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The possibility of exhaled nitric oxide (eNO) in combination with lung function as a marker of airway inflammation produced by coal mining exposure was determined presuming that workers exposed to airborne hazards would possess different concentrations of eNO and decreased lung function indices, relative to control subjects recruited from the same area. The effect of smoking was also considered. A study (exposed) group comprising 186 male subjects (aged 19-58 yr) was recruited from Newcastle coal mining companies with 86 male subjects (aged 20-64 yr) from the same area, but working outside of the coal mining location, serving as controls. The parameters examined were eNO, lung function, and variables derived from an interview-administered questionnaire survey. After adjustment for age, body weight, and smoking status, no significant differences between exposed coal mining workers and controls were found for various lung function parameters. However, the exposed group was shown to have significantly lower concentrations of eNO. In the exposed group, forced expiratory volume in 1 s (FEV(1)), forced vital capacity (FVC), and FEV(1) (%) predicted were found to be significantly different between nonsmokers and smokers. The concentrations of eNO were not significantly different between smoking and nonsmokers within the exposed group. The consideration of nonsmokers alone showed that eNO was significantly lower in the exposed group compared to the control group. The consideration of smokers alone found that eNO was significantly lower in exposed subjects. In the exposed group, no significant association was detected between eNO levels and underground work duration but a significant negative association was shown between eNO and age. Data suggest that exposure to airborne hazards in coal mining is not significantly associated with lung function changes but is correlated with decreased eNO concentrations in exposed workers. While underground work duration was not found to be significantly associated with eNO concentrations in coal mining workers in this study, the potential for using eNO as a monitoring marker still exists and further studies are needed to establish its importance.

The prevalence of asthma symptoms varies markedly throughout the world. However, the asthma mechanisms involved are not defined. Studying the effects of migration can help identify the reasons for this geographic variation. The aims of this study were to examine the prevalence of asthma symptoms, airway hyperresponsiveness (AHR), and induced sputum eosinophils in adolescents who migrate to Australia. The study was conducted in Sydney, Australia, where adolescent students completed a video symptom questionnaire, hypertonic saline challenge, sputum induction, and allergy skin testing. The 211 students had widely different cultural backgrounds, including Asian, South Pacific, Middle Eastern, European, and African countries. Among adolescents who were migrants to Australia, the prevalence of asthma symptoms was higher than that reported using a similar methodology in their country of origin. Asthma symptom prevalence was related to residence time in Australia. The prevalence of wheeze was 17.2% in recent arrivals, 20.5% in adolescents living in Australia for >2 years, and 36.3% in those living all their lifetime in Australia (P = 0.013). For every year of residence in Australia, there was an 11% increase in prevalence of current wheeze (odds ratio, 1.11; P = 0.02). This effect was not related to atopy, AHR, or eosinophilic airway inflammation. Sputum neutrophils were elevated in recent arrivals. In conclusion, adolescents who migrate to Australia report increased asthma symptoms, compared to their country of origin, and asthma symptoms are further increased for every additional year of residence in Australia. The development of wheeze after migration to Australia was independent of eosinophilic inflammation and consistent with noneosinophilic asthma mechanisms., (Copyright 2003 Wiley-Liss, Inc.)