研究：空氣污染或可致自閉症和精神分裂

A new research describes how the brains of mice are damaged by exposure to air pollution in early life.

The brain damage includes the enlargement of a part of the brain that is seen in humans who have autismand schizophrenia.

The study is published in the journal Environmental Health Perspectives.

As in autism and schizophrenia, the changes occurred predominately in males. The mice also performed poorly in tests of short-term memory, learning ability, and impulsivity.

The new findings are consistent with several recent studies that have shown a link between air pollution and autism in children.

Most notably, a 2013 study in JAMA Psychiatryreported that children who lived in areas with high levels of traffic-related air pollution during their first year of life were three times as likely to develop autism.

“Our findings add to the growing body of evidence that air pollution may play a role in autism, as well as in other neurodevelopmental disorders,” said Deborah Cory-Slechta, Ph.D., professor of environmental medicine at the University of Rochester and lead author of the study.

In three sets of experiments, Cory-Slechta and her colleagues exposed mice to levels of air pollution typically found in mid-sized US cities during rush hour.

The exposures were conducted during the first two weeks after birth, a critical time in the brain’s development. The mice were exposed to polluted air for four hours each day for two four-day periods.

In one group of mice, the brains were examined 24 hours after the final pollution exposure. In all of those mice, inflammation was rampant throughout the brain, and the lateral ventricles —chambers on each side of the brain that contain cerebrospinal fluid —were enlarged two to three times their normal size.

“When we looked closely at the ventricles, we could see that the white matter that normally surrounds them hadn’t fully developed,” said Cory-Slechta.

“It appears that inflammation had damaged those brain cells and prevented that region of the brain from developing, and the ventricles simply expanded to fill the space.”

The problems were also observed in a second group of mice 40 days after exposure and in another group 270 days after exposure, indicating that the damage to the brain was permanent.

Brains of mice in all three groups also had elevated levels of glutamate, a neurotransmitter, which is also seen in humans with autism and schizophrenia.

Most air pollution is made up mainly of carbon particles that are produced when fuel is burned by power plants, factories, and cars. For decades, research on the health effects of air pollution has focused on the part of the body where its effects are most obvious —the lungs.

That research began to show that different-sized particles produce different effects. Larger particles, the ones regulated by the Environmental Protection Agency (EPA), are actually the least harmful because they are coughed up and expelled.

But many researchers believe that smaller particles known as ultrafine particles —which are not regulated by the EPA —are more dangerous, because they are small enough to travel deep into the lungs and be absorbed into the bloodstream, where they can produce toxic effects throughout the body.

That assumption led Cory-Slechta to design a set of experiments that would show whether ultrafine particles have a damaging effect on the brain, and if so, to reveal the mechanism by which they inflict harm. The study is the first scientific work to do both.

“I think these findings are going to raise new questions about whether the current regulatory standards for air quality are sufficient to protect our children,” said Cory-Slechta.一項新研究表明，老鼠若在幼年期長期接觸污染大氣，腦部可能會受損。

這種受損包括大腦某一部分變腫大，就人類而言，變腫大的部分常出現在自閉者與精神分裂患者腦中。

相關研究結果已發佈在《環境健康透視》雜誌上。

就自閉症和精神分裂而言，這種變化更多出現在雄性之中。此外，試驗中雄性小鼠的短期記憶、學習能力和衝動性行爲均有下降。

除本實驗外，其他最近幾項研究也表明大氣污染可導致兒童自閉症。

最顯著的是2013年《美國醫學協會雜誌:精神病學分冊》上發表的一項研究，該研究顯示兒童若在一歲多時生活在交通尾氣污染嚴重地區，患上自閉症的概率是同齡兒童的三倍。

“隨着調查的深入，我們蒐集到的證據也越來越多，這些數據一致表明大氣污染和自閉症之間存在必然聯繫，污染甚至還可能引發神經系統發育障礙，”羅切斯特大學環境醫學教授德博拉•科裏•斯徹塔解釋道。

在三組試驗中，斯徹塔與同事採集了美國二線城市交通高峯期的空氣樣本，並將老鼠置於其中。

科裏•斯徹塔用出生僅兩週的老鼠進行試驗，此時正值其腦部發育的關鍵時期。試驗期間，小鼠每天要呼吸污染的空氣長達四個小時，爲期兩到四天，試驗分爲兩期進行。

試驗結束後，科裏爲第一組小鼠進行了長達二十四小時的腦部檢查。所有小鼠的大腦和側腦室均已嚴重發炎——左右腦的腦腔裏都是腦脊髓液——小鼠的大腦增大兩至三倍。

“我們仔細檢查了小鼠的腦室，發現大腦的白質未完全發育”，科裏•斯徹塔說道。

“我們觀察發現炎症損害了小鼠的腦細胞，限制了大腦的發育，腦室不斷擴張，佔滿了整個大腦。”

科裏•斯徹塔還在試驗後40天和270天分別測試了第二和第三組小鼠，發現大氣污染對腦部造成的傷害是永久性的。

三組小鼠的腦內的穀氨酸水平也明顯升高，穀氨酸是一種神經遞質，如果人類腦部的穀氨酸水平過高，則會患上自閉症和精神分裂。

空氣污染產生的主要原因是發電廠，工廠和汽車燃燒燃料後排放出的碳粒子。幾十年來，在研究大氣污染對健康的影響時，人們往往只關注病症最明顯的部位——肺。

隨着研究的深入，研究人員漸漸發現不同大小的碳顆粒對大腦的損害不同。大型碳顆粒受美國環保局監管，其實會被人體咳出或排出，危害最小。

但許多研究者認爲那些小型碳顆粒，又叫做超微顆粒——不受美國環境保護局監管——其實危害更大，因爲小型碳顆粒體積較小，可能會被吸入肺部或是融入血液，從而毒害人體。

爲驗證上述猜想，科裏•斯徹塔設計了一系列實驗，探究超微粒子是否會危害大腦，如果答案是肯定的，科裏還將深入研究超微碳粒子是如何危害人體的。科裏結合了這兩方面來研究，開創了先河。

“現在的空氣質量的監管標準能否保護我們的孩子呢？我覺得我的研究成果可能會起到警示的作用”，科裏•斯徹塔說道。