AACR2013：孕妇暴露于空气污染增加胎儿癌症风险

　　华盛顿——美国癌症研究协会(AACR)2013年会上公布的一项研究显示，如果母亲在妊娠期间曾暴露于空气污染，则其子女发生癌症的风险增加，尽管幅度不大却具有显著性。产前和1岁期间暴露于最高水平汽车尾气的儿童，发生双侧视网膜母细胞瘤和生殖细胞肿瘤的风险分别比暴露于最低水平的儿童增高19%和17%。

　　在这项为期9年的病例对照研究中，加州大学洛杉矶分校菲尔丁公共卫生学院的流行病学家Julia E. Heck博士采用第4版加州线源扩散模型系统(CALINE4)检测污染。该系统使用一队机动车辆来预测汽车空转、行驶、加速和减速时的一氧化碳(CO)排放量。

　　研究队列为加州癌症注册处收录的3,590例儿童癌症患者。所有儿童在1998~2007年间出生，年龄＜6岁。研究者将这些儿童与从加州出生记录中随机抽取的80,224例儿童进行比较。CALINE4系统基于母亲在各个妊娠期间的居住地估计当地汽车废气暴露水平。模型输入居住地1,500米半径内汽油和柴油汽车的排放量，并纳入有关交通量、道路几何形状、车辆排放率和天气模式的数据，然后根据暴露水平将研究队列按四分位数分组。研究者专门分析了CO测量值增加53/10亿的情况进行了研究。

　　结果显示，CO排放量每增加一个四分位数，则急性淋巴母细胞性白血病风险增加4%。各四分位数与视网膜母细胞瘤总体风险增加14%相关，双侧肿瘤(而非单侧肿瘤)风险显著增加(增加19%)。此外，CO排放量每增加一个四分位数，生殖细胞瘤风险增加17%。

　　CO排放量与其他肿瘤(包括急性髓性白血病、非霍奇金淋巴瘤、室管膜瘤、星形细胞瘤、神经母细胞瘤、肾母细胞瘤、肝母细胞瘤和横纹肌肉瘤)的关联不显著。

　　研究者表示，上述结果表明汽车废气污染与一些儿童癌症相关。由于该研究为回顾性分析，因此无法证明因果关系。研究结果需在其他研究中予以证实。

与癌症相关的拓展阅读： 

• NCCN2013：变革中的癌症治疗
• AACR：美国癌症研究协会限制癌症患者吸烟
• Circulation：放疗增加癌症患者心脏手术死亡率
• NEJM：痴呆花费已超过癌症和心脏病
• JNCI：端粒长度短的癌症患者生存期短 更多信息请点击：有关癌症更多资讯

A 9-year case-control study found that children who were exposed to the highest levels of traffic-related pollution prenatally and during the first year of life were 19% more likely to develop bilateral retinoblastoma and 17% more likely to develop germ cell tumors than were children who were exposed to the lowest level.

"This is the first study to report upon traffic pollution in relation to retinoblastoma or germ cell tumors, and since both of these are rare, the findings need to be replicated in other studies," Julia E. Heck, Ph.D., said in an interview at the annual meeting of the American Association for Cancer Research.

Dr. Heck, an epidemiologist at the University of California’s Fielding School of Public Health, Los Angeles, used a state air pollution modeling system to detect the patterns in her study. The California Line Source Dispersion Modeling system, version 4 (CALINE4) uses a test fleet of motor vehicles to predict traffic-related carbon monoxide emissions from vehicles in idle, cruise, acceleration, and deceleration.

Her study cohort comprised 3,590 children with cancer who were included in a California cancer registry. All were born between 1998 and 2007 and were aged younger than 6 years. She compared these children to a random selection of 80,224 children drawn form California birth records. The CALINE4 system generated estimates of local traffic exposure based on where the mothers were living during each trimester of pregnancy.

The model imputed emissions from gasoline and diesel vehicles within a 1,500-meter radius of the address. It included data on traffic volume, roadway geometry, vehicle emission rates, and weather patterns, and divided the cohort into quartiles according to exposure. Dr. Heck looked specifically at carbon monoxide measurements in increments of 53 parts per billion.

Each increase in CO emission raised the risk of acute lymphoblastic leukemia by 4%. Each quartile was associated with an overall 14% increased risk of a retinoblastoma, with the risk significantly elevated for bilateral tumors rather than unilateral tumors (a 19% increase). Dr. Heck also saw a 17% increased risk for germ cell tumors for every quartile increase in CO.

Associations with other cancers, including acute myeloid leukemia, non-Hodgkin’s lymphoma, ependymoma, astrocytoma, neuroblastoma, Wilms tumor, hepatoblastoma, and rhabdomyosarcoma, were nonsignificant.

Because Dr. Heck’s study was a retrospective analysis, it cannot prove causation. "The results need to be confirmed in other studies," she said in an interview. "But our findings do support a link between traffic pollution and some childhood cancers."

The field of childhood cancers and air pollution has not been well studied in recent years, Dr. Heck said, although there were a number of such studies in the late 1990s and early 2000s.

One was a British case-control analysis of birth and death records of 12,018 children in the United Kingdom who had been born and died from leukemia and other cancers from 1955 to 1980. The cancer-related deaths were linked to locations of rail and bus stations, ferry terminals, railways, roads, canals, and rivers (J. Epidemiol. Community Health 2005;59:755-60).

"The most striking result is the extraordinary concentration of cancer births within 0.3 km of bus/coach stations (OR = 12.5)," wrote Dr. E.G. Knox, professor emeritus at the University of Birmingham, England. "This was followed by hospitals (OR = 2.6) and heavy transport centers (OR = 1.6)."

Of the individual pollutants examined, both carbon monoxide and 1,3-butadiene more than doubled the risk of cancer.

Because the study encompassed the child’s location at birth, it demonstrated a link to prenatal exposure. "Childhood cancers are strongly determined by prenatal or early postnatal exposures to oil-based combustion gases, especially from engine exhausts," he noted. "The chief carcinogenic agent is probably 1,3-butadiene."

The National Institute for Occupational Safety and Health has recommended that 1,3-butadiene be treated as a potential occupational carcinogen, teratogen, and as a reproduction hazard.

In 2006, Dr. Knox published another study on the same group, in which he attributed about 24% of the cancers to prenatal or early life proximity to areas of high airborne pollutants. "Child cancer initiations are strongly determined by prenatal or early postnatal exposures to engine exhaust gases, probably through maternal inhalation and accumulation of carcinogens over many months," he noted. (J. Epidemiol. Community Health 2006;60:136-41).

Dr. Heck’s study was funded by the National Institutes of Health. She had no financial disclosures.