Demographics and tumor characteristics of colorectal cancers in the United States, 1998–2001


  • Genevieve Matanoski MD, DrPH,

    Corresponding author
    1. Department of Epidemiology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland
    2. District of Columbia Department of Health, Washington, District of Columbia
    • Johns Hopkins University Bloomberg School of Public Health, 111 Market Place, Suite 850, Baltimore, MD 21202, USA
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    • Fax: (410)223-1867

  • Xuguang (Grant) Tao MD, PhD,

    1. District of Columbia Department of Health, Washington, District of Columbia
    2. Division of Occupational and Environmental Medicine, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland
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  • Lyn Almon MSPH,

    1. Centers for Disease Control and Prevention, Atlanta, Georgia
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  • Aaron A. Adade PhD,

    1. District of Columbia Department of Health, Washington, District of Columbia
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  • John O. Davies-Cole PhD, MPH

    1. District of Columbia Department of Health, Washington, District of Columbia
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  • The findings and conclusions in this report are those of the authors and do not necessarily represent the views of the Centers for Disease Control and Prevention.



Descriptions of population characteristics for intestinal cancers frequently combine colon and rectal sites. However, some studies suggest that cancers of subsites in the intestinal tract may differ both by demographics and biology. Examination of colon and rectal cancers' characteristics separately could identify different risk profiles for these sites.


Data from combined National Program of Cancer Registries (NPCR) and Surveillance, Epidemiology, and End Results (SEER) databases were examined for risk characteristics by age, race, sex, and ethnicity, as well as for SEER-reported trends over 27 years.


Males had higher incidences of both colon and rectal cancers, but this predominance was greater for rectal cancers. Colon cancer rates were higher for blacks than for whites but rectal cancer rates were slightly higher for whites than for blacks. The change in incidence rates by race occurred abruptly at sites in the lower colon. Asians had low rates of colon cancer, but their rectal cancer rates were similar to those of blacks. Trends for both sites showed declines in incidence rates in whites, but slight to no change in blacks. Mortality in blacks increased until about 10 years ago.


Colon and rectal cancer sites should be studied independently because of major differences in their characteristics. Age-specific incidence rates differ by race and site. Any effect from screening is difficult to demonstrate because of changes in procedures over time, resulting in different levels of effective detection in the intestinal tract, and because of slow acceptance of screening by the public. Cancer 2006. © 2006 American Cancer Society.

Colorectal cancers (CRC) are the third most common cancer in both U.S. men and women.1 The demographic distribution of CRC mortality rates over the past 50 years has changed markedly. Previously, CRC occurred predominantly in the white population, in higher socioeconomic groups, and with similar rates in men and women.1–3 Current research indicates a shift such that now CRC mortality rates are higher in black men, and there is a suggested predominance of these cancers in lower socioeconomic populations. Since the 1970s incidence rates have been higher in men than in women, but not until the 1980s did the rate in blacks surpass that in whites.

Studies of CRC indicate differences in demographic characteristics for cancers of the colon, rectum, and colon subsites.4 Blacks have higher incidence rates of proximal colon cancers than do whites.5 Rates are higher in males than females for every site, but the M/F ratio increases from the cecum through the rectum. The ratio of proximal to distal cancers increases with age.5, 6 Rates of rectal and sigmoid cancers in Asian men and women are similar to rates in whites, but proximal cancer rates are lower in both Asians and Hispanics than in whites.6, 7 Trends in rates over time have indicated that rates of proximal colon cancers have been stable or increasing slightly.8 At the same time, left-sided or lower colon lesions have been declining rapidly, resulting in an increase in the proximal to distal cancer ratio that is more marked in women than in men.

Over the past 20 years, extensive investigation of pathogenetic events preceding the development of CRC has led to the discovery of several key genetic and epigenetic steps.9, 10 There are two distinct types of hereditary colon cancers: familial adenomatous polyposis (FAP), in which patients have a germ cell line mutation in the adenomatous polyposis coli (APC) gene, and hereditary nonpolyposis colorectal cancer (HNPCC). The FAP patient develops colon cancers that demonstrate chromosomal instability (CIN) within adenomatous polyps. HNPCC or so-called microsatellite instability (MIN) cancers have damage to the DNA mismatch repair mechanism with consequent instability at the level of nucleotides resulting in genetic changes at repetitive DNA sequences or microsatellites. Both forms of hereditary cancers have counterparts among nonhereditary cases with 80–85% of sporadic cancers representing CIN tumors and 15–20% representing MIN tumors.10

MIN and CIN tumors differ in terms of the cancer's location in the intestinal tract and demographic characteristics of patients. MIN cancers are more likely to occur in the proximal colon and are more common in blacks.9, 10 The identification of precancerous lesions is more difficult for MIN cancers because, unlike CIN cancers, they do not arise in an adenomatous polyp. Instead, they develop either de novo or in a hyperplastic' polyp or serrated adenoma. Thus, MIN cancers are not likely to be detected by screening. Cancers of the proximal colon are largely MIN cancers and thus have a poorer prognosis. This subset of colon cancers may have an increasing or stable incidence over time that is being masked by the overall decline reported for all colon cancers. Differences in the frequency of these MIN cancers may result in changing rates of and survival from colon and rectal cancers by race and sex over time.

The major aims of this study were 1) to examine colorectal cancer incidence and mortality by demographic characteristics to determine whether the data provide clues to etiology, 2) to examine incidence rates by anatomic subsites and demographic characteristics, and 3) to review analyses of trend data for 27 years and relate the trends to current CRC characteristics.


The data for this chapter are derived from both the National Program of Cancer Registries (NPCR) and the Surveillance, Epidemiology and End Results (SEER) databases that include 39 U.S. cancer registries plus the District of Columbia (D.C.) and Atlanta for the reporting period 1998–2001.11 These registries, which are identified in Table 1, designate Hispanic patients from either case records or surname matches by means of the North American Association of Central Cancer Registries (NAACCR) Hispanic Identification Algorithm (NHIA). Data on mortality are reported for the U.S. with omission of Hispanic data for the eight states that omit Hispanic designation on death records: Connecticut, Maine, Maryland, Oklahoma, New York, New Hampshire, North Dakota, and Vermont.

Table 1. Incidence Rates of Colorectal, Colon, and Rectum Cancer by Race, Sex and Ethnicity, United States, 1998–2001*
 Colorectal (Rate/100,000 persons)Colon (Rate/100,000 persons)Rectum/Rectosigmoid (Rate/100,000 persons)
  • API: Asians and Pacific Islanders.

  • *

    Data are from population-based cancer registries that participate in the National Program of Cancer Registries (NPCR) and/or the Surveillance Epidemiology and End Results (SEER) Program and meet high quality data criteria: Alabama, Alaska, Arizona, California, Colorado, Connecticut, District of Columbia, Florida, Metro Atlanta (Georgia), Hawaii, Idaho, Illinois, Indiana, Iowa, Kansas, Kentucky, Louisiana, Maine, Massachusetts, Michigan, Minnesota, Missouri, Montana, Nebraska, New Jersey, New Mexico, New York, North Carolina, Ohio, Oklahoma, Oregon, Pennsylvania, Rhode Island, South Carolina, Texas, Utah, Vermont, Washington, West Virginia, Wisconsin, Wyoming. These registries cover approximately 88% of the U.S. population.

  • Rates are per 100,000 persons and are age-adjusted to the 2000 U.S. standard population. Rates presented with 95% confidence intervals in parentheses.

  • Hispanic origin is not mutually exclusive from race categories (white, black, API).

All races55.666.147.840.646.636.115.119.511.6
(55.5, 55.8)(65.8, 66.3)(47.6, 48.0)(40.4, 40.7)(46.4, 46.9)(36.0, 36.3)(15.0, 15.1)(19.3, 19.6)(11.6, 11.7)
(54.9, 55.2)(65.4, 65.9)(46.9, 47.2)(39.8, 40.1)(45.9, 46.3)(35.2, 35.6)(15.0, 15.2)(19.4, 19.7)(11.5, 11.7)
(59.7, 60.8)(69.1, 71.1)(53.1, 54.4)(46.6, 47.5)(52.8, 54.5)(42.3, 43.4)(13.0, 13.5)(16.0, 16.9)(10.6, 11.2)
(40.1, 41.6)(46.8, 49.4)(34.3, 36.3)(27.2, 28.5)(30.4, 32.5)(24.4, 26.0)(12.6, 13.4)(15.9, 17.4)(9.6, 10.7)
(43.3, 44.4)(52.9, 54.8)(35.8, 37.1)(30.5, 31.4)(35.7, 37.3)(26.5, 27.6)(12.6, 13.1)(16.9, 17.9)(9.1, 9.7)

Age-adjusted incidence rates of colon, rectal (including rectosigmoid), and colorectal cancer by sex, race, and ethnicity for 1998–2001 are reported for data from combined NPCR and SEER registries, adjusted to the U.S. 2000 standard population using SEER*Stat software.12 Data for American Indians and Alaskan natives are under-reported and have been omitted except in analyses for all races. Age-adjusted incidence rates are examined by subsites of the colon and rectum by race and sex for the same dataset. U.S. death rates for colon and rectal cancers for 1998–2001 are examined by race, sex, and ethnicity. Incidence/mortality ratios by site, race, and sex are calculated using age-adjusted incidence and mortality. Age-specific incidence rates of colon and rectal cancers are examined by race and sex with use of a log linear scale to examine slopes of the curves.


Race and Sex

CRC incidence rates for 1998–2001 for the combined cancers were higher for blacks than for whites for both sexes (Table 1). Rates were lower among Hispanics than among whites, but Asians and Pacific Islanders (API) had the lowest rates. Males had higher rates than females for each race and Hispanics. Differences in rates by race, ethnicity or sex were significant (P < .05).

Colon cancer rates were highest in blacks for both sexes. Among all races, incidence rates were lower for rectal cancers than for colon cancers. Ratios of black to white incidence rates were higher for colon cancer (B/W = 1.18) than for rectal cancer (B/W = 0.87). For both sexes, whites had higher rectal cancer rates than blacks and Asians. Colon cancer rates were higher in males than in females for every race and Hispanics, with male/female (M/F) ratios ranging from 1.25 to 1.35. However, the male predominance was even greater for rectal (M/F = 1.7) than for colon cancers (M/F = 1.3). This predominance persisted regardless of race or ethnicity. Rectal cancer incidence rates for Asians and Hispanics were similar to those for blacks, but colon cancer incidence rates were lower than those for blacks or whites. Colon cancer rates were higher for blacks than whites, whereas the reverse was true for rectal cancer rates. These differences in incidence rates by race and sex for colon versus rectal cancers suggest possible differences in etiology, cancer pathogenesis, or other factors.

To determine the optimum point at which to divide the colorectal tract to identify differences by race and sex, we examined the rates by anatomic subsites using the same data source (Table 2). The race-specific incidence rates and B/W ratios for each site indicate that rates were higher among blacks than among whites throughout the colon to the level of the sigmoid. At that point, however, rates abruptly became approximately equal for all races. The rates among Asians were lower than among whites or blacks until the level of the descending colon. There the relationship between rates by race abruptly changed, and throughout the rectum, rates among Asians became similar to those among other races. Rates were higher in males than in females for all races at all subsites of the colon. However, the marked predominance among males seen in rectal cancers occurred abruptly at the level of the splenic flexure.

Table 2. Incidence Rates of Colon, Rectosigmoid, and Rectal Cancers by Subsite, Race, and Sex, United States, 1998–2001*
  Total (Rate/100,000)Ratio (B or API/W)Male (Rate/100,000)Female (Rate/100,000)Ratio (Male/Female)
  • API: Asians and Pacific Islanders; W, white.

  • *

    Data are from population-based cancer registries that participate in the National Program of Cancer Registries (NPCR) and/or the Surveillance Epidemiology and End Results (SEER) Program and meet high quality data criteria (see Table 1 footnote for list of registries). These registries cover approximately 88% of the U.S. population.

  • Appendix site rates are omitted since rates are low. Cancers classified as “Intestine NOS” are omitted but represent only 5% of the total cancers.

  • Rates are per 100,000 persons and are age-adjusted to the 2000 U.S. standard population.


For all races and sexes in the U.S., the incidence rate for colon cancer was 2.3 times higher and that for rectal cancer was 5.0 times higher than the corresponding death rates in 1998–2001 (Table 3). The ranking of death rates by race was similar to that of incidence rates for colon but not for rectum. For colon cancer the B/W ratio for incidence was only 1.18, but the ratio for mortality was 1.44. Compared with whites, the death rates for blacks were higher relative to the incidence rates, as reflected in the incidence/mortality (I/M) ratios. For rectal cancers, differences by race were more striking in that whites had higher incidence rates than blacks, but death rates were actually higher for blacks than for whites. These data suggest high mortality relative to incidence for both colon and rectal cancers in blacks compared with other races. Asians had the lowest incidence and mortality among all races and the highest I/M ratios for both colon and rectal cancers. In general, females had lower or equal death rates relative to incidence rates for both colon and rectal cancers, as shown by greater I/M ratios. The only exception was rectal cancer in Asian women; in that case, mortality relative to incidence was higher than in men.

Table 3. U.S. Death Rates and Incidence/Mortality Ratios for Colon and Rectum Cancers, United States, 1998–2001*
 Colon cancers (Rate/100,000 persons)Rectum cancers (Rate/100,000 persons)
  • API: Asians and Pacific Islanders.

  • *

    Incidence data are from population-based cancer registries that participate in the National Program of Cancer Registries (NPCR) and/or the Surveillance Epidemiology and End Results (SEER) Program and meet high quality data criteria (see Table 1 footnote for list of registries). Death data are from the National Vital Statistics System.

  • Death rates are age-adjusted to the 2000 U.S. standard population. Rates presented with 95% confidence intervals in parentheses.

  • Death rates do not include Hispanic and non-Hispanic data for 8 states.

US death rates
 All races17.7(17.6, 17.8)21.1(21.0, 21.3)15.2(15.1, 15.3)3.0(3.0, 3.1)3.9(3.9, 4.0)2.3(2.3, 2.4)
 White17.2(17.1, 17.3)20.6(20.5, 20.8)14.7(14.6, 14.8)3.0(3.0, 3.0)3.9(3.8, 4.0)2.3(2.3, 2.4)
 Hispanic12.5(12.2, 12.8)15.6(15.0, 16.2)10.3(10.0, 10.7)2.2(2.1, 2.4)3.0(2.8, 3.2)1.7(1.5, 1.8)
 Non-Hispanic17.4(17.3, 17.5)20.9(20.7, 21)14.9(14.8, 15)3.0(3, 3.1)3.9(3.9, 4.0)2.4(2.3, 2.4)
 Black24.7(24.4, 25.0)29.5(28.9, 30.1)21.8(21.4, 22.1)3.4(3.3, 3.6)4.6(4.4, 4.9)2.6(2.5, 2.7)
 API10.7(10.3, 11.1)13.0(12.3, 13.7)9.0(8.5, 9.5)2.2(2, 2.4)2.7(2.4, 3)1.7(1.5, 2.)0
 Colon cancersRectum cancers
Incidence/Mortality ratios
 All races2.292.212.385.05.05.0

Changes in Age-specific Incidence by Race

Figures 1 and 2 depict age-specific incidence rates of colon and rectal cancers by race and sex. These are plotted on a log-linear scale to examine the rate of increase in incidence by age. The age-specific incidence rates for colon cancer in Figure 1 indicate an increase in incidence with age with high rates in blacks and low rates in Asians for both sexes. The slopes of the curves are steeper for black men and women than for their white counterparts beginning about age 30–34 years. About age 45–55 the slopes become parallel, thus indicating the same rates of increase in incidence until about age 64. Then the slope for blacks becomes less than that for whites, leading to convergence or equal incidence rates at age 80. Both sexes follow similar patterns by race. The age-specific incidence rates for Asians were lower at all ages. However, the increase in rates with age slowed at about age 50–59 years for both sexes, after which the slopes become less steep so that the lower incidence of this cancer in Asians is even more marked at older ages.

Figure 1.

Age-specific incidence rates of colon cancer, United States, 1998–2001, log linear curve. Data are from population-based cancer registries that participate in the National Program of Cancer Registries (NPCR) and/or the Surveillance Epidemiology and End Results (SEER) Program and meet high quality data criteria (see Table 1 footnote for list of registries). These registries cover approximately 88% of the U.S. population. Solid squares indicate white; open squares, black; solid triangles, Asian/Pacific Islander.

Figure 2.

Age-specific incidence rates of rectum and rectosigmoid cancer, United States, 1998–2001, log linear curve. Data are from population-based cancer registries that participate in the National Program of Cancer Registries (NPCR) and/or the Surveillance Epidemiology and End Results (SEER) Program and meet high quality data criteria (see Table 1 footnote for list of registries). These registries cover approximately 88% of the U.S. population. Solid squares indicate white; open squares, black; solid triangles, Asian/Pacific Islander.

The pattern of age-specific incidence rates for rectal cancer is very different from the curves for colon cancer (Fig. 2). The rates of rectal cancer do not increase rapidly for young blacks, as occurred with colon cancer, and all races have similar rates to about age 60. After that age, the slope of the age-specific incidence curve in whites remains constant, and the slope for blacks decreases in steepness giving older whites increasingly higher rates than older blacks and Asians.


Contrast between Cancers of Colon and Rectum

One purpose of this chapter is to examine demographic characteristics associated with the incidence and mortality of colon and rectal cancers to identify any differences in these variables between these two sites. Theories regarding the etiology or course of cancers of the intestinal tract should conform to the basic demographic characteristics of cancers. If these characteristics differ between cancers of the colon and rectum, then studies of etiology or course of the cancers should examine the two sites separately. The analyses of incidence rates based on data from 41 NPCR and SEER registries indicate a male predominance in rates for both sites, but it is much more pronounced in the rectum than in the colon. Incidence rates are higher in blacks than in whites for colon cancer. Conversely, whites have slightly higher rates of rectal cancers than blacks. Asians and Hispanics have lower rates of colon cancer than other races or ethnic groups, but their rates of rectal cancer are similar to other races. Both the shapes and slopes of the log-linear curves of age-specific rates differ between the colon and rectum. These observations suggest that these cancers are not similar with respect to basic population characteristics. It is probable that we are looking at different cancers perhaps with different risk factors that must be examined separately.

Another question is whether the current anatomical designations used to define these cancers reflect similar distributions by race and sex. Examination of subsite data indicates that these different demographic characteristics of colon and rectum cancers actually begin in the lower colon. High black-to-white and low Asian-to-white ratios occur in the proximal colon. However, these ratios change at about the sigmoid for blacks and at the descending colon for Asians, generally reaching rates that are more similar to those of whites in the lower colon, and these relationships continue through the rectum. The male/female ratio shows a small excess in males in the upper colon, but the excess abruptly rises at the splenic flexure to the 1.5- to 1.7-fold excess commonly seen in the rectum. Thus, separation of the intestinal tract into the traditional split between colon and rectum at the rectosigmoid junction would include cancers with rectal cancer characteristics among all colon cancers. The current division is solely based on the anatomy of the tract and may not be the optimum separation for epidemiologic investigations of etiology. For such studies the division should be based on grouping by observed demographic characteristics.

Interpretation of Demographic Data

Many personal characteristics such as excess weight, physical inactivity, and poor diet are considered risk factors for colorectal cancers.13, 14 The question is whether the demographic characteristics of these cancers support the role of these factors as risks. For example, theoretically, if diet were a risk factor for CRC, then the incidence rates for males and females within a race should be more similar than the rates for different races. Yet, the predominant demographic characteristic for every race, especially for cancers below the splenic flexure, appears to be the consistently higher rates in males. Only in the proximal and transverse colon do the rates of colon cancer differ by race, with higher rates in blacks and very low rates in Asians as compared with whites. Therefore, although differences in rates by race in the upper colon support the hypothesis that diet may play a role in the risk of colon cancer, the inconsistencies in incidence by race in the rectum and descending colon, the abrupt changes in risk by race at colon subsites, and the high ratios for sex compared with race do not fit with that theory.

Many studies have noted changes in demographic characteristics of CRC based on subsite.4–8, 15 The studies have used different anatomic locations to define proximal and distal cancers. However, the demographic characteristics by subsite deserve particular attention. Normally, the expectation would be that changes in the distribution of demographic characteristics of cancers would occur gradually by subsites, but the changes seem to occur abruptly. Previous studies have suggested that changes in M/F ratios from cecum to rectum have occurred gradually.5, 16 Only Wu et al. noted abrupt changes in B/W ratios for subsites in the colon.5 The abruptness of the change in incidence for both race and sex by subsite in the lower colon in the current analysis might suggest an effect from screening, but this is unlikely to be the only reason. If screening were playing a major role, then we would expect W/B ratios in the lower colon and rectum to have increased over the past 15 or 20 years with the more widespread use of screening, especially in whites. Instead, SEER data for 1975–2001 indicate that the W/B ratio was high for rectal cancer in 1975, but by 2000 rates were almost equal for the two races.15 Furthermore, screening cannot explain the abrupt changes in racial ratios as high as the descending colon or the sex-specific changes at the splenic flexure given that screening using instruments to detect lesions above the sigmoid is a recently introduced procedure.

Evidence supports the theory that cancers might differ by site because of differences in the biologic characteristics of lesions at points along the intestinal tract.9, 10 Tumors of the upper colon have a higher proportion of MIN cancers than do cancers in the lower colon.9, 10 However, for the entire colorectal tract, the frequency of MIN cancers is only 20% of all cancers. Thus, their unequal distribution would have a greater impact on cancer rates in the upper tract than in total CRC. MIN cancers also are reported to occur more frequently in blacks and in women and to have poorer survival than CIN cancers.9 MIN cancers do not occur in adenomatous polyps, the target of screening. Therefore, increased screening with removal of polyps could potentially increase the proportion of MIN cancers among all cancers and change the ratio of cancer types at lower colorectal tract levels. Thus, increasing the proportion of MIN cancers through screening would result in poorer survival and higher B/W ratios especially in the lower colon and rectum. This outcome has not yet occurred. Still, by 2000, B/W ratios were approaching 1.00 for rectal cancers, whereas ratios had been below 1.00 about 25 years previously.15 Certainly, the existence of two cancers with major differences in genetic characteristics that are related to race and sex would suggest varying etiologic factors for these different cancer types.

The next obvious question is whether the predominance in males is related to basic physiological or other differences between the sexes. Such factors might include diet and obesity as well as drug therapies, aspirin, and hormones. The influence of many of these factors cannot be tested with the use of surveillance data. One such difference that could be examined, however, is the effect of natural premenopausal estrogens in women that might suppress CRC at early ages. If these hormones do play a preventive role, then the expectation is that age-specific incidence data would indicate that, at postmenopausal ages, women should show an increase in incidence as seen with other diseases, but none occurs. The literature also provides little support for this theory except for one study that has shown that use of postmenopausal estrogen may suppress MIN cancers specifically.17 Since these cancers represent only 20% of all CRC, any protective effect of estrogen on this tumor type may not be apparent when total cancers are studied.

Colon and rectal cancers have differences in the shapes of the age-specific incidence curves by race that may relate to the etiology or course of CRC. The results show that the slopes of incidence curves for each sex for both cancers are parallel by race for ages 40 to 60 years. The striking difference is that although the rates for ages 40–60 differ by race; for rectal cancers, all races have similar rates for this age range. Thus, the difference in incidence of colon cancer by race is primarily due to starting with incidence rates in blacks that are higher under age 40. This may represent differences related to susceptibility or to exposures in the young by race. The higher incidence rates of rectal cancers in whites occur generally because of higher rates after age 65 as compared with other races. The shapes of the age-specific incidence curves by race for both sexes are similar for colon cancer, but the slope of rectal cancer incidence is not as steep in females. These observations emphasize the need to examine these sites separately. For example, studies to explain differences in sites by race for colon cancer must focus on the youngest age group, whereas for rectal cancers the oldest age group is the major source of racial differences. In addition, the overall excess in M/F ratios for colon cancer is represented by small and varying differences by sex for each age. Rectal cancers, on the other hand, have consistently lower age-specific rates in females at all ages, which might indicate a physiologic or exposure difference in risk by sex.

For both colon and rectal cancers in males and females, the age-specific rate curves for blacks at about age 65+ have slopes that are less steep than those for whites. This change results in age-specific rates that become equal for colon cancer and that become higher in whites for rectal cancer at these older ages. Several explanations are possible for the slowing in rates of increase in incidence of colon and rectal cancers by age in blacks. This finding could result from lower rates of cancer detection, slower growth rates of cancer, or birth cohort differences in older blacks compared with whites. If birth cohort differences are the explanation for lower rates at older ages, then this would suggest a later introduction of risk factors into the black compared with the white population. Evidence in the literature suggests that CRC mortality rates for whites compared with blacks were higher around the middle of the 20th century, after which rates rose in blacks to exceed whites in the past three or more decades.2 The true explanation for the decline in the slopes of black incidence at older ages is unclear, but the differences in B/W ratios in older compared with younger ages do not occur because of an increase in the slopes of the incidence curves at age 60 in the white population.

As noted in the introduction, CRC mortality has changed its demographic characteristics over the past 40 to 50 years. In addition to changing trends in mortality, SEER incidence data from 1975 to 2001 can help track these cancer changes and determine the predicted directions of future rates.15 The published NCI data tables of joinpoint analyses permit an examination of trends from 1975 to 2001 with an evaluation of whether the rates over time are represented by a curve with a single slope or one with multiple segments having different slopes. The death rates in whites indicate a progressively steeper declining curve from 1975 to the present. In blacks, the death rates actually increased to 1990 after which there was a decline in rates that was less than half of that in whites. This pattern has resulted in the differences in mortality seen in the current analysis in which the B/W ratio for colon cancer mortality is much higher than the ratio for the incidence. For rectal cancers, there is actually a reversal in the racial ratio for incidence versus mortality with higher incidence in whites than in blacks but higher mortality in blacks. This combined effect of increasing mortality in blacks for the first 15 years of the period while whites showed declining mortality rates and subsequently a smaller decline in rates for blacks when compared with whites after that period has led to the curves becoming more divergent over time. This is a major concern because it represents a serious racial disparity that will only increase in the future if the current trends continue.

Differences in incidence trends by race have also added to the greater burden of CRC in blacks when compared with that in whites. The 27-year joinpoint analysis for 1975–2001 indicated that the incidence of colon cancer rose in both races for about the first 10 years with an increase that was three times higher in blacks than in whites. Both colon and rectal cancer incidence rates then began to decrease in whites, but there has been no decline in incidence rates for either cancer in blacks. Therefore, the reported trends indicate that the cancers are occurring at about the same incidence over the past 20 years in blacks accompanied by a mortality that rose until the last 10 years of the period and is now falling much more slowly than that of whites. The result has been high incidence rates of these cancers in blacks in recent years when compared with results from about 30 or more years ago, and death rates that show an even higher predominance in blacks.


A comparison of the incidence patterns of colon versus rectal cancers by sex, race, and age indicate major variations in demographic characteristics that suggest possible differences in etiology, pathogenesis, or screening of cancers at the two sites. The data also indicate that subsites within the lower colon have demographic characteristics similar to rectal-type cancers rather than upper-colon cancers. Data from the literature suggest that intestinal cancers may differ in genetic characteristics related to race, sex, and location in the colon. Thus, the demographic characteristics of these cancers together with basic biologic evidence suggest that investigators should be looking for a different set of risk factors for cancers of the upper colon when compared with that of the rectum and sites within the lower colon. Evaluations of effectiveness of screening programs also benefit from analysis of data by subsite since screening practices detect cancers at different levels in the colorectal tract. Rather than using divisions based solely on anatomic location, epidemiologists should divide the intestinal tract into subsites that identify risk areas on the basis of differences in demographic characteristics of populations with cancer in order to investigate etiologic risk factors for these cancers and to evaluate the impact of screening for them.

The trends in these cancers by race have indicated that unlike white incidence rates over the past 20 years, which declined, the rates in blacks have remained the same. The mortality increased in blacks until 10 years ago after which the rate has declined, but at a much slower pace than in whites. These trends suggest that the major racial disparity in these cancers that now exists will only increase in the future if trends continue.


We appreciate the in-kind support from all the contributors to this monograph and also are grateful for the contributions of Jessica King for the preparation of analytic files and to Faruque Ahmed for his leadership of the colorectal cancer monograph project.