Associations between Children's Exposure to PM2.5 and their Serum Inflammatory Responses in Taiwan

Abstract

PM2.5-induced inflammation have been demonstrated in the cellular and animal models, but few studies reported the associations of schoolchildren exposure to PM2.5 with their serum inflammatory biomarkers. Our goal was to examine whether serum inflammation was activated after children with long-term exposure to PM2.5 in an industrialized city of Taiwan. Schoolchildren (n = 183) between the ages of 6 and 12 years living in southern Taiwan were recruited to measure their serum inflammation including interferon-γ (IFN-γ), IFN-α2, interleukin 1b (IL-1b), IL-2, IL-6, IL-10, IL-13, IL-17, monocyte chemotactic protein (MCP)-1, and tumor necrosis factor (TNF-α). The subjects were sorted into three groups based on residential addresses in low-PM2.5, high-PM2.5, and traffic-related-air-pollution (TRAP)-PM2.5 areas on the basis of long-term PM2.5 pollution data from air monitoring sites collected over the past decade. Children living in the TRAP-PM2.5 areas had significantly higher TNF-α serum levels than those living in the low-PM2.5 areas. Although serum levels of MCP-1 in children exposed to low PM2.5 concentrations were lower than those in children exposure to high and TRAP PM2.5 levels, the differences were nonsignificant. Principal component (PC) analyses revealed a close association between serum MCP-1 and outdoor PM2.5 (Rotated PC2 (RPC2) and percentage of variance = 10.5%), whereas serum IFN-γ, IFN-α2, IL-1b, IL-2, IL-6, IL-10, IL-13, IL-17, and TNF-α were highly correlated (RPC1 and percentage of variance = 45.5%). Children's serum TNF-α was significantly linked to PM2.5 exposure scenarios (p = 0.031) by the test of the multivariate analysis (adjusted R 2 = 0.033, p = 0.039), but the other variables of age (p = 0.147) and gender (p = 0.291) were not statistically significant. In conclusion, serum TNF-α might be positively and significantly correlated with the longitudinal exposure of schoolchildren to PM2.5, especially among children living in TRAP-PM2.5 region.

An Insight on Microfluidic Organ-on-a-Chip Models for PM2.5-Induced Pulmonary Complications

“…Sigaud et al observed that neutrophils were released following exposure and inhalation of PM 2.5 in humans . The various inflammatory markers released include interferon-ϒ (IFN-ϒ), interleukin (IL)-4, IL-10, IL-12, and IL-13, along with the recruitment of eosinophils. , Disrupted calcium homeostasis is one of the significant mechanisms provoking disturbance due to PM 2.5 . As calcium is involved in the maintenance of normal cell physiology and functioning, increased levels can lead to stimulation of inflammation within the body and can cause damage to organs. , The toxic free radicals produced due to the inhalation of PM 2.5 lead to a subsequent increase in the levels of intracellular calcium (Ca 2+ ) ions, which can further aggravate the peroxidation process and ROS formation. , This could further lead to cell necrosis and delayed cellular apoptosis .…”

“… 31 The various inflammatory markers released include interferon-ϒ (IFN-ϒ), interleukin (IL)-4, IL-10, IL-12, and IL-13, along with the recruitment of eosinophils. 32 , 33 Disrupted calcium homeostasis is one of the significant mechanisms provoking disturbance due to PM 2.5 . As calcium is involved in the maintenance of normal cell physiology and functioning, increased levels can lead to stimulation of inflammation within the body and can cause damage to organs.…”

Effects of Residential Proximity to Industrial Zone on Respiratory Symptoms among Residents in Parit Raja, Batu Pahat

“…Many reviews reported that the pollutants released from industrial activities are associated with many acute and chronic diseases (7,8). In particular, health effects of PM 10 and PM 2.5 exposure includes pulmonary disease, heart disease, chronic bronchitis, stroke, asthma, cancers and premature mortality (9,10). Similarly, numerous reviews reported that nitrogen dioxide (NO 2 ) exposure has also been linked to cellular inflammation, bronchial hyperresponsiveness, and an aggravated risk of infection predominantly in the respiratory and cardiovascular systems (11)(12)(13)(14).…”