ReviewPostgraduate medical journal1994
Air pollution and asthma.
Review in Postgraduate medical journal, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed, 53 citations in OpenAlex.
- Thunderstorm-associated bronchial asthma: a forgotten but very present epidemic.Journal of family & community medicine · 2007Article
- Prevalence and mechanisms of development of asthma and airway hyperresponsiveness in athletes.Sports medicine (Auckland, N.Z.) · 2001Review
- Air pollution and bronchitic symptoms in Southern California children with asthma.Environmental health perspectives · 1999Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of air pollution in the increased prevalence and morbidity of asthma has been widely debated, but results to date indicate that the normally encountered levels of air pollution are unlikely to contribute to a worsening of asthma. When the levels of sulphur dioxide (SO2) are exceptionally high it is possible that asthmatic patients may have increased symptoms after exertion, since this irritant gas acts as a trigger to bronchoconstriction. There is also evidence that suspended particles may also act as an inciter of asthma symptoms when concentrations are high. Experimentally, ozone in high concentrations may increase airway responsiveness in both normal and asthmatic subjects by inducing airway inflammation, but asthmatic individuals show the same responses as normal subjects and there is little or no evidence to link increases in ambient ozone with an increase in asthma. There is little evidence that nitrogen dioxide (NO2), even at the peak levels recorded, has any significant effect on airway function in normal or asthmatic individuals. Other air pollutants which are present in lower concentrations have not been studied as extensively, but there is no convincing evidence that they cause significant respiratory symptoms in asthmatic patients. It is still possible that combinations of air pollutants may have greater effects on airway function than exposure to a single pollutant, although there is little evidence to support this. Epidemiological evidence provides little support for the idea that atmospheric pollution levels are related to the frequency of asthma symptoms or the frequency of attacks. More importantly, there is no evidence that asthma prevalence or aetiology is related to the level of air pollution. A review of currently available information therefore provides little evidence for the widely expressed view that atmospheric pollution is related to increased prevalence or morbidity of asthma or is related to the causation of asthma.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.