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Non-communicable respiratory disease and air pollution exposure in Malawi: a prospective cohort study.

  • Author(s): Rylance, Sarah
  • Jewell, Chris
  • Naunje, Andrew
  • Mbalume, Frank
  • Chetwood, John D
  • Nightingale, Rebecca
  • Zurba, Lindsay
  • Flitz, Graham
  • Gordon, Stephen B
  • Lesosky, Maia
  • Balmes, John R
  • Mortimer, Kevin
  • et al.
Abstract

Rationale

There are no population-based studies from sub-Saharan Africa describing longitudinal lung function in adults.

Objectives

To explore the lung function trajectories and their determinants, including the effects of air pollution exposures and the cleaner-burning biomass-fuelled cookstove intervention of the Cooking and Pneumonia Study (CAPS), in adults living in rural Malawi.

Methods

We assessed respiratory symptoms and exposures, spirometry and measured 48-hour personal exposure to fine particulate matter (PM2.5) and carbon monoxide (CO), on three occasions over 3 years. Longitudinal data were analysed using mixed-effects modelling by maximum likelihood estimation.

Measurements and main results

We recruited 1481 adults, mean (SD) age 43.8 (17.8) years, including 523 participants from CAPS households (271 intervention; 252 controls), and collected multiple spirometry and air pollution measurements for 654 (44%) and 929 (63%), respectively. Compared with Global Lung Function Initiative African-American reference ranges, mean (SD) FEV1 (forced expiratory volume in 1 s) and FVC (forced vital capacity) z-scores were -0.38 (1.14) and -0.19 (1.09). FEV1 and FVC were determined by age, sex, height, previous TB and body mass index, with FEV1 declining by 30.9 mL/year (95% CI: 21.6 to 40.1) and FVC by 38.3 mL/year (95% CI: 28.5 to 48.1). There was decreased exposure to PM2.5 in those with access to a cookstove but no effect on lung function.

Conclusions

We did not observe accelerated lung function decline in this cohort of Malawian adults, compared with that reported in healthy, non-smoking populations from high-income countries; this suggests that the lung function deficits we measured in adulthood may have origins in early life.

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