A cross-disciplinary evaluation of evidence for multipollutant effects on cardiovascular disease

Abstract

Overall, the evidence for multipollutant effects was often heterogeneous, and the limited number of studies inhibited making a conclusion about the nature of the relationship between pollutant combinations and cardiovascular disease.

Early Life Exposure to Air Pollution and Autism Spectrum Disorder

“…Ozone may confound relationships between PM 2.5 and ASD. 30 Therefore, we report results from two-pollutant models for each developmental window by controlling for the other pollutant in each exposure model. We additionally report results adjusted for monitored levels of nitrogen dioxide (NO 2 ), as a marker of traffic-related air pollution.…”

Evaluation of PM2.5 air pollution sources and cardiovascular health

“…Some studies have already begun to find associations between mortality and other health outcomes with source-specific PM 2.5 exposures. [16][17][18][19][20][21] Previous air pollution studies have utilized a centralized monitor to extrapolate pollution levels over their population of interest, but recent studies employ remote sensing, land-use data, and chemical transport models to better capture PM 2.5 composition at a finer geographic resolution. [22][23][24] This approach allows the combination of central monitor data and chemical transport model estimates to create more robust measures of air pollution over a given area, increasing spatial and temporal resolution of air pollution modeling.…”

“…Some studies have already begun to find associations between mortality and other health outcomes with source-specific PM 2.5 exposures. 16–21…”

Association of Short-Term Co-Exposure to Particulate Matter and Ozone with Mortality Risk

“…Even so, some studies have found a stronger association between exposure to oxidizing gases and mortality risk in areas where the PM components have a greater capacity for oxidative stress (e.g., higher excess metal content and oxidation potential) , and a synergistic effect of co-exposure to PM and O 3 through mechanisms such as neuro-immune interactions and the production of inflammation . However, a meta-analysis on a number of previous studies found uncertainty about how short-term co-exposure to PM and O 3 exerts a combined effect to lead to adverse outcomes due to inconsistencies in the end points examined, the study design, the sample size, and the way exposure levels of pollutants are estimated (i.e., the composition of pollutants and the particle size of pollutants) . For example, epidemiologic studies have shown that short-term co-exposure to PM and O 3 has a modifying effect on cardiovascular health rather than a combined effect, , while experimental studies have also shown the presence of synergistic effects, antagonistic effects, or no overall interaction between PM and O 3 .…”

“…14 For example, epidemiologic studies have shown that shortterm co-exposure to PM and O 3 has a modifying effect on cardiovascular health rather than a combined effect, 15,16 while experimental studies have also shown the presence of synergistic effects, antagonistic effects, or no overall interaction between PM and O 3 . 14 Therefore, there is an urgent need to further investigate whether there is a combined or interactive effect of short-term co-exposure to PM and O 3 on mortality using large population-based surveys. The present study aims to examine the association of shortterm co-exposure to PM and O 3 on all-cause nonaccidental, cardiovascular, and respiratory mortality in 4,276,989 people in Jiangsu Province, China, during 2014−2021.…”