MORTALITY AMONG EMPLOYEES OF LEAD BATTERY PLANTS AND LEAD-PRODUCING PLANTS, 1947-1980
MORTALITY AMONG EMPLOYEES OF LEAD BATTERY PLANTS AND LEAD-PRODUCING PLANTS, 1947-1980
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DOI：
10.5271/sjweh.2215
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发表时间：
1985-01-01
影响因子：
6.3
通讯作者：
KHEIFETS, L
中科院分区：
文献类型：
--
作者：
COOPER, WC;WONG, O;KHEIFETS, L
两个队列的男性铅工人，4519电池厂工人和2300铅生产工人，所有这些人都在1946年1月1日至1970年12月31日期间至少雇用了一年，观察了从1947年1月1日至1980年12月31日的34年期间的死亡率。截至截止日期，前一组中94.7%的患者和后一组中91.6%的患者确定了生命状态。第一组有1718人死亡，第二组有621人死亡。在每个队列中，所有原因合并的死亡率均显著高于预期，标准化死亡率比（SMR）分别为107和113。在电池厂工人中，死亡率高于预期的主要原因是恶性肿瘤（SMR 113）、其他高血压疾病（主要是肾脏疾病）（SMR 320）、慢性肾炎（SMR 222）和一组不明确的疾病（SMR 355）造成的大量死亡。在铅生产工人中，模式相似，其他高血压疾病（SMR 475）、高血压疾病（SMR 203）、慢性肾炎（SMR 265）和不明确疾病（SMR 214）导致的死亡人数显著增加。外部原因造成的死亡人数也明显过多（SMR 143）。总恶性肿瘤的SMR为113，但该值在5%水平下未显著升高。在两个队列中，脑血管疾病的死亡率均显著过高，SMR分别为93和132。比例死亡率分析表明，冶炼厂工人中死于脑血管疾病和高血压心脏病的人数过多，部分原因是冶炼厂人口中非白人的比例很高。胃、肝和肺是两个队列中导致大多数癌症死亡的部位，但SMR值升高仅在电池厂工人的胃癌和肺癌中具有统计学意义。在两个队列中，均未发生因肾脏、脑部或淋巴系统恶性肿瘤导致的过多死亡。由于1960年之前的定量信息很少，因此不可能将观察到的死亡率与铅暴露水平联系起来。据了解，过去的接触量非常高。不能排除种族、饮食、饮酒和吸烟是癌症死亡的可能混杂病因因素。
Two cohorts of male lead workers, 4 519 battery plant workers and 2 300 lead production workers, all of whom had been employed for at least one year during the period 1 January 1946 through 31 December 1970, were observed for mortality during the 34 years from 1 January 1947 through 31 December 1980. Vital status as of the closing date was determined for 94.7% of the former group and 91.6% of the latter. There were 1 718 deaths in the first cohort and 621 in the second. Mortality from all causes combined was significantly greater than expected in each cohort, the standardized mortality ratio (SMR) being 107 and 113, respectively. Among the battery plant workers the greater than expected mortality rate resulted in large part from a significant number of excess deaths from malignant neoplasms (SMR 113), other hypertensive disease (mainly renal) (SMR 320), chronic nephritis (SMR 222), and a group of ill-defined conditions (SMR 355). Among the lead production workers the pattern was similar, with a significant number of excess deaths from other hypertensive disease (SMR 475), hypertensive disease (SMR 203), chronic nephritis (SMR 265), and ill-defined conditions (SMR 214). There was also a significant excess of deaths from external causes (SMR 143). The SMR for total malignancies was 113, but this value was not significantly elevated at the 5% level. In neither cohort were deaths from cerebrovascular disease in significant excess, the SMR being 93 and 132, respectively. A proportionate mortality analysis showed that the excess deaths from cerebrovascular disease and from hypertensive heart disease among smelter workers were in part due to the high proportion of nonwhites in the smelter populations. The stomach, liver, and lungs were the sites responsible for most excess cancer deaths in both cohorts, but the elevated SMR values were statistically significant only for gastric and lung cancers in battery plant workers. There were no excess deaths from malignancies of the kidney, brain, or lymphopoeitic system in either cohort. It is impossible to relate the observed mortality to levels of lead exposure, because of meager quantitative information prior to 1960. It is known that past exposures had been very high. Ethnicity, diet, alcohol, and cigarette smoking could not be ruled out as possible confounding etiologic factors for the cancer deaths.