB) will make the final decision.

If information is insufficient for data to be extracted, we will contact the authors of the study to request additional information. If this fails, we will have to exclude the study due to insufficient information.

Assessment of risk of bias in included studies

Two authors (SM and AF) will independently assess the risk of bias of the included studies.

We will evaluate the validity of the randomised trials using the Cochrane Collaboration’s tool for assessing risk of bias as described in Chapter 8 of the Cochrane Handbook for Systematic Reviews of Interventions (Higgins 2011). We will grade each study for risk of bias in each of the following seven domains, with ratings of low risk of bias, high risk of bias or uncertain risk of bias.

  1. Random sequence generation.

  2. Allocation concealment.

  3. Blinding of participants and personnel.

  4. Blinding of outcome assessment.

  5. Incomplete outcome data.

  6. Selective reporting.

  7. Other sources of bias.

For non‐randomised studies, we will use the checklist developed by Downs 1998 to measure the quality of the studies. The criteria consist of:

  1. reporting quality (ten items);

  2. external validity (three items);

  3. internal validity in terms of bias (seven items); and

  4. internal validity in terms of confounding and selection bias (six items).

We will score each item as 'yes', 'no' or 'unable to determine'.

For ITS studies, we will use the quality criteria developed by the Cochrane EPOC group (EPOC). The quality assessment for ITS designs consists of:

  1. protection against secular changes (three items);

  2. protection against detection bias (two items);

  3. completeness of data set (one item); and

  4. reliable primary outcome measures (one item).

We will answer each item as 'done', not clear' or 'not done'.

We will resolve disagreements by discussion. If disagreement persists, a third author (AB) will make the final decision.

Measures of treatment effect

We will plot the results of each RCT as point estimates, such as risk ratios (RRs) for dichotomous outcomes, mean and standard deviation (SD) for continuous outcomes, or other type of data as reported by the authors of the studies. When the results cannot be plotted, we will describe them in the ‘Characteristics of included studies’ table, or enter the data into Additional tables.

For ITS studies, we will extract data from the original papers and re‐analyse them according to the recommended methods for analysis of ITS designs for inclusion in systematic reviews (Ramsay 2003).

Unit of analysis issues

For studies that employ a cluster‐randomised design and that report sufficient data to be included in the meta‐analysis but do not make an allowance for the design effect, we will calculate the design effect based on a fairly large assumed intra‐cluster correlation of 0.10. We base this assumption of 0.10 being a realistic estimate by analogy on studies about implementation research (Campbell 2001). We will follow the methods stated in the Cochrane Handbook for Systematic Reviews of Interventions (Higgins 2011) for the calculations.

Dealing with missing data

We will contact authors to obtain data missing in their reports that are needed for meta‐analysis.

If statistics are missing, such as SDs or correlation coefficients and they cannot be obtained from the authors, we will calculate them from other available statistics such as P values according to the methods described in the Cochrane Handbook for Systematic Reviews of Interventions (Higgins 2011).

Assessment of heterogeneity

We will assess clinical homogeneity based on similarity of population, intervention, outcome and follow‐up. We will consider populations as similar when they are exposed to either high molecular weight or low molecular weight substances, regardless of occupation or type of work. We will consider interventions as similar if they fall into one of the pre‐defined categories of interventions (as stated in the paragraph of criteria for including studies). We will consider the various asthma outcome categories as different. For the exposure outcomes we will calculate the effect of the intervention as a percentage decrease from the baseline value. We will consider this decrease of exposure as a similar outcome regardless of the type of exposure. We will regard follow‐up times of less than three months, three months to one year and more than one year as different.

In addition, we will test for statistical heterogeneity by means of the Chi2 test as implemented in the forest plot in Review Manager 5.1 software (RevMan 2011). We will use a significance level of P < 0.10 to indicate whether there is a problem with heterogeneity. Moreover, we will quantify the degree of heterogeneity using the I2 statistic, where an I2 value of 25% to 50% indicates a low degree of heterogeneity, 50% to 75% a moderate degree of heterogeneity and > 75% a high degree of heterogeneity (Higgins 2003).

Assessment of reporting biases

We will reduce the effect of reporting bias by including studies and not publications in order to avoid the introduction of duplicated data (i.e. two articles could represent duplicate publications of the same study). Following the Cho 2000 statement on redundant publications, we will attempt to detect duplicate studies and, if more articles report on the same study, we will extract data only once. We will prevent location bias by searching across multiple databases. We will prevent language bias by not excluding any article based on language. If sufficient data are available, we will assess publication bias by using a funnel plot.

Data synthesis

We will pool data from studies judged to be clinically homogeneous using Review Manager 5.1 software (RevMan 2011). If sufficient data are available, we will perform meta‐analyses. When studies are statistically heterogeneous, we will use a random‐effects model; otherwise we will use a fixed‐effect model. When using the random‐effects model, we will conduct a sensitivity check by using the fixed‐effect model to reveal differences in results. We will include a 95% confidence interval (CI) for all estimates.

For ITS studies, we will use the standardised change in level and change in slope as effect measures. We will perform meta‐analyses using the generic inverse variance method. We will enter the standardised outcomes into Review Manager 5.1 software as effect sizes, along with their standard errors (SEs).

We will use the GRADE approach as described in the Cochrane Handbook for Systematic Reviews of Interventions (Higgins 2011) and as implemented in the GRADEPro 3.2 software to present the quality of evidence and ‘Summary of findings’ tables.

The downgrading of the quality of a body of evidence for a specific outcome will be based on five factors.

  1. Limitations of study.

  2. Indirectness of evidence.

  3. Inconsistency of results.

  4. Imprecision of results.

  5. Publication bias.

The GRADE approach specifies four levels of quality (high, moderate, low and very low).

Subgroup analysis and investigation of heterogeneity

If feasible, we will perform subgroup analyses based on:

  1. the proportion of atopic subjects among study participants;

  2. type of allergen (e.g. low or high molecular weight);

  3. occupational sector (e.g. health sector); and

  4. type of asthmagen (sensitiser versus irritant agent).

Sensitivity analysis

We will a conduct a sensitivity analysis to test the robustness of our meta‐analysis results by omitting studies judged to have a high risk of bias.

Acknowledgements

We would like to thank Jos Verbeek and Jani Ruotsalainen of the Cochrane Occupational Safety and Health Review Group for the training and guidance during the first phase of this review.

Appendices

Appendix 1. Search Strategy for MEDLINE through PubMed

#1
((asthm* OR wheez* OR bronchospas* OR “airway hyperresponsiveness” OR “airway responsiveness” OR “bronchial hyperresponsiveness” OR “bronchial responsiveness” OR bronchodilator OR “bronchial spasm” OR “bronchial spasm”[MH]) NOT (animals[mh] NOT humans [mh]))
#2
(occupational diseases[MH] OR occupational exposure[MH] OR occupational exposure*[TW] OR "occupational health" OR "occupational medicine" OR work‐related OR working environment[TW] OR at work[TW] OR work environment[TW] OR occupations[MH] OR work[MH] OR workplace*[TW] OR workload OR occupation* OR worke* OR work place*[TW] OR work site*[TW] OR job*[TW] OR occupational groups[MH] OR employment OR worksite* OR industry)
#3
(effect*[tw] OR control[tw] OR controls*[tw] OR controla*[tw] OR controle*[tw] OR controli*[tw] OR controll*[tw] OR evaluation*[tw] OR program*[tw])
#4
(randomized controlled trial[pt] OR controlled clinical trial[pt] OR randomized[tiab] OR placebo[tiab] OR clinical trials as topic[mesh:noexp] OR randomly[tiab] OR trial[ti] NOT (animals[mh] NOT humans [mh]))
#5
#1 AND #2 AND #3 AND #4
#6
#1 AND #2 AND #3 NOT #4
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What's new

Date Event Description
20 April 2017 Amended This protocol has been withdrawn due to the author team's practical difficulties in carrying out the review.
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Contributions of authors

SC, SM, AB and AF conceived and designed the review. SC co‐ordinated the review process. SC wrote the protocol along with SM, AB, AF, FZ and VL. SC, SM, AB and AF developed the search strategy. GdG, DC and FV provided comments on the review.

Sources of support

Internal sources

  • Section of Occupational Medicine, Department of Internal Medicine, Geriatrics and Nefrology, University of Bologna, Italy.

External sources

  • Cochrane Occupational Safety and Health Review Group, Finland.

Declarations of interest

None known.

Notes

This protocol has been withdrawn due to the author team's practical difficulties in carrying out the review.

Withdrawn from publication for reasons stated in the review

References

Additional references

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