DOI: 10.1097/ee9.0000000000000523 ISSN: 2474-7882

Associations of current and life-course smoking and indoor environmental exposures with lung function level in early adulthood

Diana M. Hendrickx, Gerard H. Koppelman, Judith M. Vonk, Jolanda M.A. Boer, Hans Jacob L. Koefoed, Marieke Oldenwening, Roel C.H. Vermeulen, Ulrike Gehring

Background:

Lung function, expressed as forced expiratory volume in 1 second (FEV 1 ), reaches its maximum at 20–30 years of age. A lower maximal lung function has been associated with a higher risk of chronic obstructive pulmonary disease in later adulthood, but the impact of smoking and indoor environmental exposures on this maximum remains unclear.

Methods:

Using data from 858 participants of the Dutch PIAMA birth cohort (mean age: 25.7 years), we investigated associations between smoking, second-hand smoke (SHS), dampness or mold, furry pets, and gas cooking exposure with maximal lung function. Exposure data were collected via questionnaires from pregnancy through early adulthood, and life-course exposure trajectories were derived using latent class growth modeling. We assessed associations with FEV 1 and forced vital capacity (FVC) using linear regression, adjusting for potential confounders.

Results:

Pre- and post-bronchodilator spirometry was available for 846 and 806 participants, respectively. We found no associations between exposure to dampness or mold, furry pets, or gas cooking and lung function. Current and life-course active smoking was associated with higher post-bronchodilator FEV 1 , and pre- and post-bronchodilator FVC [regression coefficient β for pre-bronchodilator FVC (ml) (95% confidence interval): current (yes vs. no) 175 (68, 281), life-course (regular vs. occasional or none) 168 (55, 281)]. Current SHS was positively associated with post-bronchodilator FVC.

Conclusion:

No associations were found between indoor environmental exposures and maximal lung function in early adulthood. The observed positive associations with active smoking likely reflect bias arising from a selective uptake of smoking by individuals with higher pre-existing lung function, rather than a true physiological effect.

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