C-Reactive Protein results from dying cells and well accepted as a marker of inflammation and autoimmunity. In this study of nearly 8,000 older adults in California, mean levels of CRP significantly increased from many vehicle traffic exhaust chemicals. This included a 24.5% increase in CRP for each 10 ug/m3 increase in Particle Matter 10-2.5. CRP increased by 19.2% per each 50 ppb increase in nitrogen dioxide. Every 1 part per billion increase in benzene resulted in an additional 4.6% increase in CRP. As CRP is often elevated in many diseases from cancer to depression, these findings suggest vehicle traffic air pollution would be a significant contributing factor to many diseases.
ABSTRACT
Inhaled particles and gases can harm health by promoting chronic inflammation in the body. Few studies have investigated the relationship between outdoor air pollution and inflammation by race and ethnicity, socioeconomic status, and lifestyle risk factors. We examined associations of particulate matter (PM) and other markers of traffic-related air pollution with circulating levels of C-reactive protein (CRP), a biomarker of systemic inflammation. CRP was measured from blood samples obtained in 1994–2016 from 7,860 California residents participating in the Multiethnic Cohort (MEC) Study. Exposure to PM (aerodynamic diameter ≤ 2.5 μm [PM2.5], ≤ 10 μm [PM10], and between 2.5 and 10 μm [PM10–2.5]), nitrogen oxides (NOx, including nitrogen dioxide [NO2]), carbon monoxide (CO), ground-level ozone (O3), and benzene averaged over one or twelve months before blood draw were estimated based on participants’ addresses. Percent change in geometric mean CRP levels and 95% confidence intervals (CI) per standard concentration increase of each pollutant were estimated using multivariable generalized linear regression. Among 4,305 females (55%) and 3,555 males (45%) (mean age 68.1 [SD 7.5] years at blood draw), CRP levels increased with 12-month exposure to PM10 (11.0%, 95% CI: 4.2%, 18.2% per 10 µg/m3), PM10–2.5 (12.4%, 95% CI: 1.4%, 24.5% per 10 µg/m3), NOx (10.4%, 95% CI: 2.2%, 19.2% per 50 ppb), and benzene (2.9%, 95% CI: 1.1%, 4.6% per 1 ppb). In subgroup analyses, these associations were observed in Latino participants, those who lived in low socioeconomic neighborhoods, overweight or obese participants, and never or former smokers. No consistent patterns were found for 1-month pollutant exposures. This investigation identified associations of primarily traffic-related air pollutants, including PM, NOx, and benzene, with CRP in a multiethnic population. The diversity of the MEC across demographic, socioeconomic, and lifestyle factors allowed us to explore the generalizability of effects of air pollution on inflammation across subgroups.