Rat Lung Response to PM2.5 Exposure under Different Cold Stresses

Abstract

Ambient particulate matters and temperature were reported to have additive effects over the respiratory disease hospital admissions and deaths. The purpose of this study is to discuss the interactive pulmonary toxicities of cold stress and fine particulate matter (PM2.5) exposure by estimating inflammation and oxidative stress responses. 48 Wistar male rats, matched by weight and age, were randomly assigned to six groups, which were treated with cold stress alone (0 °C, 10 °C, and 20 °C (Normal control)) and cold stresses plus PM2.5 exposures respectively. Cold stress alone groups were intratracheal instillation of 0.25 mL normal saline, while cold stress plus PM2.5 exposure groups were intratracheal instillation of 8 mg/0.25 mL PM2.5. These procedures were carried out for three times with an interval of 48 hours for each treatment. All rats were sacrificed after 48 hours of the third treatment. The bronchoalveolar lavage fluid (BALF) was collected for analyzing inflammatory cells and cytokines, and lung homogenate MDA was determined for oxidative stress estimation. Results showed higher level of total cell and neutrophil in the BALF of PM2.5 exposed groups (p < 0.05). Negative relationships between cold stress intensity and the level of tumor necrosis factor alpha (TNF-a), C-reactive protein (CRP) interleukin-6 (IL-6) and interleukin-8 (IL-8) in BALF were indicated in PM2.5 exposure groups. Exposure to cold stress alone caused significant increase of inflammatory cytokines and methane dicarboxylic aldehyde (MDA) and decline of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity only in 0 °C exposure group (p < 0.05). The two-way ANOVA found significant interactive effects between PM2.5 exposure and cold stress in the level of neutrophil, IL-6 and IL-8 and SOD activity (p < 0.05). These data demonstrated that inflammation and oxidative stress involved in the additive effect of PM2.5 exposure and cold stress on pulmonary toxicity, providing explanation for epidemiological studies on the health effect of ambient PM2.5 and cold stress.

Cardiovascular mortality risk attributable to ambient temperature in China

“…Cold exposure was also found to increase the frequency of heart rate variability and ventricular ectopic beats 22. In addition, exposure to cold caused significant increase of inflammatory cytokines and methane dicarboxylic aldehyde and decline of superoxide dismutase (SOD) and glutathione peroxidase activity,23 and the genes involved in the hypoxia-inducible factor signalling pathway were activated in which oxidative stress-associated genes were significantly upregulated, including SOD2 and epoxide hydrolase 2 24. On the other hand, exposure to hot weather may induce profound physiological changes, such as increase in blood viscosity and cardiac output leading to dehydration, hypotension, surface blood circulation increase and even endothelial cell damage 25.…”

Working in cold environment and risk of developing rheumatoid arthritis: results from the Swedish EIRA case–control study

“…This observation indicates a possible mechanistic interaction between these exposures in RA. While there are studies that attempt to delineate the effect of acute/short-term cold exposure on the immune system, [15][16][17] studies that investigate the impact of long-term exposure to cold environment in conjunction with high physical workload on the immune system are scarce. Whether exposure to long-term cold work environment causes aberrant Rheumatoid arthritis immune reactions resulting into a chronic inflammatory disease like RA remains elusive.…”

Chronic PM2.5 exposure and risk of infant bronchiolitis and otitis media clinical encounters

“…Toxicological studies have demonstrated that chronic exposure to traffic related air pollution, such as particulate matter with a diameter of 2.5 microns or less (PM 2.5 ) can trigger an inflammatory response in rats (Luo et al 2014; Xu et al 2008; Ying et al 2015) and humans (Ostro et al 2014). To date, there have been only a few studies investigating the effects of long term PM 2.5 exposure and bronchiolitis (de Pablo-Romero et al 2015; Karr et al 2007; Karr et al 2009a; Karr et al 2009b) or OM (Brauer et al 2006; MacIntyre et al 2011; MacIntyre et al 2013), indicating evidence of a possible association (Brauer et al 2006; Karr et al 2007; MacIntyre et al 2011).…”