Toxicity Effects Of Air Pollutants On Rat Various Organs And The Adverse Effects On Human Health

Airborne pollution is one of the most predominant and urgent urban environment pollution problems in developing countries. In the north of China, airborne pollution derives from coal combustion emission, in which TSP and SO₂ are main pollutants. According to the air quality level of WHO issuance, at least 80% city dwellers are living in the unacceptable air condition, which threatens their health. By using glass microelectrode technique, immunohistochemistry SABC method and Fura-2/AM micro fluorescence detecting technique, the thesis has investigated the effects of SO₂ and its derivatives on the hippocampus neuron spontaneous activity, the BDNF expression, the intracellular Ca²⁺ concentration and the learning and memory ability. It tries to reveal the mechanism of SO₂toxicological role on central nerve system from neurobiology. It also tries to discover the oxidative damage of airborne fine particulate matter (PM2.5) at various concentrations to heart, liver, spleen, lung, kidney, brain, and testis from rats with intratracheal instillation method. What's more, it tries to investigate the influences of polluted air on cardio pulmonary for healthy human and IL-6&TNF-α in blood serum.SD male rats selected as the experiment object and given a continuous 7-day SO₂ inhalation at the concentration of 28±2mg/m³, the neuron spontaneous activity in rat hippocampus CAl was observed by using glass microelectrode in vivo. The results showed that SO₂ had such effects as neuron toxicity, which could prolong the spontaneous firing time course significantly, decrease the middle frequency firing percentage. The investigation supports the conclusion that SO₂ has the effect on restraining the neuron's excitability. In a word it has the inhibitory effect on the neuron activity. That means that SO₂ on neural toxicological role may be related to the central nervous system's disease and aging.Influence of SO₂ derivatives on the BDNF expression in the neurons ofhippocampus CA1 of rats was observed by immunohistochemistry SABC method. It showed that the number of BDNF expression in hippocampus CA1 neurons in the experiment group significantly decreased compared with the control group. The results also indicated that SO2 derivatives could inhibit the BDNF expression and induce the neurons damage.The effect of SO2 derivatives on the intracellular Ca2+ concentration in hippocampus neurons of rats was studied with Fura-2/AM micro fluorescence detection technique. Results showed that the intracellular Ca2+ concentration in experimental group significantly increased and caused the intracellular Ca overload in hippocampus neurons of rats. These results lead to a conclusion that the intracellular Ca overload in neurons is one of the main mechanisms of SO2 neural toxicological role. It may also be related to the reasons that SO2 has decreased the neuron excitability and inhibited the BDNF expression in hippocampus CA1 of rats that the prophase experiment has proved.It was discussed that SO2 influences the learning and memory function of rats by setting up passive avoidance behavior reflex to test rat's avoidance response behavior ability. It showed that SO2 significantly decreased the learning and memory function of rats. These results imply that SO2 is one of the causes of the decrease of the learning and memory function of rats, which are closely related to the intracellular Ca2+overload and changes of the neuron spontaneous. activity. It has also been proved from these results that hippocampus is the key brain area for learning and memory.The oxidative damage effects of PM25 at different concentration (1.5, 7.5, 37.5 mg/kg) on seven organs (hearts, livers, spleens, lungs, kidneys, brains and testicls) of rats were assessed by intratracheal instillation. It showed that PM2.5 instillation changed antioxidative enzymes activities and lipid peroxidation level in all organs in a dose-dependent manner. And there were also differences in the effects of oxidative damage on seven organs by instilling PM2.5 at the same concentration. These results lead to a conclusion that PM is a systemic toxic agent, not only to lung but also to other organs. Itstoxic effects might be attributed to oxidative damage mediated by prooxidant/antioxidant imbalance or excess free radicals.It was compared the cardiopulmonary function of the healthy people from polluted area and clean area in exercise and state situation using CPET. It showed that HR of TG was significantly higher than the CG at rest, while the vital capacity was significantly lower than the CG. When the load increased to AT and VO2max, the results of VO2, VO2/kg, VO2max, V02max/kg, O2P, METs, DT in CG were significantly higher than the TG. The recovery of HR in TG was relatively lagged. These results lead to the following conclusions: Airborne pollution has very important adverse effects on the cardiorespiratory function and reserve ability;the adverse effects of airborne pollution on the health undergo a gradual, long-term and chronic course. It is not easy to reflect these adverse effects at static state. Therefore CPET could more comprehensively evaluate the adverse effects of airborne pollution on cardiorespiratory damage;in normal condition, lung ventilation is not a major factor to confine the respiratory function.It was investigated the effects of airborne pollution on the expression of IL-6 and TNF-ct in serum of healthy people by the enzyme-linked immunosorbent assay (ELISA). It showed that the levels of IL-6 and TNF-a in serum in TG significantly increased compared with CG. The investigation supports the conclusion that long-term exposure in the polluted air can induce inflammatory reaction. The negative effect of the airborne contaminant may be closely related to the immune dysfunction induced by pro-inflammatory cytokine.