環境與職業化學物暴露相關之心臟血管疾病：系統性回顧

Environmental and Occupational Chemicals Exposure Related Cardiovascular Disease: Systemic Review

王建楠(Jian-Nan Wang) ； 李璧伊(Pi-I Li)

《中華職業醫學雜誌》 24卷3期 (2017/07) Pp. 215-226

摘要

日常生活環境與職場工作可能存在具有心臟毒性的化學物質，生活周遭中如空氣中懸浮微粒(particulate matter)、環境菸(environmental tobacco smoke, ETS)、揮發性有機化合物(volatile organic compounds, VOCs)等，而職場暴露於可能誘發心臟血管疾病之化學物，例如一氧化碳、有機硝化物(organic nitrates)、二硫化碳(carbon disulfide)、氟氯碳化物(chlorofluorocarbon, CFC)、含氯有機溶劑、砷化氫(arsine)、砷(arsenic)、鉛、銻(antimony)、鎘等。已有研究報告指出，即使是短期暴露細懸浮微粒PM2.5(微粒直徑小於2.5微米)，也會增加心血管疾病罹患率和死亡風險，尤其是居住在人口密度高且機動車輛頻繁往來之大都會區。在西元1952年12月5日至8日，英國倫敦為大量濃霧所覆蓋，濃霧主要成分是懸浮微粒與二氧化硫(來自家用煤碳燃燒)，急性大量暴露結果，導致濃霧期間死亡人數急速上升，尤其是本身已罹患慢性呼吸道疾病或心臟病[1]。空氣品質開始受到社會大眾及政府當局之重視，英國政府遂於西元1956年立法通過「空氣清淨法案(Clean Air Act)」，限制家用煤炭之燃燒使用。常見重要空氣污染物(air pollutants)，如二氧化碳、二硫化碳、氧化氮及微量金屬等，少數高濃度污染物可能引發立即性身負面效應，但大多數需一段時間體內累積才會致病。職場之化學物暴露，具有潛在性心臟毒性者不少，以氟氯碳化物為例，目前在工業界製程中，氟氯碳化物類化學物仍大量使用於冰箱、冷卻劑、噴霧劑等行業，用途甚廣，暴露於此類化學物之勞工應不在少數。一旦暴露於氟氯碳化物類化學物，會引發心臟對兒茶酚胺類(catecholamines)的高敏感性，因此僅少量的腎上腺素(adrenaline)便可能造成心律不整(arrythmia)的發生，加重心臟的負擔。因工作場所通風不良而大量暴露時，臨床上可能出現頭痛、頭暈、嗜睡、噁心、心跳加速或心律不整等症狀，中毒情況嚴重時，可能引發癲癇發作、心跳停止或陷入昏迷。預防措施，如透過局部排氣以減少暴露量、增加個人防護配戴等，而對於已罹患冠狀動脈疾病(coronary artery disease, CAD)、心律不整、心臟衰竭或其他心血管疾病者，應給予適當配工以避免氟氯碳化物類化學物之暴露。

關鍵字

空氣懸浮微粒 ； 環境菸 ； 心臟血管疾病 ； 二硫化碳 ； 氟氯碳化物

並列摘要

There may be existed cardiotoxic chemicals in our daily living environment and work sites. Living surroundings such as air particulate matter, environmental tobacco smoke, volatile organic compounds (VOCs), etc.; chemicals exposure probably induced cardiovascular disease in work sites, for examples carbon monoxide, organic nitrates, carbon disulfides, chlorofluocarbon (CFC), organic chlorinated solvents, arsine, arsenic, mercury, cadmium, lead, antimony, etc. Some researches pointed out that even short-term exposure of fine particulate matter PM2.5 might increase relative risks of cardiovascular morbidity and mortality, especially living in the metropolitan area with heavy traffic vehicles. In 1952 December 5-8, there was a dense fog covering the Greater London area, during this period, there was a sudden and enormous rise in mortality rate, especially among the elderly, infants, COPDs, CAD, asthma, etc., hence the goverment passed the Clean Air Act in 1956. Vascular effects of inhaled ambient particles include endothelial dysfunction and promotion of atherosclerotic lesions. Improtantly, these lesions lead to release or secretion of cytokines and chemokines, worsening cardiac complications. There existed a lot of industrail chemicals, some may be potentially cardiotoxic to human body, for example, chlorofluocarbon are widely used in refrigerators, coolers, spray-aided, solvents, etc. CFC may increased the sensitivity of cardiac response to catacholamines, even small amount adrenaline may bring about arrhythmia. Metals (cobalt, magnesium, manganese, nickel, cadmium, lead, etc.), such as cadmium, block calcium channels that affect cardiac rhythm leading to arrhythmia, others such arsenic have high affinity for sulfhydryl groups, and interfere with sulfhydryl- containing proteins, such as receptors, regulatory proteins, and transporters. Carbon disulfide has been identified as an atherogenic agent in laboratory animals. The mechanism for carbon disulfide- atheroma production may involve direct injury to the endothelium coupled with hypothyroidism (urine metabolite thiourea is a potent antithyroid substance).

並列關鍵字

air particulate matter ； environmental tobacco exposure ； carbon disulfide ； cardiovascular disease ； chlorofluocarbon