好英语网为什么空气污染如此有害？答案或许与DNA有关
The threat of air pollution grabs our attention when we see it — for example, the tendrils of smoke of Australian brush fires, now visible from space, or the poisonous soup of smog that descends on cities like New Delhi in the winter.
我们对可见的空气污染十分关注——例如，现在从太空中可以看到澳大利亚丛林大火的卷须状烟雾，或是冬天降临在新德里等城市的有毒雾霾。
But polluted air also harms billions of people on a continuing basis. Outdoors, we breathe in toxins delivered by car traffic, coal-fired plants and oil refineries. Indoor fires for heat and cooking taint the air for billions of people in poor countries. Over a billion people add toxins to their lungs by smoking cigarettes — and more recently, by vaping.
但空气污染也在持续伤害数十亿人。在户外，我们呼吸着汽车、燃煤电厂和炼油厂排放的毒素。在贫穷国家，室内烧火取暖和做饭也污染了数十亿人所呼吸的空气。超过十亿人通过吸烟或最近流行的电子烟将毒素吸入肺部。
去年12月，位于悉尼西南约90英里处的巴尔戈镇发生火灾。
Ninety-two percent of the world’s people live in places where fine particulate matter — the very small particles most dangerous to human tissues — exceeds the World Health Organization’s guideline for healthy air. Air pollution and tobacco together are responsible for up to 20 million premature deaths each year.
世界上92%的人生活在细颗粒物——对人体组织最危险的微小颗粒——超出世界卫生组织健康空气指标的地方。空气污染和烟草每年导致多达2000万人过早死亡。
Airborne toxins damage us in a staggering number of ways. Along with well-established links to lung cancer and heart disease, researchers are now finding new connections to disorders such as diabetes and Alzheimer’s disease.
空气传播的毒素伤害我们身体的方式多得惊人。除了确认与肺癌和心脏病有关外，研究人员如今还发现了与糖尿病和阿尔茨海默病等疾病的关联。
Scientists are still figuring out how air pollution causes these ailments. They are also puzzling over the apparent resilience that some people have to this modern onslaught.
科学家们仍在研究空气污染是如何导致这些疾病的。同样让他们感到困惑的是，为什么有一些人在这种现代冲击下表现出的明显抵抗力。
Some researchers now argue that the answers to these questions lie in our distant evolutionary past, millions of years before the first cigarette was lit and the first car hit the road.
一些研究人员现在认为，这些问题的答案就在我们遥远的进化史之中，在第一根香烟被点燃、第一辆汽车上路之前的数百万年里。
Our ancestors were bedeviled by airborne toxins even as bipedal apes walking the African savanna, argued Benjamin Trumble, a biologist at Arizona State University, and Caleb Finch of the University of Southern California, in the December issue of the Quarterly Review of Biology.
从还是非洲大草原上行走的双足猿之时，我们的祖先就已经被空气中的毒素所困扰，亚利桑那州立大学的生物学家本杰明·特朗布尔(Benjamin Trumble)和南加州大学的凯莱布·芬奇(Caleb Finch)在《生物学季评》(Quarterly Review of Biology)12月刊上写道。
Our forebears evolved defenses against these pollutants, the scientists propose. Today, those adaptations may provide protection, albeit limited, against tobacco smoke and other airborne threats.
科学家们提出，我们的祖先进化出了抵御这些污染物的能力。如今面对烟草烟气等空气传播的威胁，这些抵抗力可能在保护我们（尽管效力有限）。
But our evolutionary legacy may also be a burden, Dr. Trumble and Dr. Finch speculated. Some genetic adaptations may have increased our vulnerability to diseases linked to air pollution.
但特朗布尔和芬奇推测，我们的进化遗产也可能是个负担。有些基因的适应性或许会让我们在面对与空气污染有关的疾病时更脆弱。
It is “a really creative, interesting contribution to evolutionary medicine,” said Molly Fox, an anthropologist at the University of California, Los Angeles, who was not involved in the new study.
这“确实是对进化医学非常有创意和趣味的贡献，”加州大学洛杉矶分校的人类学家莫莉·福克斯(Molly Fox)说，她没有参与这项新研究。
The story begins about seven million years ago. Africa at the time was gradually growing more arid. The Sahara emerged in northern Africa, while grasslands opened up in eastern and southern Africa.
故事在大约七百万年前开始。当时的非洲正逐渐变得干旱。撒哈拉沙漠出现在北非，而非洲东部和南部则露出了草原。
The ancestors of chimpanzees and gorillas remained in the retreating forests, but our ancient relatives adapted to the new environments. They evolved into a tall, slender frame well suited to walking and running long distances.
黑猩猩和大猩猩的祖先留在了正在消失的森林里，但我们这些远祖亲戚适应了新环境。它们进化出瘦高的体格，非常适合长距离行走和奔跑。
Dr. Finch and Dr. Trumble believe that early humans faced another challenge that has gone largely overlooked: the air.
芬奇和特朗布尔认为，早期人类还面临着另一个很大程度上被忽视的挑战：空气。
Periodically, the savanna would have experienced heavy dust storms from the Sahara, and our distant ancestors may have risked harm to their lungs from breathing in the silica-rich particles.
大草原会周期性地经历来自撒哈拉的强烈沙尘暴，我们的远祖可能因吸入了含有大量硅的微粒而导致肺部受损。
“When the dust is up, we’re going to see more pulmonary problems,” Dr. Finch said. Even today, Greek researchers have found that when Sahara winds reach their country, patients surge into hospitals with respiratory complaints.
“当尘土升腾，我们就会看到更多肺部问题出现，”芬奇说。即使在今天，希腊研究人员也发现，当撒哈拉沙漠的风吹到他们国家时，就会有大批病人因为呼吸疾病涌入医院。
The dense foliage of tropical forests gave chimpanzees and gorillas a refuge from dust. But the earliest humans, wandering the open grasslands, had nowhere to hide.
茂密的热带丛林为黑猩猩和大猩猩提供了躲避尘土的避难所。但最早的人类就在空旷的草原上游荡，无处藏身。
Dust was not the only hazard. The lungs of early humans also may have been irritated by the high levels of pollen and particles of fecal matter produced by the savanna’s vast herds of grazing animals.
尘土并不是唯一的危险。花粉含量高的空气和草原上大量食草动物的粪便颗粒也可能导致早期人类的肺部不适。
Dr. Finch and Dr. Trumble maintain that scientists should consider whether these new challenges altered our biology through natural selection. Is it possible, for instance, that people who are resilient to cigarette smoke have inherited genetic variants that protected their distant ancestors from cave fires?
芬奇和特朗布尔认为，科学家应该思考这些新挑战是否通过自然选择改变了我们的生理。比如，那些对香烟烟气有抵抗力的人是否可能遗传了基因变异，而这种变异就曾保护他们的远祖免受洞穴火灾的伤害？
One way to answer these questions is to look at genes that have evolved significantly since our ancestors moved out of the forests.
要回答这一问题，其中一个办法是观察自我们祖先离开森林以来经历了显著进化的基因。
One of them is MARCO, which provides the blueprint for production of a molecular hook used by immune cells in our lungs. The cells use this hook to clear away both bacteria and particles, including silica dust.
其中之一是MARCO，它提供了制造一种分子钩的蓝图，这种分子钩为我们肺部的免疫细胞所使用。细胞用这个分子钩来清除细菌和颗粒，包括硅尘。
The human version of the MARCO gene is distinctively different from that of other apes. That transformation happened at least half a million years ago. (Neanderthals carried the variant, too.) Breathing dusty air drove the evolution of MARCO in our savanna-walking ancestors, Dr. Finch and Dr. Trumble hypothesize.
MARCO基因的人类版本与其它猿类有明显不同。这种转变至少发生在50万年前。（尼安德特人也携带这种变异基因。）芬奇和特朗布尔推测，呼吸含尘空气导致了我们在大草原上行走的祖先的MARCO基因进化。
Later, our ancestors added to airborne threats by mastering fire. As they lingered near hearths to cook food, stay warm or keep away from insects, they breathed in smoke. Once early humans began building shelters, the environment became more harmful to their lungs.
后来，我们的祖先掌握了火种，更增加了空气传播的威胁。当逗留在炉边做饭、取暖或抵御昆虫袭击时，他们就会吸入烟雾。早期人类开始建造住所后，环境对他们肺部的危害就更大了。
“Most traditional people live in a highly smoky environment,” Dr. Finch said. “I think it has been a fact of human living for us even before our species.”
“传统人类大多生活在烟雾缭绕的环境中，”芬奇说。“我认为在我们这个物种出现之前，这已经是人类生活的一个现实。”
Smoke created a new evolutionary pressure, he and Dr. Trumble believe. Humans evolved powerful liver enzymes, for example, to break down toxins passing into the bloodstream from the lungs.
他和特朗布尔都认为，烟雾制造了新的进化压力。例如，人类进化出了功能强大的肝酶来分解从肺部进入血液的毒质。
Gary Perdew, a molecular toxicologist at Penn State University, and his colleagues have found evidence of smoke-driven evolution in another gene, AHR.
宾夕法尼亚州立大学(Penn State University)的分子毒理学家加里·珀杜(Gary Perdew)和他的同事们发现了另一种在烟雾驱动下进化的基因证据，那就是AHR基因。
This gene makes a protein found on cells in the gut, lungs and skin. When toxins get snagged on the protein, cells release enzymes that break down the poisons.
这种基因会产生一种存在于肠道、肺部和皮肤细胞中的蛋白质。当毒质附着在蛋白质之上，细胞就释放出酶来分解毒素。
Other mammals use AHR to detoxify their food. But the protein is also effective against some of the compounds in wood smoke.
其它哺乳动物也利用AHR基因对食物进行排毒。但这种蛋白质对木材烟雾中的一些化合物也有效。
Compared to other species, the human version produces a weaker response to toxins, perhaps because AHR protein is not the perfect protector — the fragments it leaves behind can cause tissue damage.
与其它物种相比，人类版本的AHR基因对毒质反应较弱，或许是因为AHR蛋白质并不是完美的保护剂，它留下的碎段会造成组织损伤。
Before fire, our ancestors did not need to use AHR very often; in theory, their bodies could tolerate the limited damage the protein caused.
在学会取火之前，我们的祖先不需要经常使用AHR的能力；从理论上讲，他们的身体可以承受这种蛋白质造成的有限损伤。
But when we began breathing smoke regularly and needing the AHR protein constantly, the gene might have become dangerous to our health.
但当我们开始频繁吸入烟雾，不断需要AHR蛋白质的时候，这种基因就可能对我们的健康造成威胁。
Dr. Perdew believes that humans evolved a weaker AHR response as a way to find “a sweet spot,” a compromise that minimized the damage of airborne pollutants without causing too many side effects.
珀杜认为，人类进化出了较弱的AHR反应，是在寻找“最佳平衡点”——即将空气污染物的损害降至最低，又不会造成太多副作用的折衷办法。
These adaptations were never perfect, as evidenced by the fact that millions of people still die today from indoor air pollution. But evolution doesn’t seek perfect health.
这些适应从来都不是完美的，正如今天仍有数百万人死于室内空气污染的事实所证明的那样。但进化并不追求完美的健康。
“All that matters from an evolutionary standpoint is that you reproduce,” Dr. Perdew said. “If you die in your forties, so what? It’s kind of a cold, heartless way to think about it, but it is what it is.”
“从进化的角度来看，做重要的是保证繁殖，”珀杜说。“如果你40多岁就死了，那又怎么样呢？这是一种冷酷无情的思考方式，但事实就是如此。”
A changed atmosphere
大气的改变
Our species arrived at the Industrial Revolution two centuries ago with bodies that had been shaped for millions of years by this highly imperfect process.
我们人类在两个世纪前经历工业革命时，身体已经经历了数百万年高度不完善进化过程的塑造。
Clean water, improved medicines and other innovations drastically reduced deaths from infectious diseases. The average life expectancy shot up. But our exposure to airborne toxins also increased.
洁净的水、改进的药物和其它创新极大减少了传染病造成的死亡。平均预期寿命迅速增长。但我们所接触的空气中的毒质也增加了。
“If we compressed the last five million years into a single year, it wouldn’t be until Dec. 31, 11:40 p.m., that the Industrial Revolution begins,” Dr. Trumble said. “We are living in just the tiniest little blip of human existence, yet we think everything around us is what’s normal.”
“如果我们把过去500万年压缩成一个单一的年份，那工业革命开始的时候就得是12月31日晚上11点40分了，”特朗布尔博士说。“我们只生活在人类存在史里一个极其微小的节点上，然而却认为周遭一切就是常规。”
The Industrial Revolution was powered largely by coal, and people began breathing the fumes. Cars became ubiquitous; power plants and oil refineries spread. Tobacco companies made cigarettes on an industrial scale. Today, they sell 6.5 trillion cigarettes every year.
工业革命的动力主要源于煤炭，人类也因此开始呼吸煤炭燃烧产生的烟雾。汽车无处不在；发电厂和炼油厂遍布各地。烟草公司以工业规模生产香烟。如今，他们每年可销售6.5万亿支香烟。
Our bodies responded with defenses honed over hundreds of thousands of years. One of their most potent responses was inflammation. But instead of brief bursts of inflammation, many people began to experience it constantly.
我们的身体以几十万年磨练出的防御能力作为回应。最有效的反应之一就是炎症。但许多人不是短暂地发炎，而是持续不断地有炎症。
Many studies now suggest that chronic inflammation represents an important link between airborne toxins and disease. In the brain, for example, chronic inflammation may impair our ability to clear up defective proteins. As those proteins accumulate, they may lead to dementia.
如今许多研究表明，慢性炎症是空气中毒质与疾病之间的重要联系。例如在大脑中，慢性炎症可能损害我们清除缺陷型蛋白质的能力。这些蛋白质的累积可能会导致失智。
Pathogens can hitch a ride on particles of pollutants. When they get in our noses, they can make contact with nerve endings. There, they can trigger even more inflammation.
病原体可以搭上污染颗粒物的便车。当它们进入我们的鼻子，就能接触到神经末梢。在那里，它们会引发更多炎症。
“They provide this highway that’s a direct route to the brain,” Dr. Fox, of the University of California, Los Angeles, said. “I think that’s what makes this a particularly scary story.”
“它们提供了一条通向大脑的高速公路，”加州大学洛杉矶分校的福克斯说。“所以我认为这是件特别可怕的事情。”
Some genetic variants that arose in our smoky past may offer some help now. They might allow some people to live long despite smoking, Dr. Finch and Dr. Trumble suggest.
我们因烟熏缭绕的过往而产生的一些基因变异，现在或许能提供一些帮助。芬奇和特朗布尔认为，一些人尽管吸烟可能还是可以很长寿。
But the researchers have studied another gene for which the opposite seems to be true: a variant that was once helpful has become harmful in an age of rising air pollution.
但研究人员研究了另一种基因，其结果似乎刚好相反：在空气污染日益严重的时代，曾经有用的基因变体已经有害了。
The variant, ApoE4, first came to light because it drastically raises the risk of developing Alzheimer’s disease. More recently, researchers have also discovered that ApoE4 increases the risk that exposure to air pollution leads to dementia.
ApoE4基因突变首次被发现是因为它大大增加了阿尔茨海默病的风险。最近，研究人员还发现ApoE4会增加暴露于污染空气而导致失智的风险。
But these studies were restricted to industrialized countries. When researchers looked to other societies — such as farmers in poor villages in Ghana, or indigenous forest-dwellers in Bolivia — ApoE4 had a very different effect.
但这些研究仅限于工业化国家的范畴。而当研究人员观察其他社会时——如加纳贫穷村庄的农民，或是玻利维亚的森林原住民——ApoE4的影响就大大不同。
In these societies, infectious diseases remain a major cause of death, especially in children. Researchers have found that in such places, ApoE4 increases the odds that people will survive to adulthood and have children.
在这些社会中，传染病仍是死亡主因，特别是对儿童。研究人员发现，在这些地方，ApoE4增加了人们活到成年并生育后代的几率。
Natural selection may have favored ApoE4 for hundreds of thousands of years because of this ability to increase survival. But this gene and others may have had harmful side effects that remained invisible until the sooty, smoky modern age.
几十万年来，自然选择一直青睐ApoE4，或许正是因为它这种提高人类生存率的能力。但这种基因和其它基因可能产生的有害副作用，直到被烟熏黑的现代才被发现。