Lanier Anne P, Holck Peter, Ehrsam Day Gretchen, Key Charles
Office of Alaska Native Health Research, Division of Community Health Services, Alaska Native Tribal Health Consortium, Anchorage, Alaska, USA.
Pediatrics. 2003 Nov;112(5):e396. doi: 10.1542/peds.112.5.e396.
The primary purpose of this study was to examine the occurrence of cancer in Alaska Native (AN) children (under age 20). Although several studies have compared differences in cancer incidence between white and black children, few have examined cancer among Alaska Natives/American Indians. We know of no published article describing cancer incidence in AN children. We compared our findings with those of American Indian children of New Mexico and of Alaska white children. Data on mortality, survival, and prevalence are also included. Alaska Native is the term used collectively for the inhabitants whose ancestors occupied the area before European contact of what is now the state of Alaska. Alaska Natives include Eskimo, Indian, and Aleut groups. Although the 3 major groups differ in culture, language, and probably genetics, there are similarities in numerous social and economic indicators. The Northern Eskimo of Alaska (Inupiat) are related to Canadian and Greenland Inuit. Indians in Alaska include Athabaskan (in the interior of the state), who share commonalities with Canadian Athabaskan as well as with Navajo and Apache in the southwestern United States. Tlingit, Haida, and Tsimshian groups reside primarily in the southeast panhandle of the state. The panhandle Indian groups are similar to those of British Columbia.
Data on cancer incidence are from the Alaska Native Tumor Registry, 1969-1996. We studied children under age 20 to make our results comparable to national data as presented in the National Cancer Institute's Surveillance, Epidemiology and End Results (SEER) Pediatric Monograph. Population data for AN are based on census data and Indian Health Service intercensal estimates. Data for US whites and New Mexico Indians are from the National Cancer Institute's SEER program. Calculations were made using SEERStat software. Data for Alaska whites are for the years 1996-2000. (The Alaska Cancer Registry has collected data for all Alaskans only since 1996). Odds ratios (ORs) of rates with 95% confidence intervals (CIs) were calculated.
The rate among all AN children (both sexes) for all cancers combined is similar to that of US whites (OR: 1.0; 95% CI: 0.8-1.1). Examination of childhood cancer rates by ethnicity, however, reveal that rates are significantly lower for Indian (OR: 0.6; 95% CI: 0.4-0.8) but not significantly different for Eskimo or Aleut children. For most International Classification of Childhood Cancers groups, incidence rates for AN children are also similar to those of US whites. However, AN children are at significantly higher risk for hepatic tumors (OR: 13.1; 95% CI: 7.9-20.5), particularly hepatocellular carcinoma (OR: 43.8; 95% CI:24.4-75.1) and retinoblastoma (OR: 2.8; 95% CI: 1.3-5.3). By ethnic group, rates for hepatocellular carcinoma are significantly high only for Eskimo. Rates for all AN children are lower for neuroblastoma (OR: 0.1; 95% CI: 0.1-0.6) and lymphoma (OR: 0.5; 95% CI: 0.3-0.9), particularly Hodgkin's disease (OR: 0.2; 95% CI: 0.0-0.5). On the basis of 5 years of data, rates for Alaska white children do not seem to differ from those of US white children. Because of our findings of differences between AN and US whites, we reviewed data of other relevant populations, specifically American Indian data from the New Mexico SEER registry. Using SEER data and SEER software, we calculated rates for New Mexican American Indians (NMAI) and compared them with US white rates. Rates for all cancers combined among NMAI are significantly lower than for US white (OR: 0.8). However, similar to AN children, the rate among NMAI for retinoblastoma is higher compared with US whites (OR: 2.5; 95% CI:1.4-4.5). Similar to AN, NMAI also seem to be at low risk for neuroblastoma (OR: 0.2; 95% CI: 0.1-0.7), lymphoma as a group (OR: 0.1; 95% CI: 0.0-0.3), and, specifically, Hodgkin's disease (OR: 0.1; 95% CI: 0.0-0.4). Rates among NMAI children are low for central nervous system tumors (OR: 0.5; 95% CI: 0.3-0.7). The average annual age-adjusted cancer mortality rate among AN children is lower but not significantly lower than that of US white children (28.6 vs 37.3 per million).
Comparison of AN rates for all cancers combined are similar to those of US and Alaska white children but seem higher than those of NMAI. Differences between AN and US whites exist for select International Classification of Childhood Cancers groups. The most striking rate differences are found in hepatic tumors, largely because of elevated rates of hepatitis B-associated hepatocellular carcinoma. All children in our study with hepatocellular carcinoma were hepatitis B antigen positive. A statewide hepatitis B virus immunization program was begun in late 1982. Although 16 children who were born before 1983 developed hepatocellular carcinoma, no children who were born in the 20 years since hepatitis B immunization was instituted among infants have received a diagnosis of hepatocellular carcinoma, a significant difference. Comparing AN and US white childhood cancer rates after removing hepatocellular carcinoma cases from both populations results in an OR of 0.8 (95% CI: 0.7-1.0). Thus, if no increase in other childhood cancers occurs in the coming generations, then rates for childhood cancer may soon be significantly lower than those in US white children. Rates are low for all lymphomas, largely because of very low rates of Hodgkin's disease. Rates are also low for neuroblastoma. It is reassuring that rates for AN children are not in excess and do not seem to be increasing. There is concern among the population regarding environmental exposure, including ionizing radiation. Our data do not show excess childhood leukemia or thyroid cancers, malignancies for which radiation is known to increase risk.
本研究的主要目的是调查阿拉斯加原住民(AN)儿童(20岁以下)的癌症发病情况。尽管已有多项研究比较了白人和黑人儿童癌症发病率的差异,但很少有研究关注阿拉斯加原住民/美洲印第安人的癌症情况。我们未发现有已发表的文章描述AN儿童的癌症发病率。我们将研究结果与新墨西哥州的美洲印第安儿童以及阿拉斯加白人儿童的结果进行了比较。研究还纳入了死亡率、生存率和患病率数据。阿拉斯加原住民是对其祖先在欧洲人接触现今阿拉斯加州这片区域之前就已居住在此的居民的统称。阿拉斯加原住民包括爱斯基摩人、印第安人和阿留申人群体。尽管这三大群体在文化、语言以及可能的基因方面存在差异,但在众多社会和经济指标上具有相似性。阿拉斯加的北爱斯基摩人(因纽皮特人)与加拿大和格陵兰的因纽特人有亲缘关系。阿拉斯加的印第安人包括阿萨巴斯卡人(分布在该州内陆),他们与加拿大的阿萨巴斯卡人以及美国西南部的纳瓦霍人和阿帕奇人有共同之处。特林吉特、海达和钦西安群体主要居住在该州东南部的狭长地带。该狭长地带的印第安群体与不列颠哥伦比亚的群体相似。
癌症发病率数据来自阿拉斯加原住民肿瘤登记处,时间跨度为1969 - 1996年。我们研究20岁以下的儿童,以便使我们的结果能够与美国国立癌症研究所的监测、流行病学和最终结果(SEER)儿科专论中呈现的全国数据进行比较。AN的人口数据基于人口普查数据和印第安卫生服务机构两次人口普查期间的估计值。美国白人及新墨西哥州印第安人的数据来自美国国立癌症研究所的SEER项目。使用SEERStat软件进行计算。阿拉斯加白人的数据为1996 - 2000年期间的(阿拉斯加癌症登记处自1996年起才开始收集所有阿拉斯加人的数据)。计算了率的比值比(OR)及其95%置信区间(CI)。
所有AN儿童(男女皆有)的所有癌症综合发病率与美国白人相似(OR:1.0;95%CI:0.8 - 1.1)。然而,按种族对儿童癌症发病率进行分析发现,印第安儿童的发病率显著较低(OR:0.6;95%CI:0.4 - 0.8),但爱斯基摩或阿留申儿童的发病率无显著差异。对于大多数儿童癌症国际分类组,AN儿童的发病率也与美国白人相似。然而,AN儿童患肝肿瘤的风险显著更高(OR:13.1;95%CI:7.9 - 20.5),尤其是肝细胞癌(OR:43.8;95%CI:24.4 - 75.1)和成视网膜细胞瘤(OR:2.8;95%CI:1.3 - 5.3)。按种族分组,仅爱斯基摩人肝细胞癌的发病率显著较高。所有AN儿童神经母细胞瘤(OR:0.1;95%CI:0.1 - 0.6)和淋巴瘤(OR:0.5;95%CI:0.3 - 0.9)的发病率较低,尤其是霍奇金病(OR:0.2;95%CI:0.0 - 0.5)。基于5年的数据,阿拉斯加白人儿童的发病率似乎与美国白人儿童无异。由于我们发现AN与美国白人之间存在差异,我们审查了其他相关人群的数据,特别是来自新墨西哥州SEER登记处的美洲印第安人数据。使用SEER数据和SEER软件,我们计算了新墨西哥州美洲印第安人(NMAI)的发病率,并将其与美国白人的发病率进行比较。NMAI所有癌症综合发病率显著低于美国白人(OR:0.8)。然而,与AN儿童相似,NMAI成视网膜细胞瘤的发病率高于美国白人(OR:2.5;95%CI:1.4 - 4.5)。与AN相似,NMAI患神经母细胞瘤(OR:0.2;95%CI:0.1 - 0.7)、淋巴瘤总体(OR:0.1;95%CI:0.0 - 0.3)以及特别是霍奇金病(OR:0.1;95%CI:0.0 - 0.4)的风险似乎也较低。NMAI儿童中枢神经系统肿瘤的发病率较低(OR:0.5;95%CI:0.3 - 0.7)。AN儿童的年均年龄调整癌症死亡率低于美国白人儿童,但差异不显著(每百万分别为28.6和37.3)。
AN所有癌症综合发病率与美国及阿拉斯加白人儿童相似,但似乎高于NMAI。在特定的儿童癌症国际分类组中,AN与美国白人之间存在差异。最显著的发病率差异见于肝肿瘤,这主要是由于乙型肝炎相关肝细胞癌的发病率升高。我们研究中的所有肝细胞癌患儿乙型肝炎抗原均为阳性。1982年末开始了一项全州范围的乙型肝炎病毒免疫接种计划。尽管1983年之前出生的16名儿童患了肝细胞癌,但自婴儿接种乙型肝炎疫苗后的20年里,没有儿童被诊断为肝细胞癌,这是一个显著差异。从两个群体中去除肝细胞癌病例后比较AN和美国白人儿童癌症发病率,得出OR为0.8(95%CI:0.7 - 1.0)。因此,如果未来几代儿童其他癌症发病率不增加,那么儿童癌症发病率可能很快会显著低于美国白人儿童。所有淋巴瘤的发病率都较低,这主要是因为霍奇金病的发病率极低。神经母细胞瘤的发病率也较低。令人欣慰的是,AN儿童的发病率并未过高且似乎没有上升。该人群对包括电离辐射在内的环境暴露存在担忧。我们的数据未显示儿童白血病或甲状腺癌过多,而辐射已知会增加这些恶性肿瘤的风险。