Background

Chronic exposures to particulate matter with an aerodynamic diameter < 2.5 μm (PM_2.5) and ozone pollution can affect respiratory function. ARDS, an often lethal respiratory failure, is most common among older adults. However, few epidemiology studies have investigated an association between air pollution and the risk of ARDS.

Methods

This observational study was conducted to estimate air pollution exposures at the ZIP code level and hospital admissions with ARDS among US Medicare beneficiaries aged ≥ 65 years from 2000 to 2012. A two-pollutant generalized linear mixed model, adjusting for sex, age, race, median household income, smoking, and weather, was applied.

Results

There were a total of 1,164,784 hospital admissions with ARDS in the cohort. Increases of 1 µg/m³ in annual average PM_2.5 and of 1 parts per billion in annual average ozone were associated with increases in annual hospital admission rates for ARDS of 0.72% (95% CI, 0.62-0.82) and 0.15% (95% CI, 0.08-0.22), respectively. In low-pollution regions (annual average PM_2.5 level < 12 µg/m³ and annual average ozone level < 45 parts per billion), the same annual increase in PM_2.5 and ozone were associated with increases in annual hospital admission rates for ARDS of 1.50% (95% CI, 1.27-1.72) and 0.27% (95% CI, 0.16-0.38).

Conclusions

Long-term exposures to PM_2.5 and ozone were associated with increased risk of ARDS among older adults in the United States, including exposures below current annual US National Ambient Air Quality Standards.

Although prediagnostic circulating concentrations of the immune activation markers soluble CD27 (sCD27), sCD30 and chemokine ligand-13 (CXCL13) have been associated with non-Hodgkin lymphoma (NHL) risk, studies have been limited by sample size in associations with NHL subtypes. We pooled data from eight nested case-control studies to investigate subtype-specific relationships for these analytes. Using polytomous regression, we calculated odds ratios (ORs) with 95% confidence intervals (CIs) relating study-specific analyte tertiles to selected subtypes vs controls (n = 3310): chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL; n = 623), diffuse large B cell lymphoma (DLBCL; n = 621), follicular lymphoma (FL; n = 398), marginal zone lymphoma (MZL; n = 138), mantle cell lymphoma (MCL; n = 82) and T cell lymphoma (TCL; n = 92). We observed associations with DLBCL for elevated sCD27 [OR for third vs first tertile (ORT3 ) = 2.2, 95% CI = 1.6-3.1], sCD30 (ORT3  = 2.0, 95% CI = 1.6-2.5) and CXCL13 (ORT3  = 2.3, 95% CI = 1.8-3.0). We also observed associations with sCD27 for CLL/SLL (ORT3  = 3.3, 95% CI = 2.4-4.6), MZL (ORT3  = 7.7, 95% CI = 3.0-20.1) and TCL (ORT3  = 3.4, 95% CI = 1.5-7.7), and between sCD30 and FL (ORT3  = 2.7, 95% CI = 2.0-3.5). In analyses stratified by time from phlebotomy to case diagnosis, the sCD27-TCL and all three DLBCL associations were equivalent across both follow-up periods (<7.5, ≥7.5 years). For other analyte-subtype comparisons, associations were stronger for the follow-up period closer to phlebotomy, particularly for indolent subtypes. In conclusion, we found robust evidence of an association between these immune markers and DLBCL, consistent with hypotheses that mechanisms related to immune activation are important in its pathogenesis. Our other findings, particularly for the rarer subtypes MZL and TCL, require further investigation.