Evaluation of the efficacy of a web-based work-related asthma educational tool

<p><i>Background</i>: Work-related asthma (WRA) has been estimated to account for 15–20% of adult asthma cases. Studies have indicated that a substantial number of asthma patients have inadequate knowledge of work-related effects on their disease, which may contribute to suboptimal asthma control. A Canadian web-based educational tool on WRA was developed to address this knowledge gap in the population. <i>Objective</i>: To evaluate the effectiveness of this web-based tool. <i>Methods</i>: Participants were recruited prior to a routine visit at a tertiary care asthma clinic in Toronto. A brief WRA knowledge questionnaire was developed and administered immediately before and after using of the web-based educational tool, and one year later. <i>Results</i>: The study sample (<i>N</i> = 34) was mostly female (68%) with a mean age of 50.7 (SD, 17.2). Participants demonstrated significant improvement in questionnaire scores following interaction with the tool. The mean score increased from 76% (SEM = 2.1) to 84% (SEM = 1.7) (<i>p</i> = 0.001). On average, scores improved on 12 of the 13 questionnaire items. A 1-year follow-up of a sample of 19 participants demonstrated a slight reduction in mean scores, from 86% (SEM = 1.9) to 84% (SEM = 1.9), but still demonstrated a trend towards a higher score than the baseline (78%; SEM = 2.9; <i>p</i> = 0.08). <i>Conclusions</i>: Our findings suggest that the educational tool has a positive effect on WRA knowledge, and that knowledge may be retained long-term. Future studies are needed in non-tertiary care clinic populations which may possess less baseline knowledge of WRA.</p

Genetic variants in <i>TNF</i><b>α</b>, <i>TGFB1, PTGS1</i> and <i>PTGS2</i> genes are associated with diisocyanate-induced asthma

<div><p></p><p>Diisocyanates are the most common cause of occupational asthma, but risk factors are not well defined. A case-control study was conducted to investigate whether genetic variants in inflammatory response genes (<i>TNFα, IL1α, IL1β, IL1RN, IL10, TGFB1, ADAM33, ALOX-5, PTGS1, PTGS2</i> and <i>NAG-1/GDF15</i>) are associated with increased susceptibility to diisocyanate asthma (DA). These genes were selected based on their role in asthmatic inflammatory processes and previously reported associations with asthma phenotypes. The main study population consisted of 237 Caucasian French Canadians from among a larger sample of 280 diisocyanate-exposed workers in two groups: workers with specific inhalation challenge (SIC) confirmed DA (DA⁺, <i>n</i> = 95) and asymptomatic exposed workers (AW, <i>n</i> = 142). Genotyping was performed on genomic DNA, using a 5′ nuclease PCR assay. After adjusting for potentially confounding variables of age, smoking status and duration of exposure, the <i>PTGS1</i> rs5788 and <i>TGFB1</i> rs1800469 single nucleotide polymorphisms (SNP) showed a protective effect under a dominant model (OR = 0.38; 95% CI = 0.17, 0.89 and OR = 0.38; 95% CI = 0.18, 0.74, respectively) while the <i>TNFα</i> rs1800629 SNP was associated with an increased risk of DA (OR = 2.08; 95% CI = 1.03, 4.17). Additionally, the <i>PTGS2</i> rs20417 variant showed an association with increased risk of DA in a recessive genetic model (OR = 6.40; 95% CI = 1.06, 38.75). These results suggest that genetic variations in <i>TNFα, TGFB1, PTGS1</i> and <i>PTGS2</i> genes contribute to DA susceptibility.</p></div