Workplace irritant exposures: Do they produce true occupational asthma?
To describe the features of irritant-induced asthma and discuss the diagnosis in relation to differing workplace irritant exposures and symptomatic responses.
A review of MEDLINE articles on this topic from January 1, 1985, through December 31, 2001 was performed.
The author selected relevant articles for inclusion in the review.
Many reports indicate that unintentional high-level respiratory irritant exposures can induce the new onset of asthma. Cases that meet strict criteria for a syndrome of irritant-induced asthma, termed reactive airways dysfunction syndrome, can be diagnosed with relative certainty. Several reports of irritant-induced asthma, especially prevalence studies, have relied on historical data or have otherwise modified the reactive airways dysfunction syndrome criteria for diagnosis (eg, expanding the definition to include the symptom onset several days after exposure). Such modifications, or inclusion of cases with incomplete documentation, likely increase diagnostic sensitivity but may reduce the certainty of diagnosis for individual cases. Expanding exposure criteria to moderate or long-term low-level irritant exposures causes difficulty in excluding transient irritant exacerbation of underlying asthma or coincidental onset of asthma during working life. Although recent population studies suggest a greater relative risk of asthma in occupations with expected low-to-moderate respiratory irritant exposures, currently no objective laboratory tests exist to exclude coincidental asthma in such patients.
Irritant-induced asthma can be produced by high-level unintentional respiratory irritant exposures at work or outside the workplace. Lower levels of exposure to respiratory irritants at work are more common, and additional studies are needed to determine the airway effects of such exposures.
Available from: Mats G Fredrikson
- "This can be described as a new onset of an –irritant-induced asthma within 24 hours after a single exposure to high concentrations of a respiratory irritant gas, fumes or vapour (Tarlo 2003). Subsequently a discussion has arisen about the existence of a low-level RADS (Kipen et al. 1994; Tarlo 2000), as well as the idea of a " not so sudden " irritant-induced asthma (Banks 2001). "
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ABSTRACT: This case-control study was undertaken to elucidate the controversy concerning whether low-level, long-term exposure to non-sensitising air pollution at workplaces may cause asthma.
A case-control study of 192 adult-onset asthma cases aged 20-65 years and 323 controls was conducted in the southeast of Sweden. Cases were identified from computerised registers from the region, diagnosed 2000-2004 and diagnoses were confirmed via medical files. Referents were randomised from the population register of the region. Exposure was monitored by a 16-page questionnaire. Special attention was devoted to identifying and in the final analyses excluding subjects exposed to sensitising agents.
Three years or more of occupational exposure to air pollution from dust, smoke, fumes or vapours before the year of diagnosis by analyses adjusting for age yielded an increased risk for asthma (OR = 2.3, 95% CI 1.2-4.2) in men, while in women, no risk was seen. In a multiple logistic regression analysis in men without allergy in childhood, a significant risk was seen (OR = 2.8, 95% CI 1.07-7.4), when subjects exposed to identified allergens were excluded. In women, no excess risk was observed from occupational air pollution.
The results of this study support an association between occupational exposure to low level non-sensitising air pollution and adult-onset asthma in men.
Available from: PubMed Central
- "Some researchers have proposed expanding the definition of RADS to include more than one short-term high-level exposure and onset of symptoms up to 7 days after exposure; others go even further to include chronic exposure to low levels of irritants. However, these suggestions have not been widely accepted as an expansion of the definition and would make it even more difficult to differentiate RADS from other causes of airway hyperresponsiveness [18,19]. "
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ABSTRACT: : Work-related asthma is asthma that is caused or exacerbated by exposures at work. It is the most common form of occupational lung disease in developed countries. It has important impacts on the health and well-being of the affected individual, as well as consequences for society because of unemployment issues and workers' compensation claims. With ongoing exposure, occupational asthma can result in persistent airway hyperresponsiveness and, possibly, permanent disability for the individual. Thus, it is important for the clinician to be able to diagnose this disorder as quickly and accurately as possible. The evaluation of a patient with work-related asthma can be extensive. It includes obtaining a consistent history, identifying the cause in the workplace, and confirming the diagnosis with objective tests. After a diagnosis has been made, treatment must sometimes go beyond the medications used for nonoccupational asthma and include interventions to minimize or completely remove the individual from exposure to the causal agent if he or she has sensitizer-induced occupational asthma. In addition, once an individual has been identified with occupational asthma, steps should be taken to prevent the development of this disorder in other workers. The purpose of this article is to review the current literature and provide the clinician with a stepwise approach to the diagnosis and management of a patient with work-related asthma.
Available from: Maritta Jaakkola
- "For example, nicotine induces placental vasoconstriction, which leads to hypoxia of the fetus and consequently impaired maturation of the lungs. Irritant substances in ETS may induce chronic inflammation in the airways that could lead to a form of irritant-induced asthma (Tarlo 2003). In addition, animal studies and even some studies in children have suggested that in the presence of tobacco smoke exposure, hypersensitivity reactions to allergens are stronger. "
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ABSTRACT: Asthma is a multifactorial airway disease that arises from a relatively common genetic background interphased with exposures to allergens and airborne irritants. The rapid rise in asthma over the past three decades in Western societies has been attributed to numerous diverse factors, including increased awareness of the disease, altered lifestyle and activity patterns, and ill-defined changes in environmental exposures. It is well accepted that persons with asthma are more sensitive than persons without asthma to air pollutants such as cigarette smoke, traffic emissions, and photochemical smog components. It has also been demonstrated that exposure to a mix of allergens and irritants can at times promote the development phase (induction) of the disease. Experimental evidence suggests that complex organic molecules from diesel exhaust may act as allergic adjuvants through the production of oxidative stress in airway cells. It also seems that climate change is increasing the abundance of aeroallergens such as pollen, which may result in greater incidence or severity of allergic diseases. In this review we illustrate how environmental tobacco smoke, outdoor air pollution, and climate change may act as environmental risk factors for the development of asthma and provide mechanistic explanations for how some of these effects can occur.
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