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Acute exposure to biomass smoke causes oxygen desaturation in adult women
  1. Om P Kurmi1,
  2. Santosh Gaihre2,
  3. Sean Semple2,
  4. Jon G Ayres1
  1. 1Institute of Occupational and Environmental Medicine, School of Health and Population Sciences, University of Birmingham, Edgbaston, Birmingham, UK
  2. 2Scottish Centre for Indoor Air, Population Health Sciences, Division of Applied Health Sciences, School of Medicine, University of Aberdeen, Aberdeen, UK
  1. Correspondence to Om Kurmi, Institute of Occupational and Environmental Medicine, School of Health and Population Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK; o.kurmi{at}bham.ac.uk

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Long-term exposure to biomass fuel smoke indoors is causally associated with chronic obstructive pulmonary disease (COPD)1 but the effect of acute exposures has not been studied. Should acute effects occur, this might increase the risk of an exacerbation of pre-existing lung disease. We studied acute changes in lung function and oxygen saturation in individuals exposed regularly to biomass smoke in Nepal.

Spirometry (EasyOne spirometer using American Thoracic Society (ATS) criteria) and oxygen saturation data were collected from 26, randomly selected, life-long non-smoking women (mean±SD age 38.0±11.7 years) before and after cooking (morning or evening). Smoke concentrations were measured using a DustTrak (TSI, Shoreview, Minnesota, USA) during cooking events and expressed as PM2.5 (particulate matter of <2.5 μm in diameter).2

Geometric mean (range) PM2.5 exposures were 2742 (1951–3853) μg/m3 for a mean±SD period of 164±34 min.

Spirometry results are presented in table 1. Taking the best values, group mean forced expiratory volume in 1 s (FEV1) was 1.95 litres (77% predicted), group mean forced vital capacity (FVC) was 2.44 litres (84% predicted) and group mean FEF25–75 (forced expiratory flow between 25% and 75% of FVC) 2.19 l/s (60% predicted). Three (12.5%) women had COPD (2 severe and 1 moderate, GOLD (Global Initiative on Obstructive Lung Disease classification), 8 (33%) had a restrictive defect ranging from mild to severe and 9 (37.5%) had small airways disease. When rested after cooking FEV1 and FEF25–75 fell but not significantly (FEV1: morning p=0.264 and evening p=0.421; FEF25–75 morning p=0.142 and evening p=1.000)) when re-tested after cooking.

Table 1

Best values for lung function and change in oxygen saturation during cooking (∆SaO2) for each individual—all individuals were women

All subjects had normal SaO2 (arterial oxygen saturation) values before cooking but values fell significantly after cooking (mean difference before and after cooking in the morning, −1.56%, 95% CI −0.94 to 2.18 (p<0.001) and in the evening, −1.53%, 95% CI −0.76 to 2.30 (p=0.001)). Heart rate fell significantly after the morning cooking period (−5.4±9.7, 95% CI 10.3 to 0.6, p=0.029) but not during the evening (−0.7±8.5, 95% CI 5.2 to 3.9, p=0.751). The changes were independent of fuel type and were more likely to be seen in those with abnormal lung function especially if the defect was severe.

This study suggests that women in low and middle income countries regularly exposed to biomass smoke who have chronic lung disease might be more at risk of hypoxia if they have marginal gas exchange when exposed acutely to biomass smoke. Consequently, while biomass smoke exposure contributes to the development of COPD, once established in an individual continued smoke exposure may further impair gas exchange, putting individuals at risk of cardiopulmonary decompensation.

These changes in SaO2 did not relate to acute changes in lung function during cooking suggesting that the acute changes in SaO2 were due to ventilation–perfusion imbalance. This could be due to inhalation of fine particles causing small airway narrowing3 or could affect pulmonary capillary blood flow either by a direct toxic effect from the particles or through autonomic nervous system stimulation.

In summary, these findings suggest that acute exposure to biomass smoke in women with small airways disease or restrictive lung disease is associated with blood deoxygenation, suggesting that in these individuals continued exposures may increase the risk of disease exacerbation.

Acknowledgments

We are extremely grateful to Pradeep Raj Dali for his help in the selection of the sampling locations and coordinating with the house members. We would like to thanks all the participants for taking part in this study.

References

View Abstract

Footnotes

  • Funding University of Birmingham.

  • Competing interests None.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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