Article(id=1208516105614790935, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1208516099369464789, articleNumber=null, orderNo=null, doi=10.11855/j.issn.0577-7402.2022.01.0072, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=research-article, receivedDate=1619539200000, receivedDateStr=2021-04-28, revisedDate=null, revisedDateStr=null, acceptedDate=1631030400000, acceptedDateStr=2021-09-08, onlineDate=1766062292683, onlineDateStr=2025-12-18, pubDate=1643299200000, pubDateStr=2022-01-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1766062292683, onlineIssueDateStr=2025-12-18, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1766062292683, creator=13701087609, updateTime=1766062292683, updator=13701087609, issue=Issue{id=1208516099369464789, tenantId=1146029695717560320, journalId=1189873630562394117, year='2022', volume='47', issue='1', pageStart='1', pageEnd='101', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=0, createTime=1766062291230, creator=13701087609, updateTime=1766062975431, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1208518969208738485, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1208516099369464789, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1208518969208738486, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1208516099369464789, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=72, endPage=77, ext={EN=ArticleExt(id=1208516106491400521, articleId=1208516105614790935, tenantId=1146029695717560320, journalId=1189873630562394117, language=EN, title=Impacts of air pollution and climate change on kidney diseases: Progress in biological mechanisms, columnId=1190243275882729994, journalTitle=Medical Journal of Chinese People’s Liberation Army, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

Kidney diseases have become an important public health problem worldwide that threatens human health. In addition to traditional risk factors such as advanced age, hypertension, and diabetes, environmental pollution, especially the air pollution and climate change, are also major risk factors for chronic kidney disease. The exposure of airborne particulate matter or gaseous pollutants has been found to be closely associated with the incidence of chronic kidney disease, decline of kidney function, and poor prognosis of patients. As the main manifestation of global climate change, climate warming could also lead to acute kidney injury and nephrolithiasis. This paper reviews the progress in the epidemiological research of the impacts of air pollution and climate change on kidney diseases, in order to provide reference for air pollution control, climate governance, and the development of prevention and control strategies for kidney diseases.

, correspAuthors=Lu-Xia Zhang, authorNote=null, correspAuthorsNote=
*E-mail:
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肾脏疾病已成为全球范围内危害人类健康的重要公共卫生问题。除高龄、高血压、糖尿病等传统因素外,环境污染也是引发肾脏疾病的重要危险因素,尤其是大气污染及气候因素对肾脏健康的影响不可忽视。大气颗粒物及气态污染物暴露与肾脏疾病的发生、肾功能下降及患者的不良预后密切相关。气候变暖作为全球气候变化的最主要表现,同样会引起急性肾损伤及肾结石等疾病。本文对国内外大气污染及气候因素对肾脏疾病的影响及其生物学机制研究进展进行综述,以期为治理大气污染、应对气候变化,以及制定肾脏疾病人群防治策略提供依据。

, correspAuthors=张路霞, authorNote=null, correspAuthorsNote=
张路霞,E-mail:
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杨超,医学博士,助理研究员,主要从事慢性肾脏病及相关慢性疾病的流行病学研究

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大气污染及气候因素对肾脏疾病的影响及其生物学机制研究进展
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杨超 1, 2, 3 , 李鹏飞 3 , 张路霞 1, 2, 3, 4, *
解放军医学杂志 | 综述 2022,47(1): 72-77
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解放军医学杂志 | 综述 2022, 47(1): 72-77
大气污染及气候因素对肾脏疾病的影响及其生物学机制研究进展
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杨超1, 2, 3, 李鹏飞3, 张路霞1, 2, 3, 4, *
作者信息
  • 1北京大学第一医院肾内科/北京大学肾脏病研究所,北京 100034
  • 2中国医学科学院免疫介导肾病诊治创新单元,北京 100034
  • 3浙江省北大信息技术高等研究院,杭州 311215
  • 4北京大学健康医疗大数据国家研究院,北京 100191
  • 杨超,医学博士,助理研究员,主要从事慢性肾脏病及相关慢性疾病的流行病学研究

通讯作者:

张路霞,E-mail:
Impacts of air pollution and climate change on kidney diseases: Progress in biological mechanisms
Chao Yang1, 2, 3, Peng-Fei Li3, Lu-Xia Zhang1, 2, 3, 4, *
Affiliations
  • 1Department of Nephrology, Peking University First Hospital/Peking University Institute of Nephrology, Beijing 100034, China
  • 2Research Units of Diagnosis and Treatment of Immune-Mediated Kidney Diseases, Chinese Academy of Medical Sciences, Beijing 100034, China
  • 3Advanced Institute of Information Technology, Peking University, Hangzhou 311215, China
  • 4National Institute of Health Data Science at Peking University, Beijing 100191, China
出版时间: 2022-01-28 doi: 10.11855/j.issn.0577-7402.2022.01.0072
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肾脏疾病已成为全球范围内危害人类健康的重要公共卫生问题。除高龄、高血压、糖尿病等传统因素外,环境污染也是引发肾脏疾病的重要危险因素,尤其是大气污染及气候因素对肾脏健康的影响不可忽视。大气颗粒物及气态污染物暴露与肾脏疾病的发生、肾功能下降及患者的不良预后密切相关。气候变暖作为全球气候变化的最主要表现,同样会引起急性肾损伤及肾结石等疾病。本文对国内外大气污染及气候因素对肾脏疾病的影响及其生物学机制研究进展进行综述,以期为治理大气污染、应对气候变化,以及制定肾脏疾病人群防治策略提供依据。

大气污染  /  气候变化  /  慢性肾脏病  /  急性肾损伤  /  流行病学

Kidney diseases have become an important public health problem worldwide that threatens human health. In addition to traditional risk factors such as advanced age, hypertension, and diabetes, environmental pollution, especially the air pollution and climate change, are also major risk factors for chronic kidney disease. The exposure of airborne particulate matter or gaseous pollutants has been found to be closely associated with the incidence of chronic kidney disease, decline of kidney function, and poor prognosis of patients. As the main manifestation of global climate change, climate warming could also lead to acute kidney injury and nephrolithiasis. This paper reviews the progress in the epidemiological research of the impacts of air pollution and climate change on kidney diseases, in order to provide reference for air pollution control, climate governance, and the development of prevention and control strategies for kidney diseases.

air pollution  /  climate change  /  chronic kidney disease  /  acute kidney injury  /  epidemiology
杨超, 李鹏飞, 张路霞. 大气污染及气候因素对肾脏疾病的影响及其生物学机制研究进展. 解放军医学杂志, 2022 , 47 (1) : 72 -77 . DOI: 10.11855/j.issn.0577-7402.2022.01.0072
Chao Yang, Peng-Fei Li, Lu-Xia Zhang. Impacts of air pollution and climate change on kidney diseases: Progress in biological mechanisms[J]. Medical Journal of Chinese People’s Liberation Army, 2022 , 47 (1) : 72 -77 . DOI: 10.11855/j.issn.0577-7402.2022.01.0072
肾脏疾病由于其高患病率、高致残率、高医疗花费、低知晓率等特征,已成为危害人类健康的重要公共卫生问题[1-2]。慢性肾脏病(chronic kidney disease,CKD)是肾脏疾病中最为常见的一类疾病,据报道2017年全球共有CKD患者6.98亿,其中我国约1.3亿[3-4]。此外,近年来全球范围内急性肾损伤(acute kidney injury,AKI)发病率呈明显上升趋势,病死率居高不下[5-6]。肾脏疾病是多因素导致的复杂疾病,传统危险因素包括高龄、高血压、糖尿病、高尿酸血症等[7]。此外,环境污染也是引发肾脏疾病的重要因素,包括大气污染、气候因素、有机溶剂、重金属污染、生物毒素及农业杀虫剂等[1,8]。由于在过滤过程中的毒素汇集,肾脏易受环境危险因素毒性效应的影响[8]。多项流行病学研究提示,大气污染及气候因素对人体健康的影响不可忽视,尤其是大气污染已成为导致我国人口死亡及健康寿命损失的第4位危险因素[9-11]。近年来,越来越多的研究开始关注环境污染因素中大气污染及气候因素对肾脏疾病发生、发展及预后的影响,本文对国内外相关流行病学研究进展进行综述。
大气颗粒物(particulate matter,PM)及二氧化氮(nitrogen dioxide,NO2)是目前全球多数地区大气污染的主要组分,前者由悬浮在空气中的有机及无机物的固体或液体颗粒混合物组成,后者主要来源于燃料燃烧的过程,尤其与交通产生的废气排放密切相关[12]。当前,世界卫生组织、欧洲环境署、美国环境保护署及我国生态环境部已对PM及NO2等多种常见污染物浓度进行日常监测。来自美国等国家的多项研究证实,大气污染物浓度升高与CKD发病风险的增加明显相关[13-14]。Metha等[13]研究美国波士顿地区退伍军人的数据发现,大气细颗粒物(particular matter with an aerodynamic diameter ≤2.5 μm,PM2.5)长期暴露可降低估算肾小球滤过率(estimated glomerular filtration rate,eGFR),提高CKD的发病风险。Bragg-Gresham等[15]探讨了美国3143个县医疗保险人群PM2.5长期暴露与CKD发病风险的关联效应,发现PM2.5暴露浓度从第1上升至第3四分位数水平时,CKD发病风险增加至1.05[95%置信区间(confidence interval,CI) 1.03~1.07]倍。另一项整合了美国退伍军人数据的大型队列研究显示,暴露于可吸入颗粒物(particular matter with an aerodynamic diameter ≤10 μm,PM10)及气态污染物NO2、一氧化碳(carbon monoxide,CO),同样可以增加CKD的发病风险,其中,上述污染物每增加1个四分位间距,CKD发生风险分别增加至原来的1.07(95%CI 1.05~1.08)倍、1.09(95%CI 1.08~1.11)倍及1.10(95%CI 1.08~1.11)倍[16]。韩国一项纳入24 407例30岁以上成年人的全国性调查发现,PM10及NO2长期暴露与eGFR水平下降有关,差异有统计学意义;但在调整其他混杂因素之后,这两种大气污染物与CKD发病风险增加的关系变得无统计学意义[14]
在我国,大气污染对肾脏危害效应的研究较少,且研究结论不完全一致。国内一项研究利用我国13个省市47 204例研究对象的横断面调查数据,结合卫星遥感数据反演的大气PM2.5浓度,分析了PM2.5长期暴露对CKD患病风险的影响,结果显示,我国大气PM2.5浓度每增加10 μg/m3,CKD及蛋白尿发生风险比值比分别为1.28(95%CI 1.22~1.35)及1.39(95%CI 1.32~1.47),并且此种效应的作用在城市高于农村,对年轻人(<65岁)、男性、非糖尿病及非心血管疾病人群的影响更大,提示这些人群有可能是大气污染相关效应的易感人群[17]。来自我国台湾地区的研究显示,在台北市8497例65岁及以上老年人群中,暴露于较高浓度的PM10与CKD发病风险增加密切相关[18]。Yang等[19]研究台北市年度健康体检数据发现,PM10年均暴露浓度每增加1个四分位间距(5.83 μg/m3),CKD发病风险增加至1.15(95%CI 1.07~1.23)倍,但该研究未发现PM2.5长期暴露与CKD发病风险的显著关联。此外,另一项来自我国台湾地区的研究表明,PM2.5、NO2、NO、二氧化硫(sulfur dioxide,SO2)的短期暴露会增加肾病综合征的发病风险[20]。Wang等[21]对四川省绵阳市7071例女性健康居民的研究显示,大气污染物的短期暴露同样能引起eGFR水平显著下降,日均污染物暴露量每增加1个四分位间距[1.04~1.50 m3/(kg·d)],eGFR水平下降0.78(95%CI 0.45~1.11) ml/(min·1.73 m2),从而增加CKD的发病风险。
美国开展的一项大样本研究对近250万例受试者进行了8.5年的观察,结果显示:PM2.5长期暴露浓度每增加10 μg/m3,eGFR下降超过30%及终末期肾脏病的发生风险分别增加至原来的1.28(95%CI 1.18~1.39)倍及1.26(95%CI 1.17~1.35)倍[22]。该团队还发现PM10、NO2、CO长期暴露均与CKD的疾病进展及不良预后密切相关[16]。一项纳入了全球14项研究的Meta分析结果显示,PM2.5、PM10、NO2、CO、SO2、臭氧(ozone,O3)等大气污染物不同程度的长期暴露均会导致CKD患者的肾功能下降,其中PM10年平均暴露浓度每增加10 μg/m3,eGFR水平下降0.83(95%CI 0.12~1.54) ml/(min·1.73 m2)[23]。另一项在上海市3622例住院患者中开展的研究发现,PM10长期暴露还可显著降低eGFR水平,该效应在男性、65岁以上、体重指数<24及未患高血压的人群中更为明显[24]
膜性肾病作为一种自身免疫相关的原发性肾小球疾病,以大量蛋白尿、低蛋白血症、高度水肿、高脂血症为主要临床表现,环境因素对其发病机制的影响也颇为重要。国内有学者在全国范围内开展了一项关于肾脏病理类型转变与大气污染的流行病学调查,涵盖了我国282个城市938家医院的7万余例肾活检资料,时间跨度为2004-2014年,结果显示,我国膜性肾病以每年13%的增幅呈显著增加的趋势,这种增加与PM2.5长期暴露及平均空气质量指数密切相关,而且此种关系呈非线性:在PM2.5>70 μg/m3的地区,其浓度每增加10 μg/m3,发生膜性肾病的风险增加至1.14(95%CI 1.10~1.18)倍,而在PM2.5<60 μg/m3的地区,这一效应明显减弱;其他类型的肾小球肾炎则相对稳定[25]
全球气候变化作为当前全球性的热点问题,同样影响着人类的健康与安全。气候变暖是全球气候变化的最主要表现及直接影响之一,有可能增加多种疾病的发生风险及增高死亡率,例如,高温会增加循环系统的负担,使机体失去调节内部温度的能力,进而导致热痉挛、热衰竭、中暑甚至死亡[11,26]。自1950年以来,全球热浪频率及强度不断上升,不仅增高了AKI的发生率及住院率,也导致了媒介传染病及肾病的增多[27-28]。在2003年的欧洲热浪期间,肾衰竭为导致死亡的主要原因,其中老年人及合并CKD的患者为主要易感人群[27-28]。来自美国的最新研究表明,仅经历一天的酷热即可使终末期肾脏病患者当日的住院风险增加至原来的1.27(95%CI 1.13~1.43)倍,死亡风险增至1.31(95%CI 1.01~1.70)倍,且在合并充血性心力衰竭、慢性阻塞性肺疾病及糖尿病的患者中该效应更加显著,提示在指南中应当考虑加强对极端高温天气下肾脏疾病患者管理的建议[29]
环境温度及炎热指数升高是肾结石形成的危险因素之一,主要与炎热导致大量出汗、尿量减少,以及尿液矿物质及盐过饱和有关。来自美国及韩国的两项研究均证实,日平均气温的大幅上升可显著增加肾结石的发生风险:在美国,日平均气温从10 ℃升至30 ℃,肾结石的发生风险增加36%~39%[30]。在韩国,日平均气温29 ℃时的肾结石发生风险是13 ℃时的2.54(95%CI 1.67~3.87)倍[31]。国外有学者估计,到21世纪末,全球平均气温将升高1.0~4.5 ℃,可导致肾结石及梗阻性肾病的患病人数明显增加,同时也将带来巨大的医疗支出[32]。在过去50年间,我国平均气温升高了0.5~0.8 ℃,上升幅度高于全球平均水平,预计未来气候变化将更加剧烈[33],但目前尚无研究评估我国长期气候变化对肾结石等相关疾病的影响。
反复高温暴露还可导致热应激性肾病——一种可能由气候变化引发的不明原因CKD,主要见于中美洲、南美洲、非洲、印度及斯里兰卡等地区,好发人群为在高热天气下务农的年轻男性(如甘蔗种植者)。热应激性肾病的临床表现与间质性肾炎相似,其病理特点包括间质纤维化、肾小管萎缩及间质单核细胞浸润等[8]。目前认为,反复发生热应激、脱水、生活及职业条件较差是热应激性肾病的主要致病原因[27,34]。在巴西的萨尔瓦多,当地政府已经采取一系列措施,并启动了“工人健康和效率计划(worker health and efficiency program)”来提升工作条件,以降低热应激性肾病的发生率[34]。此外,气温升高还会增加大气蒸发及水汽量,导致大多数地区极端降水事件的频率及强度增加,进而引发一些由水污染所致的极端天气事件性肾脏病[27]
大气污染及气候因素对肾脏疾病影响的机制多样,短期或长期暴露对机体健康的影响存在较大差异,目前尚未完全阐明。既往研究提示,炎症反应、氧化应激、细胞毒性反应、DNA修复及甲基化异常、DNA氧化及碎片、组蛋白乙酰化、晶体肾损害、肾脏血管血液流变学改变、热应激及脱水等可能是潜在的生物学机制[34-36]。最新的动物实验结果表明,部分大气污染物会渗透到肺泡组织并随血液作用于肾脏,由颗粒物诱发的肺部炎性介质也可能溢出到循环中,导致全身炎症及氧化应激,诱导白细胞及血小板激活,过氧化物酶增加,细胞因子表达增强,活性氧(reactive oxygen species,ROS)生成增多,生成抗磷脂酶A2受体(PLA2R)抗体,从而引起肾脏免疫复合物沉积,而且ROS还能导致线粒体活动、蛋白质结构及DNA损伤,进一步引起肾脏损害,可能表现为肾小球硬化、系膜扩张、肾小管萎缩及血管损伤[22,37]
此外,沉积在肺泡中的PM2.5等颗粒物会激活机体自主神经系统,诱发自主神经系统失衡及交感神经兴奋,抑制副交感神经系统,并促进全身炎症反应及其他器官的氧化应激和损伤[8]。这一过程还会引起血管收缩及内皮功能障碍,导致肾脏组织的炎症及肾血管内皮损伤[38]。有研究表明,长期暴露于PM2.5的大鼠肾脏出现以弥漫性髓质浸润及局灶性肾小球周围浸润为主的慢性炎症,使肾组织中巨噬细胞大量增加,进一步引起纤维化斑块形成及肾小管基底膜增厚[39]。相比于PM2.5,亚微米级颗粒物(particular matter with an aerodynamic diameter≤1 μm,PM1)的粒径更小,且在大气中停留时间长、输送距离远,甚至可以进入循环或淋巴系统,有可能对人体健康产生更大的危害[40]。但是,当前由于部分毒性代谢机制尚不完全明确,大气污染及气候因素对肾脏的危害效应及具体生物学机制仍需更多的流行病学及基础研究证据支持。
当前,国内外已开展了多项环境因素对肾脏疾病影响的流行病学研究,发现多种大气污染物及气候因素与不同类型肾脏疾病的发生、发展及预后密切相关,主要关注点为PM2.5、PM10与CKD的关联效应。此外,其他环境污染因素,如有机溶剂、重金属、生物毒素、农业杀虫剂、二手烟等,也逐渐受到研究者的广泛关注。因此,建议相关部门基于既往研究证据,通过推动立法及健康教育,提倡绿色交通、清洁能源、清洁食物与饮水,加强工农业职业防护,提升公众对环境污染的防护意识,并针对大气污染及气候因素实施三级预防策略及综合性防治措施,以减轻相关污染物可能带来的健康危害。
既往研究主要将健康医疗相关数据与不同来源、不同类型的环境监测数据进行匹配、整合及利用,通过时间序列、病例交叉、队列研究及空间分析技术等分析环境暴露因素的影响程度,研究结果对促进环境保护及国民健康起到了重要推动作用[41-44]。但是,目前相关循证医学研究证据仍较为有限,证据水平较低,未能全面、系统地明确多维度大气污染和气候因素对肾脏疾病的影响及其作用机制,罕有研究评估大气污染与气候变化之间的协同作用,不利于开展人群层面的肾脏病防治工作。既往研究具有以下局限性:(1)研究人群的代表性及结论的外推性有限,缺乏全国范围内不同地区多种大气污染物暴露对不同类型肾脏疾病进展和预后的影响及机制研究;(2)多数研究大气污染物暴露浓度采集的空间分辨率只能精确到10 km,数据的精确性受到一定限制;(3)气态污染物与肾脏疾病的关联性研究相对较少,且研究结论不完全一致;(4)气候因素与肾脏疾病之间的研究证据较少,维度较单一,我国以高温为主要环境因素的研究匮乏;(5)缺乏多维度环境因素对肾脏疾病时空分布特征影响的系统性定量评估,未对不同维度或同一维度内不同环境因素之间的交互作用进行深入探究。
近年来,随着健康医疗大数据的积累及挖掘利用,医学、公共卫生与环境领域的跨学科交叉研究不断创新,大数据研究成果相继涌现。诸如地理探测器等新型空间统计学方法及深度学习算法的发展[43,45],也为挖掘传统方法难以分析的高维变量及其交互作用、探究肾脏疾病相关环境因素提供了良好的方法学工具。当前,我国肾脏疾病谱正发生变迁且存在明显地区差异性,个体层面的影响因素尚不能完全解释此种差异[46];而且,我国的PM2.5等大气污染物暴露浓度远高于欧美、日本等发达国家[47]。在此背景下,通过融合真实世界医疗大数据与大气污染和气候变化的监测数据,建立大型的环境与自然人群或专病队列,可以全面挖掘影响肾脏疾病发生发展的环境因素及其剂量-反应关系,以在人群层面为我国肾脏疾病防控策略的制定提供参考,最终有效应对大气污染及气候变化,遏制我国不断上升的肾脏疾病负担。
  • 国家自然科学基金(82003529)
  • 国家自然科学基金(91846101)
  • 北京市科技新星计划交叉学科合作课题(Z191100001119008)
  • 中国医学科学院医学与健康科技创新工程项目(2019-I2M-5-046)
  • 北大百度基金(2019BD017)
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2022年第47卷第1期
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doi: 10.11855/j.issn.0577-7402.2022.01.0072
  • 接收时间:2021-04-28
  • 首发时间:2025-12-18
  • 出版时间:2022-01-28
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  • 收稿日期:2021-04-28
  • 录用日期:2021-09-08
基金
National Natural Science Foundation of China(82003529)
国家自然科学基金(82003529)
National Natural Science Foundation of China(91846101)
国家自然科学基金(91846101)
Beijing Nova Programme Interdisciplinary Cooperation Project(Z191100001119008)
北京市科技新星计划交叉学科合作课题(Z191100001119008)
Chinese Academy of Medical Sciences Innovation Fund for Medical Sciences(2019-I2M-5-046)
中国医学科学院医学与健康科技创新工程项目(2019-I2M-5-046)
Peking University-Baidu Fund(2019BD017)
北大百度基金(2019BD017)
作者信息
    1北京大学第一医院肾内科/北京大学肾脏病研究所,北京 100034
    2中国医学科学院免疫介导肾病诊治创新单元,北京 100034
    3浙江省北大信息技术高等研究院,杭州 311215
    4北京大学健康医疗大数据国家研究院,北京 100191

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张路霞,E-mail:
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2种不同金属材料的力学参数

Family
属数
Number of
genus
种数
Number of
species
占总种数比例
Percentage of
total species (%)

Genus
种数
Number of
species
占总种数比例
Percentage of total
species (%)
鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39
多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39
红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
小菇属 Mycena 11 5.26
光柄菇属 Pluteus 5 2.39
红菇属 Russula 17 8.13
栓菌属 Trametes 5 2.39
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