de Silva P E, Christophers A J
AMCOSH Occupational Health Services, Werribee, Victoria, Australia.
J Paediatr Child Health. 1997 Feb;33(1):12-7. doi: 10.1111/j.1440-1754.1997.tb00984.x.
It has come to be generally accepted that low levels of lead exposure may result in mental deficit. This causal inference is based on claimed time precedence of the lead exposure and on biological plausibility. The objective of this study is to argue that mental deficit causes pica which causes lead exposure (i.e. to support the theory of reverse causation).
The literature since the 1930s has been interpreted in the light of our own long experience in the investigation of lead exposure in children and adults to support the arguments in favour of reverse causation.
The arguments for reverse causation are based on: (i) analogy with mental retardation which causes increased lead exposure; (ii) the results of published prospective studies that show a special relationship between blood lead levels at 24 months and intelligence tested later, exactly what would be predicted by the reverse causation theory; and (iii) on an alternative explanation for mental retardation following lead encephalopathy (i.e. that mental retardation following encephalopathy is due to anoxia and not due to a direct destructive effect on the brain neurones). The arguments, which have been proposed for the conventional view, are rejected for the following reasons: (i) none of the prospective studies have found a relationship between cord blood lead levels and intelligence tested later, undermining the argument based on time precedence of lead exposure; and (ii) there is no convincing evidence that lead poisoning, short of encephalopathy, causes mental retardation.
We believe that the reverse causation hypothesis is a more plausible explanation of the facts.
低水平铅暴露可能导致智力缺陷这一观点已被广泛接受。这种因果推断基于铅暴露被宣称的时间先后顺序以及生物学合理性。本研究的目的是论证智力缺陷导致异食癖，而异食癖导致铅暴露（即支持反向因果关系理论）。
自20世纪30年代以来的文献，结合我们自身在儿童和成人铅暴露调查方面的长期经验进行解读，以支持有利于反向因果关系的论点。
支持反向因果关系的论据基于：（i）与导致铅暴露增加的智力迟钝进行类比；（ii）已发表的前瞻性研究结果，这些结果显示24个月时的血铅水平与之后测试的智力之间存在特殊关系，这正是反向因果关系理论所预测的；（iii）对铅中毒性脑病后智力迟钝的另一种解释（即脑病后的智力迟钝是由于缺氧，而非对脑神经元的直接破坏作用）。针对传统观点提出的论据，因以下原因被驳回：（i）没有一项前瞻性研究发现脐血铅水平与之后测试的智力之间存在关系，削弱了基于铅暴露时间先后顺序的论点；（ii）没有令人信服的证据表明，除脑病外的铅中毒会导致智力迟钝。
我们认为反向因果关系假说对这些事实的解释更具合理性。
