Airway Sensitivity of Asthmatics To Sulfur Dioxide

Horstman, Donald H.; Roger, L. Jack; Kehrl, Howard; Hazucha, Milan J.

doi:10.1177/074823378600200307

Cited by 53 publications

(32 citation statements)

References 7 publications

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“…This heterogeneity of response appears to be unrelated to basic demographic details but may reflect variation in individual sensitivity to pollution, as in the laboratory exposures of asthmatic subjects to O 3 or SO 2 are known to produce a spectrum of physiological effects [33,34].…”

Section: Discussionmentioning

confidence: 99%

Asthmatic bronchial hyperresponsiveness varies with ambient levels of summertime air pollution

Taggart¹,

Čustović²,

Francis³

et al. 1996

Eur Respir J

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It is widely believed that the mechanisms of action of outdoor air pollutants are the same as those found in the laboratory, although few studies have attempted to clarify this issue. This study investigates the relationship of asthmatic bronchial hyperresponsiveness (BHR), a marker of airway inflammation, and pulmonary function to ambient levels of summertime air pollution.Thirty eight nonsmoking adult asthmatic subjects underwent repeated measurement of methacholine BHR, using Yan's method, at differing levels of air pollution (O 3 , SO 2 , NO 2 , smoke) during summer 1993.A total of 109 evaluable tests were performed: 31 subjects completed three or more challenge tests, and seven managed two. Levels of all pollutants remained within current World Health Organization (WHO) Guidelines for Health. Changes in BHR were found to correlate significantly with changes in the levels of 24 h mean SO 2 , NO 2 and smoke; 48 h mean NO 2 and smoke; 24 h lag NO 2 ; although the effect was only small, accounting for approximately 10% of the variability in within-subject BHR between visits. Twenty four hour lag NO 2 was also associated with forced vital capacity (FVC).In conclusion, in subjects with asthma, methacholine bronchial hyperresponsiveness varies with ambient levels of summertime air pollution. This suggests that changes in airway inflammation underlie the increased respiratory morbidity known to accompany pollution episodes.

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Section: Discussionmentioning

confidence: 99%

Asthmatic bronchial hyperresponsiveness varies with ambient levels of summertime air pollution

Taggart¹,

Čustović²,

Francis³

et al. 1996

Eur Respir J

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“…There is evidence that they can also cause bronchoconstriction (ibid. ; [107]). In general, these effects are reversible, and do not necessarily constitute a risk of disease in healthy subjects.…”

Section: Short-term Irritant-related Reductions In Functionmentioning

confidence: 99%

“…Asthmatics appear to be more susceptible to short-term peak concentration of air pollutants, although there is a broad range of sensitivity [4,17,107,108]. Oral breathing produces larger and quicker effects, as does exercise.…”

Section: Pm/o 3 and Copdmentioning

confidence: 99%

Epidemiological studies of the respiratory effects of air pollution

Lebowitz¹

1996

Eur Respir J

112

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Environmental epidemiological studies of the health effects of air pollution have been major contributors to the understanding of such effects. The chronic effects of atmospheric pollutants have been studied, but, except for the known respiratory effects of particulate matter (PM), they have not been studied conclusively. There are ongoing studies of the chronic effects of certain pollutant classes, such as ozone, acid rain, airborne toxics, and the chemical form of PM (including diesel exhaust).Acute effects on humans due to outdoor and indoor exposures to several gases/fumes and PM have been demonstrated in epidemiological studies. However, the effects of these environmental factors on susceptible individuals are not known conclusively. These acute effects are especially important because they increase the human burden of minor illnesses, increase disability, and are thought to decrease productivity. They may be related to the increased likelihood of chronic disease as well. Further research is needed in this latter area, to determine the contributions of the time-related activities of individuals in different microenvironments (outdoors, in homes, in transit). Key elements of further studies are the assessment of total exposure to the different pollutants (occurring from indoor and outdoor sources) and the interactive effects of pollutants.Major research areas include determination of the contributions of indoor sources and of vehicle emissions to total exposure, how to measure such exposures, and how to measure human susceptibility and responses (including those at the cellular and molecular level). Biomarkers of exposures, doses and responses, including immunochemicals, biochemicals and deoxyribonucleic acid (DNA) adducts, are beginning to promote some basic knowledge of exposure-response, especially the mechanisms. These will be extremely useful additions to standard physiological, immunological, and clinical instruments, and the understanding of biological plausibility. The outcomes of all this work will be the management of risks and the prevention of respiratory diseases related to air pollution. Eur Respir J., 1996Respir J., , 9, 1029Respir J., -1054 This work was supported by USA-NHLBI SCOR Grant HL14136.Previously published reviews of this series 1. Sandström T. Respiratory effects of air pollutants: experimental studies in humans. Eur Respir J 1995; 8: 976-995. 2. Chitano P, Hosselet JJ, Mapp CE, Fabbri LM. Effects of oxidant air pollutants on the respiratory system: insights from experimental animal research. Eur Respir J 1995; 8: 1357-1371. Heyder J, Takenaka S. Long-term canine exposure studies with ambient air pollutants. Eur Respir J 1996; 9: 571-584. This review of epidemiological studies of the respiratory effects of exposures to air pollutants follows excellent reviews of experimental studies in animals and humans that have recently appeared in the Journal [1][2][3]. It has relied both on prior reviews of the topic and on the extensive literature of the major research reports...

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“…1 2 The same response occurs in asthmatic people at lower concentrations especially if they are exercising at the time. [2][3][4][5][6] The response is typically maximal within 5 minutes and resolves spontaneously after 30-60 minutes. 1 5 7 It is prevented and relieved by inhaled 2 agonists.…”

mentioning

confidence: 99%

Point source sulphur dioxide peaks and hospital presentations for asthma.

Donoghue

Thomas

1999

Occup Environ Med

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Objective-To examine the eVect on hospital presentations for asthma of brief exposures to sulphur dioxide (SO 2 ) (within the range 0-8700 µg/m 3 ) emanating from two point sources in a remote rural city of 25 000 people. Methods-A time series analysis of SO 2 concentrations and hospital presentations for asthma was undertaken at Mount Isa where SO 2 is released into the atmosphere by a copper smelter and a lead smelter. The study examined 5 minute block mean SO 2 concentrations and daily hospital presentations for asthma, wheeze, or shortness of breath. Generalised linear models and generalised additive models based on a Poisson distribution were applied. Results-There was no evidence of any positive relation between peak SO 2 concentrations and hospital presentations or admissions for asthma, wheeze, or shortness of breath. Conclusion-Brief exposures to high concentrations of SO 2 emanating from point sources at Mount Isa do not cause suYciently serious symptoms in asthmatic people to require presentation to hospital. (Occup Environ Med 1999;56:232-236)

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Airway Sensitivity of Asthmatics To Sulfur Dioxide

Cited by 53 publications

References 7 publications

Asthmatic bronchial hyperresponsiveness varies with ambient levels of summertime air pollution

Asthmatic bronchial hyperresponsiveness varies with ambient levels of summertime air pollution

Epidemiological studies of the respiratory effects of air pollution

Point source sulphur dioxide peaks and hospital presentations for asthma.

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