You are here

  • Home
  • Archive
  • Volume 76, Issue 12
  • Accelerated lung function decline in an aluminium manufacturing industry cohort exposed to PM2.5: an application of the parametric g-formula

Article Text

Article menu
Download PDFPDF
Workplace
Accelerated lung function decline in an aluminium manufacturing industry cohort exposed to PM2.5: an application of the parametric g-formula
  1. Andreas M Neophytou1,2,
  2. Sadie Costello2,
  3. Sally Picciotto2,
  4. Elizabeth M Noth2,
  5. Sa Liu2,3,
  6. Liza Lutzker2,
  7. John R Balmes2,
  8. Katharine Hammond2,
  9. Mark R Cullen4,
  10. Ellen A Eisen2
  1. 1 Environmental and Radiological Health Sciences, Colorado State University, Fort Collins, Colorado, USA
  2. 2 School of Public Health, Division of Environmental Health Sciences, University of California Berkeley, Berkeley, California, USA
  3. 3 School of Health Sciences, Purdue University, West Lafayette, Indiana, USA
  4. 4 Department of Internal Medicine, Stanford University School of Medicine, Stanford, California, USA
  1. Correspondence to Dr Andreas M Neophytou, Environmental and Radiological Health Sciences, Colorado State University, Fort Collins, CO 80523, USA; andreas.neophytou{at}colostate.edu

Abstract

Objective Occupational dust exposure has been associated with accelerated lung function decline, which in turn is associated with overall morbidity and mortality. In the current study, we assess potential benefits on lung function of hypothetical interventions that would reduce occupational exposure to fine particulate matter (PM2.5) while adjusting for the healthy worker survivor effect.

Methods Analyses were performed in a cohort of 6485 hourly male workers in an aluminium manufacturing company in the USA, followed between 1996 and 2013. We used the parametric g-formula to assess lung function decline over time under hypothetical interventions while also addressing time-varying confounding by underlying health status, using a composite risk score based on health insurance claims.

Results A counterfactual scenario envisioning a limit on exposure equivalent to the 10th percentile of the observed exposure distribution of 0.05 mg/m3 was associated with an improvement in forced expiratory volume in one second (FEV1) equivalent to 37.6 mL (95% CI 13.6 to 61.6) after 10 years of follow-up when compared with the observed. Assuming a linear decrease and (from NHANES reference values), a 20 mL decrease per year for a 1.8 m-tall man as they age, this 37.6 mL FEV1 loss over 10 years associated with observed exposure would translate to approximately a 19% increase to the already expected loss per year from age alone.

Conclusions Our results indicate that occupational PM2.5 exposure in the aluminium industry accelerates lung function decline over age. Reduction in exposure may mitigate accelerated loss of lung function over time in the industry.

  • epidemiology
  • respiratory
  • PM10-PM2.5-ultrafine
  • aluminium
  • statistics

https://doi.org/10.1136/oemed-2019-105908

Statistics from Altmetric.com

    Request Permissions

    If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

    View Full Text

    Footnotes

    • Contributors AMN was responsible for data analyses and manuscript preparation. SC, SP and JRB assisted with interpretation of findings and critically reviewed the manuscript. EMN, SL and KH participated in data collection and assessment as well as critically reviewing the manuscript. LL assisted with data management and critically reviewing the manuscript. MRC initiated the original study and critically reviewed the manuscript. EAE and AMN devised the concept of the current study and critically reviewed the manuscript.

    • Funding This study was supported by the National Institutes of Health, Institute of Aging (R01-AG026291), the Centers for Disease Control and Prevention, National Institute of Occupational Safety and Health (R01 OH009939).

    • Competing interests KH has received compensation as a member of the scientific advisory board for Alcoa, Inc. (Pittsburgh, Pennsylvania) and for consulting for Alcoa, Inc. in the past. MRC has received salary support from Alcoa, Inc. through contracts with Stanford University (Stanford, California).

    • Patient consent for publication Not required.

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

    • Data availability statement As an alternative to providing a de-identified data set to the public domain, we allow access for the purpose of re-analyses or appropriate “follow-on” analyses to any qualified investigator willing to sign a contractual covenant with the host institution limiting the use of data without direct PHI/PII identifiers, in accordance to HIPAA regulations, and with a 15-day manuscript review for compliance purposes. For access to the data, interested parties can contact the study PI, Dr. Mark Cullen, at mrcullen@stanford.edu.