Air pollution reaches deep into kids’ DNA

Exposure to air pollution impacts the methylation of immunoregulatory genes among children, and alters their immune cell and blood pressure profiles, according to a recent study.

“Whereas most air pollution health studies have focused on adults, some of which already have overt clinical cardiac disease, a strength of our study was the inclusion of participants in a young age group, allowing us to investigate air pollution effects on cardiovascular and immune functioning before clinical symptomatology,” the researchers said.

The study included 221 schoolchildren (aged 6–8 years; 46 percent girls) who were living in a city known to have elevated pollution. Multivariate partial least squares (PLS) showed that both short- and long-term exposure to fine particulate matter (PM_2.5), carbon monoxide (CO), and ozone (O₃) were key pollution parameters that could predict most of the methylation in immunoregulatory genes. [Sci Rep 2021;11:4067]

Multivariable-adjusted regression analysis confirmed the initial findings, showing that the methylation of CpG sites of immunoregulatory genes independently correlated with exposure to air pollution.

For instance, high PM_2.5 exposure 1 month before sampling was linked to increased methylation in several CpG sites on the interleukin (IL) -4 and -10 genes, as well as on the interferon-γ (IFNγ) and FoxP3 genes. Similarly, CpG sites on the IL-4, IL-10, and IFNγ genes saw heightened methylation following elevated CO exposure a month prior.  Similar effects were reported for O₃.

“Here we demonstrated air pollution as a predictor of DNA methylation of four immunoregulatory genes: IL-4, IL-10, Foxp3, and IFNγ. Overall, acute exposure to CO, O₃, and PM_2.5 was associated with methylation of numerous CpG sites,” the researchers said.

“The largest effect size was for the association of CO levels at 15 days prior to blood draw to a CpG site in the promoter region of the IL-10 gene,” they added.

Exposure to air pollution also triggered dysregulation in immune cell profiles. Multivariable PLS analysis identified PM_2.5, CO, and O₃ as main predictors, along with 5-, and 6-ringed polycyclic aromatic hydrocarbons (PAH₄₅₆). Percentages of helper T cell (Th) subtypes 1, 2, and 17 were most affected.

As with immunoregulatory genes, exposure to PM_2.5 1–3 months before sampling correlated with altered Th1 and Th17 profiles. Th2, on the other hand, increased after high PM_2.5 exposure the day before as well as with higher CO exposure 1 day to 3 months prior.

In addition, CD4+ and CD8+ cells were correlated with chronic PAH₄₅₆ exposure; B cells and CD4+ cells were linked with nitrogen dioxide exposure the day before.

Air pollution also impacted blood pressure, explaining 21.0 percent and 5.1 percent of the variance in systolic and diastolic blood pressure, respectively. Air pollution also accounted for 7.0 percent of pulse pressure variance.

“In conclusion, we find that air pollution exposure is linked to methylation of immunoregulatory genes, immune cell profiles and blood pressure, suggesting that even at a young age, the immune and cardiovascular systems are negatively impacted by air pollution,” they added.