葉蕊蕊
鉛作業(yè)住院患者不同血鉛負(fù)荷量與血壓水平及心電圖改變的關(guān)系
葉蕊蕊
[摘要]目的通過(guò)對(duì)血鉛水平異常者的病例對(duì)照研究,探討血鉛水平對(duì)鉛作業(yè)工人血壓及心電圖的影響。方法選取某鋼鐵廠確診為職業(yè)性慢性血鉛水平異常者45人(慢性血鉛中毒20人,慢性血鉛升高25人)為病例組,同時(shí)選取該廠不接觸鉛的工人30人為對(duì)照組,監(jiān)測(cè)血壓、心電圖等檢查結(jié)果進(jìn)行對(duì)比分析。結(jié)果收縮壓水平從高到低依次為慢性血鉛中毒組[(126.0±11.4)mmHg]、慢性血鉛升高組[(120.6±8.99) mmHg]和對(duì)照組[(112.5±5.2) mmHg],組間兩兩比較差異均具有統(tǒng)計(jì)學(xué)意義(P<0.05);舒張壓水平從高到低依次為慢性血鉛中毒組[(76.3±9.0) mmHg]、慢性血鉛升高組[(72.4±6.8) mmHg]和對(duì)照組[(68.7±4.7) mmHg],組間兩兩比較差異均具有統(tǒng)計(jì)學(xué)意義(P<0.05);各類心電圖異??傮w檢出率從高到低依次為慢性血鉛中毒組(65.0%)、慢性血鉛升高組(40.0%)和對(duì)照組(16.7%),差異具有統(tǒng)計(jì)學(xué)意義(趨勢(shì)χ2值=11.930,P=0.001)。結(jié)論鉛可導(dǎo)致收縮壓與舒張壓升高,以及心電圖的異常率上升,且血鉛水平越高上述問(wèn)題越嚴(yán)重。
[關(guān)鍵詞]鉛中毒;血壓;心電圖;職業(yè)暴露
作者單位: 230022合肥安徽省第二人民醫(yī)院內(nèi)科
鉛在工業(yè)中廣泛應(yīng)用,而鉛的危害性越來(lái)越得到關(guān)注。鉛及其化合物可以通過(guò)呼吸道、消化道等不同途徑進(jìn)入人體,導(dǎo)致人體內(nèi)血鉛異常,而鉛并不是人體必需的微量元素,在人體內(nèi)沒(méi)有任何生理功能,所以體內(nèi)微量的鉛就會(huì)威脅人類的健康[1]。近年來(lái)研究大多局限于鉛對(duì)造血系統(tǒng)、神經(jīng)系統(tǒng)及消化系統(tǒng)的影響[2],關(guān)于鉛對(duì)心血管功能的影響國(guó)內(nèi)研究比較少。本文通過(guò)對(duì)鉛作業(yè)人員的血壓和心電圖進(jìn)行調(diào)查分析,探討鉛作業(yè)工人不同血鉛水平與血壓水平以及心電圖變化的關(guān)系,為該人群鉛暴露而誘發(fā)的相關(guān)健康問(wèn)題的防治提供依據(jù)。
1對(duì)象與方法
1.1研究對(duì)象選取某鋼鐵廠在職業(yè)病防治所住院治療的職業(yè)性慢性血鉛水平異常者45例,均為男性爐前工,依據(jù)《中華人民共和國(guó)國(guó)家職業(yè)衛(wèi)生標(biāo)準(zhǔn)GBZ37-2002》,將其分為慢性鉛中毒組(血鉛水平>600 μg/L)20例,年齡28~50(39.5±6.9)歲,工齡3~21(12.3±6.2)年,高中及中專文化程度17例,大專及以上文化程度3例;慢性血鉛升高組(血鉛水平> 400 μg/L)25例,年齡28~47(38.6±6.0)歲,工齡3~21(12.7±5.6)年,高中及中專文化程度20例,大專及以上文化程度5例;對(duì)照組為該廠體檢的不接觸鉛的男性工人(血鉛水平<200 μg/L) 30例,年齡29~52(40.6±7.0)歲,工齡2~24(12.9±6.7)年,高中及中專文化程度26例,大專及以上文化程度4例,3組人員年齡、工齡及文化程度組間比較差異均無(wú)統(tǒng)計(jì)學(xué)意義(P>0.05)。
1.2方法3組人員均按職業(yè)病檢查常規(guī)詢問(wèn)職業(yè)史、既往史、臨床表現(xiàn)等,并進(jìn)行體檢和常規(guī)檢查。心血管指標(biāo):①血壓測(cè)定:采用汞柱式血壓計(jì)測(cè)量血壓,檢查者休息15 min,取仰臥位右手臂置于心臟同一水平,外展45°,測(cè)量安靜狀態(tài)下血壓2次,取其平均血壓值。②心電圖:SCHILLER-AT-102全自動(dòng)心電圖分析儀常規(guī)描記12導(dǎo)聯(lián),必要時(shí)加做18導(dǎo)聯(lián)心電圖,心電圖診斷以黃宛編著的《臨床心電圖學(xué)》第6版為依據(jù)。
2結(jié)果
2.13組人員血壓檢測(cè)結(jié)果慢性血鉛中毒組收縮壓(126.0±11.4) mmHg,舒張壓(76.3±9.0) mmHg;慢性血鉛升高組收縮壓(120.6±8.99) mmHg,舒張壓(72.4±6.8) mmHg;對(duì)照組收縮壓(112.5±5.2) mmHg,舒張壓(68.7±4.7) mmHg,3組人員收縮壓與舒張壓經(jīng)方差分析,差異有統(tǒng)計(jì)學(xué)意義(F收=16.051,F(xiàn)舒=7.626,P均<0.05)。兩兩比較結(jié)果詳見(jiàn)表1。
2.23組人員心電圖比較各類心電圖異??傮w檢出率(包括竇性心動(dòng)過(guò)緩、傳導(dǎo)阻滯、ST-T改變和左室高電壓)從高到低依次為慢性血鉛中毒組(65.0%,13/20),慢性血鉛升高組(40.0%,10/25),對(duì)照組為(16.7%,5/30),經(jīng)χ2趨勢(shì)檢驗(yàn)顯示,3組心電圖異常檢出率差異具有統(tǒng)計(jì)學(xué)意義(趨勢(shì)χ2值=11.930,P=0.001)。其中,各類心電圖異常檢出率的組間比較中,竇性心動(dòng)過(guò)緩和ST-T改變?cè)?組間的檢出率比較差異均具有統(tǒng)計(jì)學(xué)意義,而傳導(dǎo)阻滯和左室高電壓檢出率的組間比較差異均無(wú)統(tǒng)計(jì)學(xué)意義。詳見(jiàn)表2。
注:收縮壓的組間兩兩比較(LSD法):慢性血鉛中毒組與慢性血鉛升高組比較,P=0.037;慢性血鉛中毒組與對(duì)照組比較,P<0.001;慢性血鉛升高組與對(duì)照組比較,P=0.001。舒張壓的組間兩兩比較(LSD法):慢性血鉛中毒組與慢性血鉛升高組比較,P=0.062;慢性血鉛中毒組與對(duì)照組比較,P<0.001;慢性血鉛升高組與對(duì)照組比較,P=0.045
表2 3組對(duì)象各種EKG異常例數(shù)比較[例(%)]
注:傳導(dǎo)阻滯及左室高電壓在3組人員間比較時(shí)采用校正的卡方值
3討論
本次研究結(jié)果顯示,在血壓水平的組間比較上,收縮壓與舒張壓水平均表現(xiàn)為慢性血鉛中毒組最高,其次為慢性血鉛升高組,而對(duì)照組最低,結(jié)果表明血鉛水平的異??蓪?dǎo)致血壓的升高,且有血鉛水平越高個(gè)體血壓水平越高的趨勢(shì)。其機(jī)制可能通過(guò)以下幾個(gè)途徑:①影響緩激肽系統(tǒng)和腎素-血管緊張素-醛固酮系統(tǒng)[3],通過(guò)抑制鈉泵相關(guān)蛋白和腎素-血管緊張素系統(tǒng)作用于平滑肌鈣離子信號(hào)系統(tǒng)[4],改變鈣離子激活的血管平滑肌細(xì)胞的增殖和收縮,增強(qiáng)血管對(duì)收縮激素如去甲腎上腺素的反應(yīng)性,引起血管收縮。②通過(guò)底物磷酸化,改變蛋白激酶C活性經(jīng)Ca2+/cAMP作用于血管平滑肌細(xì)胞,引起血管收縮,血壓升高[5]。③鉛誘導(dǎo)細(xì)胞活性氧產(chǎn)生,經(jīng)細(xì)胞活性氧鏈產(chǎn)生過(guò)氧離子,使超氧化物歧化酶下降,一氧化氮下降,血管平滑肌收縮,血壓上升[6]。④鉛干擾脂質(zhì)代謝,可使體內(nèi)的氧自由基增多,產(chǎn)生過(guò)氧化脂質(zhì),引起高脂血癥,導(dǎo)致動(dòng)脈硬化,使得血壓升高[7]。⑤鉛作用于腎小管使其集合管對(duì)水的通透性升高,引起腎小球細(xì)胞壞死,間質(zhì)纖維化,腎小管變性,導(dǎo)致血壓升高[8]。
本次研究結(jié)果顯示,在心電圖的組間比較上,心電圖異??傮w檢出率表現(xiàn)為慢性血鉛中毒組最高、其次為慢性血鉛升高組、對(duì)照組最低,結(jié)果表明血鉛水平的異??蓪?dǎo)致心電圖異??傮w檢出率升高,且有血鉛水平越高心電圖異??傮w檢出率越高的趨勢(shì),其機(jī)制可能為:① 鉛能抑制心肌收縮力和傳導(dǎo)系統(tǒng),降低心肌細(xì)胞興奮性,鉛與ATP形成lead-ATP復(fù)合體,影響細(xì)胞內(nèi)質(zhì)子梯度,抑制線粒體呼吸,使ATP濃度進(jìn)行性降低,影響心肌收縮。② 有研究者用30 μmol/L的鉛液灌注小鼠心臟,發(fā)現(xiàn)鉛引起冠狀動(dòng)脈收縮,影響心臟舒張的代償性機(jī)制,從而使得冠脈血流下降。③ 鉛對(duì)心肌細(xì)胞微粒體膜的陽(yáng)離子轉(zhuǎn)運(yùn)酶能夠產(chǎn)生影響,使鈣離子在心肌細(xì)胞內(nèi)聚集,導(dǎo)致鈣離子轉(zhuǎn)運(yùn)異常,從而引起心肌細(xì)胞功能紊亂。④ 血鉛水平升高可引起左室肥大,左室肥大與血鉛水平明顯相關(guān)[9]。⑤ 鉛改變心血管系統(tǒng)對(duì)縮血管物質(zhì)的反應(yīng)性及血管平滑肌表達(dá),增加心肌負(fù)荷。
綜上所述,本次研究結(jié)果顯示,長(zhǎng)期的血鉛水平高于正常會(huì)引起血壓和心電圖改變,對(duì)心血管系統(tǒng)可造成暫時(shí)性或永久性的損害。也有學(xué)者[10]認(rèn)為驅(qū)鉛治療后,心電圖和血壓的異常率能夠下降,部分心電圖可以基本恢復(fù)正常,高血壓例數(shù)能夠顯著降低,血壓水平能夠接近正常水平。這些都說(shuō)明及時(shí)有效的治療,能夠減輕或逆轉(zhuǎn)心血管系統(tǒng)的損害,表明鉛對(duì)心血管系統(tǒng)的損害具有可逆性。因此,加強(qiáng)鉛作業(yè)人員的自我防護(hù)意識(shí),做好個(gè)人防護(hù),定期進(jìn)行職業(yè)健康體檢,監(jiān)測(cè)血壓、心電圖,做到早發(fā)現(xiàn)、早診斷、早治療,對(duì)鉛作業(yè)人員心血管疾病的預(yù)防有重要意義[11]。
參考文獻(xiàn)
[1]魏群英, 魏靜麗, 王愛(ài)琴, 等. 329例慢性職業(yè)性鉛中毒患者治療前后心電圖的變化[J]. 國(guó)際護(hù)理學(xué)雜志, 2012, 31(6):1140-1142.
[2]趙麗敏, 郭連霞, 吳逸明. 焦作市某蓄電池廠鉛作業(yè)人員心電圖調(diào)查分析[J]. 河南預(yù)防醫(yī)學(xué)雜志, 2011, 22(5):361-363.
[3]Loew M, Hoffmann M, Hahmann H, et al. Genotype combinations of plasminogen activator inhibitor-l and angiotensin-converting enzyme genes and risk for early onset of coronary heart disease[J]. Eur J Cardiovasc Prey Rehabi, 2006, 13(3):449-456.
[4]Tanabe N, Amano S, Tatsumi K, et al. Angiotensin-converting enzyme gene polymorphisms and prognosis in chronic thromboembolic pulmonary hypertension[J]. Circ J, 2006, 70(9): 1174-1179.
[5]Hernberg S. Lead poisoning in a historical perspective[J]. Am J Ind Med, 2000, 38(3): 244-254.
[6]Rahman S, Khalid N, Zaidi JH, et al. Non-occupational lead exposure and hypertension in Pakistan adults[J]. J Zhejiang Univ Sci B, 2006, 7(9):732-737.
[7]Kristal-boneh E, Coller D, Froom P, et al. The association between occupational lead exposure and scrum cholesterol and lipoprotein levels J[J]. Am J Public Health, 1999, 89: 1083-1087.
[8]戴繼舫. 鉛的心血管毒理及與高血壓的關(guān)系[J].中國(guó)公共衛(wèi)生, 2002, 18(3):397-399.
[9]Cheng Y, Schwartz J, Vokonas PS, et al. Electrocardiographic conduction disturbances in association with low-level lead exposure :the normative aging study[J]. Am J Cardiol, 1998, 82(5): 594-599.
[10] 吳鈞芳. 鉛作業(yè)工人血鉛 鋅卟啉水平與心電 血壓變化的研究[D]. 南昌: 南昌大學(xué), 2009.
[11] 夏安莉, 李杰, 劉敏. 鉛對(duì)作業(yè)工人心電圖的影響[J].中國(guó)工業(yè)醫(yī)學(xué)雜志, 2007, 20(2):721.
(2014-11-04收稿2015-02-01修回)
Relationship between different blood lead load of hospitalized patients engaged in work related to lead and their blood pressure as well as their electrocardiogram changes
YeRuirui
AnhuiNo.2People′sHospital,Hefei230022,China
[Abstract]ObjectiveThrough the case-control study of the workers with abnormal blood lead level, to explore the effects of blood lead level on the blood pressure and electrocardiogram of the workers. MethodsForty-five workers from a certain steel works who were diagnosed as having chronic abnormal blood lead level were selected (20 workers were diagnosed as chronic blood lead poisoning, 25 workers were diagnosed as having chronic elevated blood lead) as the case group; meanwhile 30 workers from the same steel woks who had physical examination and out of touch with lead were selected as control group, then their blood pressure was monitored and electrocardiogram examination results were analyzed. ResultsThe systolic blood pressure levels of the workers from high to low in turn were chronic blood lead poisoning group [(126.0±11.4) mmHg], chronic elevated blood lead group [(120.6±8.99) mmHg] and the control group [(112.5±5.2) mmHg], and the comparative differences between any two groups were all statistically significant; the diastolic blood pressure levels of the workers from high to low in turn were chronic blood lead poisoning group [(76.3±9.0) mmHg], chronic elevated blood lead group [(72.4±6.8)mmHg] and the control group [(68.7±4.7)mmHg], and the comparative differences between any two groups were all statistically significant; the overall detection rate of all kinds of abnormal electrocardiogram (ECG) from high to low of the workers in turn was chronic blood lead poisoning group (65.0%), chronic elevated blood lead group (40.0%) and the control group(16.7%) (χ2=11.930,P=0.001). ConclusionLead can result in higher systolic blood pressure and diastolic blood pressure, and a rising rate of abnormal ECG; moreover, the higher blood lead levels is, the more obvious of the above problems.
[Key words]Lead poisoning;Blood pressure;Electrocardiogram;Occupational exposure
doi:10.3969/j.issn.1000-0399.2015.04.021