贵州省是燃煤型氟中毒是严重的省份，氟中毒是环境与基因综合作用的结果。研究表明氧化应激是慢性氟中毒的重要发病机制，植物化学物具有较强的抗氧化活性且广泛存在日常膳食中。少量动物实验研究表明植物化学物可以拮抗过量氟所致的氧化损伤，提示植物化学物可能预防氟中毒，但尚无流行病学研究证据；亦无抗氧化酶（SOD和GPx）基因多态性与氟中毒的关联性及它们之间的相互作用对氟中毒易感性的影响报道。为此，本研究拟采用1:1病例对照研究，收集500对病例和对照的膳食等问卷资料及生物样本，检测分析膳食及血清植物化学物含量、氧化/抗氧化水平和抗氧化酶基因多态性，揭示植物化学物对氟中毒的作用性质和强度，阐明抗氧化酶基因多态性与氧化应激及氟中毒的关系，探索环境与抗氧化酶基因交互作用对氟中毒易感性的影响。为筛选氟中毒的高危人群提供理论基础，为从抗氧化途径选择针对性的措施预防和/或治疗氟中毒提供科学依据。

The most severe area of the coal-burning endemic fluorosis is located in Guizhou province of China. Fluorosis is the result of the combined effects of environmental and genetic. Studies suggest that oxidative stress is an important pathogenesis of chronic fluorosis. Phytochemicals exhibit strong antioxidant activity and are widespread present in our daily diet. Several studies have showed that phytochemicals attenuated oxidative damage induced by excessive fluoride in animal, which indicated that phytochemicals may prevent the risk of fluorosis. However, up to date, there are no epidemical studies have investigated the overall effect of multiple oxidantive phytochemicals on endemic fluorosis. Furthermore, no studies have examined the associations between antioxidant enzymes (SOD and GPx) gene polymorphism and endemic fluorosis and reported the influence of interaction to the susceptibility of fluorosis. To address this issue，we will perform a 1:1 matched case-control study, including 500 pairs of coal-burning endemic fluorosis case and control, to collect dietary intake et al by questionnaire, blood and urine samples. Dietary consumption of phytochemicals and blood or urine concentrations of phytochemicals will be assessed. Antioxidant enzymes gene polymorphisms and blood oxidative/anti-oxidative levels also will be examined. Our results will reveal the effects size and strenth of various phytochemicals on endemic fluorosis, and clarify the associations between antioxidant enzymes gene polymorphisms and endemic fluorosis, and explore influence of interaction between phytochemicals, urine fluorine and antioxidant enzymes gene polymorphisms to the susceptibility of fluorosis. Moreover, our findings will form a theoretical foundation for screening high risk population of endemic fluorosis and provide theoretical evidences for prevention and/or treatment of endemic fluorosis by via antioxidant approach.