Air pollution is linked to brain inflammation, which accelerates tumorigenesis and neurodegeneration. The molecular mechanisms that connect air pollution with brain pathology are largely unknown but seem to depend on the chemical composition of airborne particulate matter (PM).
Ljubimova et al., sourced ambient PM from Riverside, California, and selectively exposed rats to coarse (PM2.5-10: 2.5-10 µm), fine (PM<2.5: <2.5 µm), or ultrafine particles (UFPM: <0.15 µm). They characterized each PM type via atomic emission spectroscopy and detected nickel, cobalt and zinc within them. They then exposed rats separately to each PM type for short (2 weeks), intermediate (1-3 months) and long durations (1 year). All three metals accumulated in rat brains during intermediate-length PM exposures. Via RNAseq analysis we then determined that intermediate-length PM2.5-10 exposures triggered the expression of the early growth response gene 2 (EGR2), genes encoding inflammatory cytokine pathways (IL13-Rα1 and IL-16) and the oncogene RAC1. Gene upregulation occurred only in brains of rats exposed to PM2.5-10 and correlated with cerebral nickel accumulation. We hypothesize that the expression of inflammation and oncogenesis-related genes is triggered by the combinatorial exposure to certain metals and toxins in Los Angeles Basin PM2.5-10 1).
Epidemiological research has shown that exposure to fine particulate matter pollution (PM2.5) is associated with a reduction in cognitive function in older adults. However, primary evidence comes from high-income countries, and no specific studies have been conducted in low and middle-income countries where higher air pollution levels exist.
To estimate the association between the exposure to PM2.5 and cognitive function in a nationally representative sample of older Mexican adults and the associated effect modifiers.
Data for this study were taken from the National Survey of Health and Nutrition in Mexico carried out in 2012. A total of 7986 older adults composed the analytical sample. Cognitive function was assessed using two tests: semantic verbal fluency and three word recall. The annual concentration of PM2.5 was calculated using satellite data. Association between exposure to PM2.5 and cognitive function was estimated using two-level logistic and linear regression models.
In adjusted multilevel regression models, each 10 μg/m3 increase in ambient PM2.5 raised the odds of a poorer cognitive function using the three-word memory test (OR = 1.37, 95% CI: 1.08, 1.74), and reduced the number of valid animal named in the verbal fluency test (β = -0.72, 95% CI: -1.05, -0.40). Stratified analyses did not yield any significant modification effects of age, sex, indoor pollution, urban/rural dwelling, education, smoking and other factors.
This study supports an association between exposure to PM2.5 concentrations and cognitive function in older adults. This is particularly relevant to low- and middle-income countries, which are marked by a rapid growth of their aging population and high levels of air pollution 2).
Spontaneous intracerebral hemorrhage (sICH) has a high mortality rate. Research has demonstrated that the occurrence of sICH is related to air pollution. This study used big data analysis to explore the impact of air pollution on the risk of sICH in patients of differing age and geographic location. 39,053 cases were included in this study; 14,041 in the Taipei region (Taipei City and New Taipei City), 5537 in Taoyuan City, 7654 in Taichung City, 4739 in Tainan City, and 7082 in Kaohsiung City. The results of correlation analysis indicated that there were two pollutants groups, the CO and NO₂ group and the PM2.5 and PM10 group. Furthermore, variations in the correlations of sICH with air pollutants were identified in different age groups. The co-factors of the influence of air pollutants in the different age groups were explored using regression analysis. This study integrated Taiwan National Health Insurance data and air pollution data to explore the risk factors of sICH using big data analytics. They found that PM2.5 and PM10 are very important risk factors for sICH, and age is an important modulating factor that allows air pollutants to influence the incidence of sICH 3).
Negatively impacts pulmonary, cardiovascular, and central nervous systems. Although its influence on brain cancer is unclear, toxic pollutants can cause blood-brain barrier disruption, enabling them to reach the brain and cause alterations leading to tumor development. By gene microarray analysis validated by quantitative RT-PCR and immunostaining Ljubimova et al, examined whether rat (n=104) inhalation exposure to air pollution particulate matter (PM) resulted in brain molecular changes similar to those associated with human brain tumors. Global brain gene expression was analyzed after exposure to PM (coarse, 2.5-10μm; fine, <2.5μm; or ultrafine, <0.15μm) and purified air for different times, short (0.5, 1, and 3 months) and chronic (10 months), for 5h per day, four days per week. Expression of select gene products was also studied in human brain (n=7) and in tumors (n=83). Arc/Arg3.1 and Rac1 genes, and their protein products were selected for further examination. Arc was elevated upon two-week to three-month exposure to coarse PM and declined after 10-month exposure. Rac1 was significantly elevated upon 10-month coarse PM exposure. On human brain tumor sections, Arc was expressed in benign meningiomas and low-grade gliomas but was much lower in high-grade tumors. Conversely, Rac1 was elevated in high-grade vs. low-grade gliomas. Arc is thus associated with early brain changes and low-grade tumors, whereas Rac1 is associated with long-term PM exposure and highly aggressive tumors. In summary, exposure to air PM leads to distinct changes in rodent brain gene expression similar to those observed in human brain tumors 4).