急,请问前人说得那个汞中毒和家具的机经在哪儿？

听力段子：汞污染

　　汞是在常温下唯一呈液态的金属元素。在自然界里大部分汞与硫结合成硫化汞（HgS），亦称“辰砂”或“朱砂”，广泛地分布在地壳表层。辰砂及其多晶体偏辰砂是主要的含汞矿源。随着自然的演化，环境的各个因素中都可能含有汞，形成汞的天然本底。汞的本底对判断环境中的汞污染程度很有意义。地壳中汞的平均丰度为0.08ppm，土壤中为0.03～0.3ppm，大气中为0.1～1.0ppt。汞在大气中呈蒸汽态，因而雨水中也有汞，平均浓度为0.2ppb。水中汞的本底浓度，内陆地下水为0.1ppb，海水为0.03一2ppb，泉水可达80ppb以上，湖水、河水一般不超过0.1ppb。

　　人类活动造成水体汞污染，主要来自氯碱、塑料、电池、电子等工业排放的废水。据估计，1970～1979年全世界由于人类活动直接向水体排放汞的总量约1．6万吨；排向大气的总汞量达10万吨左右；排入土壤总汞约为10万吨，而排向大气和土壤的也将随着水循环回归入水体。

　　由于天然本底情况下汞在大气、土壤和水体中均有分布，所以汞的迁移转化也在陆、水、空之间发生。大气中气态和颗粒态的汞随风飘散，一部分通过湿沉降或干沉降落到地面或水体中。土壤中的汞可挥发进入大气，也可被降水冲淋进入地面水和渗透入地下水中。地面水中的汞一部分由于挥发而进入大气，大部分则沉淀进入底泥。底泥中的汞，不论呈何种形态，都会直接或间接地在微生物的作用下转化为甲基汞或二甲基汞。二甲基汞在酸性条件可以分解为甲基汞。甲基汞可溶于水，因此又从底泥回到水中。水生生物摄入的甲基汞，可以在体内积累，并通过食物链不断富集。受汞污染水体中的鱼，体内甲基汞浓度可比水中高上万倍，危及鱼类并通过食物链危害人体。

　　汞虽然是一种累积性毒物，但人体对汞具有一定的排泄能力。试验表明，成年人每天摄人0.025毫克的甲基汞，由于人体排泄能力使之不会在身体内累积，若摄入量超过人体的排泄能力，会在体内累积。日本的水俣病，就是在大脑中累积了甲基汞，损害脑组织所致。在人体其他组织中的金属汞，可能氧化成离子状态，并转移到肾中蓄积起来。人体受汞慢性中毒的临床表现，主要是神经性症状，有头痛、头晕、肢体麻木和疼痛、肌肉震颤、运动失调等。大量吸入汞蒸汽会出现急性汞中毒，其症候为肝炎、肾炎、蛋白尿和尿毒症等。这类病有严重的后遗症和较高的死亡率，还可以通过母体遗传给婴儿。在我国松花江和蓟河流域的一些渔民体内有明显的汞积累，而且已经出现了“拟似水俣病”的病人。

　　由于汞的毒性强，产生中毒的剂量就小，因此我国饮水、农田灌溉，都要求汞的含量不得超过0.001毫克／升，渔业用水要求汞不得超过0.005毫克／升。
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　　汞中毒，通常又叫“水俣病”。首次出现是在1933年的日本九州熊本县。刚才所提到的５号病，实际上就是汞中毒。汞中毒有一定的征兆性，开始是走路不稳，面容痴呆，尔后耳聋眼瞎，重者全身麻痹，最后精神失常，以至死亡。这是因为汞中毒是一种神经中毒，可以造成全身性的神经损害。但是汞中毒又是可以预测的。当时在日本就发现了一种猫，被称为舞蹈猫。原本正常的猫，走路变得摇摇晃晃，就像跳舞一样。为什么猫会先得病呢？这是因为猫去吃水俣湾里的鱼，而水俣湾的水受到污染汞含量超标。汞被鱼吸收富集，再通过食物链转到猫和人的体内。猫因为吃鱼多，所以先中毒。猫得了舞蹈病，也就是水俣病，这时人还可以进行及时的救治。这是因为人体内的汞含量还没有达到临界值，一旦到达临界值，就很难进行治疗了。所以说，汞中毒还是有一定的可预见性的。

　　还有就是，在香港有一些人发现自己经常感冒，总感觉很累，经常头痛、失眠、颈椎痛、腰痛，而且久治不愈。经过化验，发现这些人体内的汞比一般人都高，病因就是这些人爱吃海鱼。类似的情况在日本水俣，农民的发病率就要比渔民低得多。概括地讲，在被污染的水域浅水鱼的汞含量相对较高，深海鱼类相比较来说则低得多。

Furniture

The conservatism of the early English colonists in North American, their strong attachment to the English way of doing things, would play a major part in the furniture that was made in New England. The very tools that the first New England furniture makers used were, after all, not much different from those used for centuries-even millennia: basic hammers, saws, chisels, planes, augers, compasses, and measures.

These were the tools used more or less by all people who worked with wood: carpenters, barrel makers, and shipwrights. At most the furniture makers might have had planes with special edges or more delicate chisels, but there could not have been much specialization in the early years of the colonies.

               The furniture makers in those early decades of the 1600's were known as "joiners", for the primary method of constructing furniture, at least among the English of this time, was that of mortise-and-tenon joinery. The mortise is the hole chiseled and cut into one piece of wood, while the tenon is the tongue of protruding element shaped from another piece of wood so that it fits into the mortise; and another small hole is then drilled (with the auger) thought the mortised end and the tenon so that a whittled peg can secure the joint-thus the term "joiner". Panels were fitted into slots on the basic frames. This kind of construction was used for making everything from houses to chests.

Relatively little hardware was used during this period. Some nails-forged by hand-were used, but no screws or glue, hinges were often made of leather, but metal hinges were also used. The cruder varieties were made by blacksmiths in the colonies, but the finer metal elements were imported. Locks and escutcheon plates-the latter to shield the wood from the metal key-would often be imported.

Above all, what the early English colonists imported was their knowledge of familiarity with, and dedication to the traditional types and designs of furniture they knew in England.

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