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An international team of scientists has made a breakthrough in identifying how air pollution causes lung cancer in people who have never smoked, a development that could help medical experts prevent and treat tumours.
一個國際科學家團隊在確定空氣汙染如何導致從不吸菸的人患上肺癌方面取得了突破，這一進展可能有助於醫學專家預防和治療腫瘤。
Researchers found the fine particles in polluted air cause inflammation in the lungs, which activates pre-existing cancer genes that had been dormant. It was previously believed that air pollution triggered genetic mutations that lead to cancer.
研究人員發現，汙染空氣中的細顆粒物會導致肺部炎症，從而啟用先前一直處於休眠狀態的癌症基因。先前，人們認爲空氣汙染會引發基因突變，導致癌症。
The findings, based on research led by the Francis Crick Institute in London and funded by Cancer Research UK, were released at the European Society for Medical Oncology Congress in Paris on Saturday.
這項研究由倫敦弗朗西斯•克里克研究所領導，由英國癌症研究所資助，研究結果於週六在巴黎舉行的歐洲醫學腫瘤學會大會上公佈。
As fewer people smoke, air pollution is emerging more clearly as a cause of tumours in the lungs. An estimated 300,000 lung cancer deaths per year worldwide are caused by very fine pollutant particles with a diameter below 2.5 microns, known as PM2.5, which are emitted in vehicle exhaust and fossil fuel combustion.
隨著吸菸的人越來越少，空氣汙染越來越明顯地成爲導致肺部腫瘤的原因。據估計，全球每年有30萬人死於肺癌，原因是汽車尾氣和化石燃料燃燒排放的直徑小於2.5微米的非常細的汙染物顆粒，即PM2.5。
“Our study has fundamentally changed how we view lung cancer in people who have never smoked,” said project leader Charles Swanton. “Cells with cancer-causing mutations accumulate naturally as we age, but they are normally inactive. We’ve demonstrated that air pollution wakes these cells up in the lungs, encouraging them to grow and potentially form tumours.”
項目負責人查爾斯•斯旺頓(Charles Swanton)說：「我們的研究從根本上改變了我們對從未吸菸人羣肺癌的看法。隨著我們年齡的成長，具有致癌突變的細胞會自然積累，但它們通常不活躍。我們已經證明，空氣汙染會喚醒肺部的這些細胞，促使它們生長，並可能形成腫瘤。」
The project is part of a £14mn Cancer Research UK programme to understand how lung cancer starts and progresses. The scientists analysed data about PM2.5 exposure and lung cancer in 400,000 people from the UK, Taiwan and South Korean, and carried out laboratory experiments with mice, human cells and tissues.
該項目是英國癌症研究項目的一部分，該項目耗資1400萬英鎊，旨在瞭解肺癌的開始和發展過程。科學家們分析了來自英國、臺灣和南韓的40萬人的PM2.5暴露和肺癌數據，並對小鼠、人體細胞和組織進行了實驗室實驗。
Two important environmental carcinogens, tobacco smoke and ultraviolet light, damage DNA and create mutations that generate tumours. But the researchers found no evidence that PM2.5 particles directly mutate DNA, which prompted them to look for a different explanation.
兩種重要的環境致癌物，菸草煙霧和紫外線，會破壞DNA併產生產生腫瘤的突變。但研究人員沒有發現PM2.5顆粒直接突變DNA的證據，這促使他們尋找另一種解釋。
They found that the particles caused inflammation, which activated pre-existing mutations in genes that drive the development of many lung cancers.
他們發現，這些顆粒會引發炎症，從而啟用驅動許多肺癌發展的基因中已經存在的突變。
“The mechanism we’ve identified could ultimately help us to find better ways to prevent and treat lung cancer in never smokers,” said Swanton. “The next step is to discover why some lung cells with mutations become cancerous when exposed to pollutants while others don’t.”
斯旺頓說：「我們確定的機制最終可以幫助我們找到更好的方法來預防和治療從不吸菸的人患肺癌。下一步是發現爲什麼一些突變的肺細胞暴露在汙染物中會癌變，而另一些不會。」
The findings may be applicable to other cancers associated with air pollution, including mesothelioma and tumours of the throat and mouth, said Emilia Lim, another member of the Crick research team. “Ninety-nine per cent of the world’s population lives in areas which exceed annual World Health Organization limits for PM2.5, underlining the public health challenges posed by air pollution across the globe,” she added.
克里克研究小組的另一名成員艾米利亞·林(Emilia Lim)說，這一發現可能適用於與空氣汙染有關的其他癌症，包括間皮瘤和咽喉和口腔腫瘤。她補充說：「世界上99%的人口生活在PM2.5超標的地區，這凸顯了全球空氣汙染對公共健康構成的挑戰。」
One way to counteract the harmful effect of air pollution may be to block a molecule called interleukin-1beta, which plays a key role in the inflammatory response to PM2.5. The team found that this approach worked in mice.
抵制空氣汙染的有害影響的一種方法可能是阻斷一種叫做白細胞介素-1 beta的分子，這種分子在對PM2.5的炎症反應中起著關鍵作用。研究小組發現，這種方法在小鼠身上起了作用。
Tony Mok, professor of medical oncology at the Chinese University of Hong Kong, who was not involved in the study, said the research findings were “intriguing and exciting”.
沒有參與這項研究的香港中文大學腫瘤醫學教授莫樹錦(Tony Mok)表示，研究結果「有趣而令人興奮」。
“It means that we can ask whether, in the future, it will be possible to use lung scans to look for precancerous lesions in the lungs and try to reverse them with medicines,” he said.
他說：「這意味著我們可以詢問，在未來，是否有可能使用肺部掃描來尋找肺部的癌前病變，並試圖用藥物逆轉病變。」
He joined Swanton in emphasising the importance of reducing air pollution to lower the risk of disease.
他和斯旺頓一樣，強調減少空氣汙染對降低疾病風險的重要性。
“We have known about the link between pollution and lung cancer for a long time, and we now have a possible explanation for it,” Mok said. “As consumption of fossil fuels goes hand in hand with pollution and carbon emissions, we have a strong mandate for tackling these issues — for both environmental and health reasons.”
莫樹錦說：「我們早就知道汙染和肺癌之間的聯繫，現在我們有了一個可能的解釋。由於化石燃料的消耗與汙染和碳排放的同時增加，我們有強有力的緊迫感來解決這些問題——無論是出於環境原因還是健康原因。」