Background
Description of the condition
Work-related rhinitis and rhinosinusitis are major problems for workers worldwide. Rhinitis is defined by the British Society for Allergy and Clinical Immunology as an inflammatory condition of the nose, which is characterised by intermittent or persistent symptoms consisting of nasal congestion, sneezing, rhinorrhoea and itching (Scadding 2008; Zhao 2012). Work-related rhinitis (WRR), also known as occupational rhinitis, is caused by conditions attributable to a work-specific environment rather than stimuli encountered outside the workplace; it can be categorised into onset WRR or an exacerbation of pre-existing rhinitis due to workplace exposures (Moscato 2009). For its part, rhinosinusitis is defined as an inflammatory condition of the nose and paranasal sinuses characterised by nasal blockage, obstruction, congestion or discharge. It may be accompanied by facial discomfort or reduced sense of smell, supported by endoscopic signs of nasal polyps, mucopurulent discharge or mucosal oedema, primarily from the middle meatus. Mucosal changes within the osteomeatal complex and sinuses may also be apparent in a CT scan (Fokkens 2012). Rhinitis and rhinosinusitis are part of the same aetiological spectrum, and their occupational forms, WRR and work-related rhinosinusitis (WRRS), cause increased sickness absence, loss of productivity and increased medical expenses. Work productivity losses attributable to allergic rhinitis in the USA in 1995 were estimated to be between USD 2.4 billion and USD 4.6 billion (Crystal-Peters 2000). As WRR and WRRS involve both allergic and non-allergic components, and not all allergic rhinitis is due to WRR or WRRS, those estimates are of limited usefulness in estimating the cost of WRR and WRRS. Estimates for the overall cost burden of WRR and WRRS have not been reported.
Although the prevalence of WRR and WRRS varies from 2% to 87% across settings, depending on the presence of different workplace risk factors, it is consistently reported to be more common than occupational asthma, another well-known illness on the same spectrum (Moscato 2009; Siracusa 2000). Certain occupations are reported to have increased risk of WRR, including furriers, bakers, livestock breeders, food-processing workers, veterinarians, farmers, electronic or electrical products assemblers, boat builders and workers in the detergent industry (Elliott 2005; Gautrin 2001; Hytonen 1997; Sarlo 2003; Zhao 2012).
There are several aetiological categories of rhinitis and rhinosinusitis (Slavin 2010).
Irritational: non-specific inflammation of the nose that has no immunologic or allergic basis. Exposure to substances such as cigarette smoke, formalin and capsaicin results in the release of substance P, a sensory transmitter that triggers a neurogenic inflammatory response. This type of WRR is seen in people who work in an enclosed environment and who are exposed to materials such as paints, talcum and coal dust.
Corrosive: the result of exposure to a high concentration of irritating and soluble chemical gases, causing sufficient nasal inflammation that the mucosa may break down and ulcerate, similar to a chemical burn. Common causes include exposure to substances with high water solubility and chemical reactivity, such as chlorine, sulphur dioxide, ammonia and formaldehyde. Corrosive WRR can lead to permanent changes in physiological functions of the nose, such as loss of smell.
Immunologic: allergic response that may or may not be IgE-mediated, with resultant early and late nasal and sinus reactions, respectively.
Annoyance: incident in individuals with a heightened olfactory awareness to substances such as perfumes and detergents. The likelihood of developing annoyance reactions is increased by nasal polyposis, sinusitis, smoking and overuse of over-the-counter nasal decongestants or illicit drugs. However, the category of annoyance is not included consistently in all definitions (Moscato 2009), as other causes such as psychosocial factors are considered likely to contribute to this reaction.
Certain high-molecular weight particles have a tendency to elicit an allergic response (Ameille 2013). An example of this is psyllium, a major component of popular bulk-forming laxatives affecting people who work in laxative-producing factories or nurses who dispense the medication. Similarly, guar gum is commonly reported as a cause of WRR in the food and carpet industries. Carpet workers may become sensitive to guar gum through its use as a fixator for dye and fibre as well as an insulator in rubber cables.
Description of the intervention
Because WRR and WRRS are part of a spectrum, they are likely to respond similarly to interventions. Primary prevention involves eliminating or controlling exposure to sensitising agents in order to prevent individuals from developing the condition, while secondary prevention applies many of the same interventions as a way to control or treat people who have already acquired WRR or WRRS. While elimination of the sensitising agent is the ideal intervention, reducing occupational exposure, for example through the use of personal protective equipment like respirators, should be considered if this is not an option.
The Hazard Identification Risk Assessment and Risk Control (HIRARC) framework is commonly used as a basis for occupational health and safety measures, and it generally prioritises risk control options in the following orders; elimination of the agent or compound; substitution with a less sensitising agent; engineering controls;administrative controls; training and education; and personal protective equipment. Curti 2012 have applied a very similar formula to classify measures to control occupational asthma, whose aetiology overlaps considerably with WRR and WRRS as a disease entity. Thus, this classification constitutes a good basis for our Cochrane review.
How the intervention might work
Eliminating workplace exposure to sensitising agents or substituting these agents with non-sensitising agents theoretically would be the most effective approaches to minimising the incidence of work-related rhinitis, and it is known to prevent WRR and WRRS and work-related asthma (Wright 2014). However, total elimination is usually hard to achieve because changing industrial production relies on technological changes. Curti 2012 were able to provide a few appropriate examples, including the removal of some chemical compounds from radiology units when digital imaging came into use (Liss 2003) and the substitution of glutaraldehyde with other chemicals less likely to sensitise in the sterilisation process of medical instruments (Fujita 2006). If elimination or substitution are not feasible, engineering controls including process enclosure, ventilation, process or equipment modification can also reduce exposure. One good example is the encapsulation of enzymes in detergent production (Schweigert 2000).
Administrative controls, such as job rotation or adoption of rest periods, can limit the number of exposed workers or their duration of exposure. At the same time, manager and staff training and education in workplace safety practices and in the selection and proper use of respiratory protective devices (Dressel 2007; HSE 2013), can increase compliance with protective measures (Sakunkoo 2012) and reduce WRR and WRRS. Logically, training should also be accompanied by the provision of personal protective equipment to reduce workers’ exposure to sensitising agents (Sakunkoo 2012).
Primary prevention of WRR or WRRS might also be achieved by excluding people with a high possibility of sensitisation from high-risk jobs. For example, a Cochrane review on pre-employment examinations found that the inclusion of a bronchial challenge reduced occupational asthma (Mahmud 2010).
Why it is important to do this review
Rhinitis is a difficult condition to treat. In published Cochrane reviews on various medical interventions that mainly target the individuals in treating allergic rhinitis and related illnesses, some show a benefit (Calderon 2007; Radulovic 2010; Taramarcaz 2003), while others are inconclusive (Cheng 2006; Harvey 2007; Mishra 2012; Nasser 2010; Nurmatov 2012; Sacks 2011).
There are several relevant non-Cochrane reviews published over the last 12 years that cover part of our topic.
Balkissoon 2002 and Chan 2009 provide a general overview of work-related rhinitis, including diagnosis and management strategies. However, the papers did not evaluate a specific intervention or a type of management strategy adapted to the workplace. There was also a lack of sufficient clarity on the crucial steps in a systematic review. Hellgren 2008 is also an overview paper, but it focuses on "new insights on occupational rhinosinusitis, including the impact on health-related quality of life". Zacharek 2004 gives an overview on the pathophysiology of persistent rhinosinusitis at the molecular level.
Marple 2009 provides a relatively recent and comprehensive overview of chronic rhinosinusitis, including work-related rhinosinusitis. However, there was no specific intervention evaluated in accordance to the steps required in a systematic review.
In recent years, two very similar reviews on occupational rhinitis have been published by the European Academy of Allergy and Clinical Immunology (EAACI) (EAACI 2008; Moscato 2009). Their key message relates to primary prevention of occupational rhinitis by focusing on reducing exposure to potentially sensitising agents. As examples of effective prevention resulting from reduction of exposure, the reviews mention strategies used in enzyme detergent producers, platinum refining workers, laboratory workers and health care workers using latex gloves.
The review by Vandenplas 2010 summarises the scientific evidence on sensitiser-induced occupational asthma and rhinitis that has been published during the past five years. It includes the findings and recommendations of the above-mentioned reviews by EAACI Task Force on Occupational Rhinitis (EAACI 2008; Moscato 2009).
From the above, it appears that to date, there has not been a Cochrane review that assesses the effect of workplace interventions on the incidence and severity of work-related rhinitis and rhinosinusitis. However, there is one Cochrane review that deals with pre-employment examinations for preventing occupational injury and disease in workers (Mahmud 2010). There is another Cochrane review on prevention of respiratory tract symptoms, infections and asthma by remediating buildings damaged by dampness and mould (Sauni 2015). Because the focus of these two published Cochrane reviews is at least partly the same as in our review, we will exclude studies on pre-employment examinations and building remediations (Mahmud 2010; Sauni 2015) from our review on primary prevention of WRR or WRRS. Another review in progress will examine the effects of workplace interventions as a treatment for WRR and WRRS.