# Cross-sectional evaluation of exposure to ozone, nitrogen dioxide, and particulate mass levels on circulating immune markers in women in the California Teachers Study

## TL;DR

This study found that higher ozone exposure in women is linked to increased immune markers related to inflammation and immune cell activation.

## Contribution

The study identifies specific immune pathways linking ozone exposure to adverse health outcomes in women.

## Key findings

- Elevated ozone exposure was associated with increased levels of IL-1β, IL-8, sTNFR2, and sgp130.
- Ozone exposure was consistently linked to pro-inflammatory/macrophage activation and B-cell activation pathways.
- NO2 was associated with increased TNFα levels at shorter exposure windows.

## Abstract

Exposure to ambient air pollutants, specifically ozone (O3), nitrogen dioxide (NO2), ultrafine, fine or coarse particulate matter (PM0.1, PM2.5, and PM10), has been linked to a number of adverse health outcomes, including cardiovascular disease. Changes in immune response may be a key mechanism underlying these effects. Within the California Teachers Study cohort, we conducted a cross-sectional analysis of 1,898 women to assess the associations between exposure to O3, NO2, PM0.1, PM2.5, and PM10 and 15 immune markers measured from serum samples collected in 2015. Daily residential exposures to O3, NO2, PM0.1, PM2.5, and PM10 were estimated by a validated chemical transport model and averaged over 12-, 3-, and 1-month periods prior to blood draw. Fifteen immune markers (categorized as quartiles) were estimated per interquartile range (IQR) of air pollutant exposures using multivariable ordinal logistic regressions adjusted for age, body mass index, and respective pollutants. Immune markers were also grouped into immune pathways (pro-inflammatory/macrophage activation, B-cell activation, and T-cell activation). After applying Bonferroni correction, elevated exposure to O3 levels at all three exposure windows were associated with elevated circulating levels of IL-1β (interleukin-1 beta), IL-8 (interleukin 8), sTNFR2 (soluble tumor necrosis factor receptor 2), and sgp130 (soluble glycoprotein 130). Elevated O3 at 3- and 1-month periods were associated with increased levels of sCD27 (soluble cluster of differentiation 27) and BAFF (B-cell activating factor). In pathway analyses, O3 was consistently and significantly associated with the pro-inflammatory/macrophage activation pathway (12-month OR = 1.49, 3-month OR = 1.57, 1-month OR = 1.54) and with B-cell activation at all three exposure windows (12-month OR = 1.24, 3-month OR = 1.53, 1-month OR = 1.41). NO2 was positively associated with TNFα at the 3- and 1-month exposure windows. For the PM size fractions, sporadic, mainly inverse, associations with immune markers were observed. Elevated O3 exposure up to one year prior to blood draw was associated with elevated immune markers related to pro-inflammatory response, macrophage activation, and B cell activation. These findings suggest potential immunologic pathways linking air pollution to adverse health outcomes in women.