[Skip to Content]
Sign In
Individual Sign In
Create an Account
Institutional Sign In
OpenAthens Shibboleth
Purchase Options:
[Skip to Content Landing]
Citations 0
From the Centers for Disease Control and Prevention
December 27, 2000

HIV-Related Knowledge and Stigma—United States, 2000

JAMA. 2000;284(24):3118-3119. doi:10.1001/jama.284.24.3118
HIV-Related Knowledge and Stigma—United States, 2000

MMWR. 2000;49:1062-1064

1 table omitted

An essential component of efforts to prevent new human immunodeficiency virus (HIV) infections in the United States is the use of voluntary HIV counseling and testing by persons at risk for HIV, especially members of underserved populations.1 To increase the number of persons at risk for HIV who receive voluntary HIV counseling and testing services, barriers to these services must be identified and removed. The stigmatization of persons infected with HIV and the groups most affected by HIV, including men who have sex with men and illicit drug users, is a barrier to testing.2,3 Measuring public attitudes and knowledge about HIV transmission to determine the prevalence and the correlates of stigmatizing attitudes is important for guiding efforts to remove barriers to HIV prevention. This report describes the results of a national public opinion survey conducted through the Internet to measure indicators of HIV-related stigma and knowledge of HIV transmission. The findings indicate that most persons do not have stigmatizing views.

During August-September 2000, Research Triangle Institute conducted an Internet-based, household survey in a sample of 7493 adults aged ≥18 years. The sample was proportionately selected from a nationally representative panel of approximately 45,000 households. To establish the panel, a sample of U.S. households obtained through random-digit-dialed telephone sampling was offered Internet access and equipment in exchange for participation in weekly surveys. Surveys were conducted using a standard television set connected to the Internet, and responses were entered using a remote control. A module on HIV-related stigma and knowledge of transmission was included in a larger survey on health and aging. This analysis is based on 5641 respondents (75.3%) who answered the question on HIV stigma.

The survey included one question that was considered a proxy indicator for a stigmatizing attitude. Participants were identified who strongly agreed or agreed with the statement "People who got AIDS [acquired immunodeficiency syndrome] through sex or drug use have gotten what they deserve." Although this question addresses only one element of HIV/AIDS stigma, for this report, these answers were considered a "stigmatizing" response. Two questions concerned knowledge about HIV transmission. Persons who responded that it was very unlikely or impossible to become infected through sharing a glass or being coughed or sneezed on were considered informed; those who stated that it was very likely, somewhat likely, or somewhat unlikely were classified as misinformed. Percentage estimates were weighted to provide representative estimates, and confidence intervals (CIs) and p-values were computed using SUDAAN.

Among the 5641 respondents, 40.2% (95% CI = 38.8%-41.6%) responded that HIV transmission could occur (i.e., it was very likely, somewhat likely, or somewhat unlikely) through sharing a glass, and 41.1% (CI = 39.7%-42.5%) responded that it could occur from being coughed or sneezed on by an HIV-infected person. A total of 18.7% responded that persons who acquired AIDS through sex or drug use have gotten what they deserve. Stigmatizing responses were more common among men (21.5%), whites (20.8%), persons aged ≥55 years (30.0%), those with only a high school education (22.1%), those with an income <$30,000 (23.4%), and those in poorer health compared with others (23.6%). For both transmission questions, approximately 25% of those who were misinformed gave stigmatizing responses, compared with approximately 14% who were informed (p<0.05).

Reported by:

DA Lentine, JC Hersey, VG Iannacchione, GH Laird, K McClamroch, L Thalji, Research Triangle Institute, Research Triangle Park, North Carolina. Prevention Informatics Office, Office of the Director; Behavioral Intervention Research Br, Div of HIV/AIDS Prevention-Intervention Research and Support, National Center for HIV, STD, and TB Prevention, CDC.

CDC Editorial Note:

The findings in this report suggest that most U.S. adults do not hold stigmatizing views about persons with HIV infection or AIDS. However, a substantial minority gave a response that suggests they may have stigmatizing attitudes about persons with HIV. The smallest proportion of respondents who gave this response was black, the racial/ethnic group with the highest rates of AIDS in the United States. Significantly more of the respondents who were misinformed about HIV transmission gave a stigmatizing response, suggesting that increasing understanding about behaviors related to HIV transmission may result in lower levels of stigmatizing beliefs about infected persons. However, many other factors are probably related to stigma.

Early HIV diagnosis and entry into health care have both individual and societal benefits: improved health and productivity, reduced hospitalization costs, and decreased transmission from persons who do not know their HIV status.1 Because most HIV-infected persons probably will adopt safer sexual behaviors after the diagnosis of HIV infection,4,5 increasing the number of infected persons who know their serostatus is an important prevention goal. However, HIV-infected persons who fear being stigmatized are typically reluctant to acknowledge risk behaviors, avoid seeking prevention information, and may experience real or perceived barriers to prevention and other health-care services.2,3 Therefore, public health measures that encourage access to HIV testing by reducing stigma (e.g., social marketing campaigns targeted to high risk, stigmatized populations; sexuality and cultural sensitivity training for health-care providers; and anonymous testing opportunities) strengthen HIV-prevention efforts.

The findings in this report are subject to at least two limitations. First, the results are based on only one question about stigma, which comprises a range of attitudes, beliefs, and behaviors. Second, the survey did not include persons who do not own a telephone, persons in institutions, the transient or homeless, and those living on military installations. Despite these limitations, the sampling methods eliminated the main bias in earlier Internet samples (i.e., a lack of universal access to the Internet) while preserving the advantages of Internet surveys. In addition, the panel closely matched the overall U.S. population with respect to age, race/ethnicity, sex, education, and income.

Stigma includes prejudice and active discrimination directed toward persons either perceived to be or actually infected with HIV and the social groups and persons with whom they are associated.3 Overcoming stigma is an important step in persons seeking to know their HIV status. Measurements such as those conducted in this study help to direct and assess efforts to overcome these barriers.

Valdiserri RO. HIV counseling and testing: its evolving role in HIV prevention.  AIDS Educ Prev.1997;9:2-13.
Chesney M, Smith A. Critical delays in HIV testing and care: the potential role of stigma.  American Behavioral Scientist.1999;42:1162-74.
Herek G. AIDS and stigma.  American Behavioral Scientist.1999;42:1106-16.
CDC.  Adoption of protective behaviors among persons with recent HIV infection and diagnosis—Alabama, New Jersey, and Tennessee, 1997-1998.  MMWR Morb Mortal Wkly Rep.2000;49:512-5.
Weinhardt LS, Carey MP, Johnson BT, Bickham NL. Effects of HIV counseling and testing on sexual risk behavior: a meta-analytic review of published research, 1985-1997.  Am J Public Health.1999;89:1397-405.
Update: West Nile Virus Activity—Eastern United States, 2000

MMWR. 2000;1044-1047

1 figure omitted

Data reported to CDC through the West Nile Virus (WNV) Surveillance System have shown an increase in the geographic range of WNV activity in 2000 compared with 1999, the first year that WNV was reported in the Western Hemisphere.1 In response to this occurrence of WNV, 17 states along the Atlantic and Gulf coasts, New York City, and the District of Columbia conducted WNV surveillance, which included monitoring mosquitoes, sentinel chicken flocks, wild birds, and potentially susceptible mammals (e.g., horses and humans).2 In 1999, WNV was detected in four states (Connecticut, Maryland, New Jersey, and New York).3 In 2000, epizootic activity in birds and/or mosquitoes was reported from 12 states (Connecticut, Delaware, Maryland, Massachusetts, New Hampshire, New Jersey, New York, North Carolina, Pennsylvania, Rhode Island, Vermont, and Virginia) and the District of Columbia. Of the 13 jurisdictions, seven also reported severe neurologic WNV infections in humans, horses, and/or other mammal species. This report presents surveillance data reported to CDC from January 1 through November 15.

During 2000, 18 (14 from New York and four from New Jersey) persons were hospitalized with severe central nervous system illnesses caused by WNV. Patients ranged in age from 36 to 87 years (mean: 62 years); 12 were men. Of the New York patients, 10 resided in Richmond County (Staten Island), two in Kings County (Brooklyn), one in Queens County, and one in New York County (Manhattan). Of the New Jersey patients, two resided in Hudson County, and one each in Bergen and Passaic counties. Epizootic activity in birds and/or mosquitoes preceded the onset of human illness in all of these counties. Diagnoses were confirmed either by ELISA for WNV-specific IgM in cerebrospinal fluid or by a four-fold rise in WNV-specific neutralizing antibody in paired serum samples. Dates of illness onset ranged from July 20 to September 13. Of the 18 patients, one died (case fatality rate: 6%), and one is in a persistent vegetative state. In addition, WNV infection was documented in a mildly symptomatic woman residing in Fairfield County, Connecticut.

Veterinary surveillance has identified WNV infections in 65 horses with severe neurologic disease from 26 counties in seven states (27 horses in New Jersey; 24 in New York; seven in Connecticut; four in Delaware; and one each in Massachusetts, Pennsylvania, and Rhode Island). Illness onsets in these horses ranged from August 15 to October 29. WNV infection has been confirmed in 26 other mammals; of these, 25 were from 10 counties in New York (14 bats, four rodents, three rabbits, two cats, two raccoons), and one was from Connecticut (skunk).

WNV was isolated from or WNV gene sequences were detected in 470 mosquito pools in 38 counties in five states (352 pools in New York, 54 in New Jersey, 46 in Pennsylvania, 14 in Connecticut, and four in Massachusetts). Of the 470 reported WNV-infected pools, Culex species accounted for 418, including 222 Cx. pipiens/restuans, 126 Cx. pipiens, 35 Cx. salinarus, 11 Cx. restuans, and 24 unspecified Cx. pools. Ochlerotatus species (formerly in Aedes genus)4 accounted for 29 positive pools, including nine Oc. japonicus, nine Oc. triseriatus, eight Oc. trivittatus, and one each of three other Oc. species. Aedes species accounted for 18 positive pools, including 16 Ae. vexans, one Ae. albopictus, and one unspecified Ae. pool. In addition, WNV was detected in three pools of Culiseta melanura, one pool of Psorophora ferox, and one pool of Anopheles punctipennis.

A total of 4139 WNV-infected dead birds were reported from 133 counties in 12 states (New York reported 1263 birds; New Jersey, 1125; Connecticut, 1116; Massachusetts, 442; Rhode Island, 87; Maryland, 50; Pennsylvania, 34; New Hampshire, seven; Virginia, seven; Delaware, one; North Carolina, one; and Vermont, one) and the District of Columbia (five). Crows were the most frequently reported WNV-infected species. Since 1999, WNV has been identified in 76 avian species in the United States. WNV infection also was documented in specimens collected from six previously seronegative sentinel chickens in six counties in two states (New Jersey, four and New York, two).

Reported by:

A Novello, MD, D White, PhD, L Kramer, PhD, C Trimarchi, MS, M Eidson, DVM, D Morse, MD, B Wallace, MD, P Smith, MD, State Epidemiologist, New York State Dept of Health; S Trock, DVM, New York State Dept of Agriculture; W Stone, MS, Dept of Environmental Conservation, Albany; B Cherry, VMD, J Kellachan, MPH, V Kulasekera, PhD, J Miller, MD, I Poshni, PhD, C Glaser, MPH, New York City Dept of Health, New York. W Crans, PhD, Rutgers Univ, New Brunswick; F Sorhage, VMD, E Bresnitz, MD, State Epidemiologist, New Jersey Dept of Health and Senior Svcs. T Andreadis, PhD, Connecticut Agricultural Experiment Station, New Haven; R French, DVM, Univ of Connecticut, Storrs; M Lis, DVM, Connecticut Dept of Agriculture; R Nelson, DVM, D Mayo, ScD, M Cartter, MD, J Hadler, MD, State Epidemiologist, Connecticut Dept of Public Health. B Werner, PhD, A DeMaria, Jr, MD, State Epidemiologist, Massachusetts Dept of Public Health. U Bandy, MD, State Epidemiologist, Rhode Island Dept of Health. J. Greenblatt, MD, State Epidemiologist, New Hampshire Dept of Health. P Keller, M Levy, MD, State Epidemiologist, District of Columbia Dept of Public Health. C Lesser, MS, Maryland Dept of Agriculture; R Beyer, C Driscoll, DVM, Maryland Dept of Natural Resources; C Johnson, DVM, J Krick, PhD, A Altman, MS, D Rohn, MPH, R Myers, PhD, L Montague, J Scaletta, MPH, J Roche, MD, State Epidemiologist, Maryland Dept of Health and Mental Hygiene. B Engber, ScD, N Newton, PhD, T McPherson, N MacCormack, MD, State Epidemiologist, North Carolina Dept of Health. G Obiri, DrPH, J Rankin, Jr, DVM, State Epidemiologist, Pennsylvania Dept of Health. P Tassler, PhD, P Galbraith, DMD, State Epidemiologist, Vermont Dept of Health. S Jenkins, VMD, R Stroube, MD, State Epidemiologist, Virginia Dept of Health. D Wolfe, MPH, H Towers, VMD, W Meredith, PhD, A Hathcock, PhD, State Epidemiologist, Delaware Div of Public Health. Animal, Plant, and Health Inspection Svc, US Dept of Agriculture. National Wildlife Health Center, US Geologic Survey, Madison, Wisconsin. P Kelley, MD, Walter Reed Army Institute of Research, District of Columbia. M Bunning, DVM, US Air Force, Frederick, Maryland. Arbovirus Diseases Br, Div of Vector Borne Infectious Diseases, National Center for Infectious Diseases; and EIS officers, CDC.

CDC Editorial Note:

Although the WNV epizootic has persisted in the four states originally affected in 1999 and expanded into eight additional states and the District of Columbia, only 18 humans with severe neurologic illness attributed to WNV were reported in 2000 compared with 62 in 1999.5 However, severe neurologic illness occurs in <1% of infected persons, suggesting that approximately 2000 persons may have been infected during 2000. Although some decrease in severe human illness may be attributable to vector-control and other prevention activities, experience in Europe shows that the incidence of human illness can be variable and outbreaks sporadic.6 Because widespread WNV epizootic activity probably will persist and expand in the United States, larger outbreaks of WNV infection and human illness are possible if adequate surveillance, prevention activities, and mosquito control are not established and maintained.

A major objective of WNV surveillance is to detect epizootic activity early so that intervention can occur before severe human illnesses. In 2000, all 18 persons with severe neurologic disease became ill after WNV-infected dead birds were identified in their county of residence, suggesting that avian surveillance data are a sensitive indicator of epizootic transmission that may portend human illness. However, of 133 counties reporting WNV-infected birds, only seven (5%) reported at least one person with severe neurologic illness. The presence of WNV-positive mosquito pools may indicate a greater potential for severe human illness as six (16%) of the 38 counties with positive pools reported at least one severely ill person. But these pools were identified before the onset of human illness in only five of these counties. Further analysis of 2000 surveillance data, including an assessment of the timing, number, and geographic location of WNV-infected birds, and an assessment of mosquito-trapping activities, infection rates, and species identified are required to further interpret these data.

As occurred in 1999, the number of reported WNV illnesses in horses peaked and persisted after human illnesses.7 Although more data are needed to determine the reasons for this relative delay, it appears that horses are not a sensitive sentinel for the prediction of human illness.

The continued geographic expansion of WNV indicates the need for expanded surveillance and prevention activities. Surveillance should include monitoring WNV infection in birds, humans, and veterinary species and in mosquitoes, particularly when WNV activity has been identified.5 Prevention should include programs that (1) eliminate mosquito-breeding habitats in public areas; (2) control mosquito larvae where these habitats cannot be eliminated; (3) promote the increased use of personal protection and the reduction of peridomestic conditions that support mosquito breeding; and (4) implement adult mosquito control when indicated by increasing WNV activity or the occurrence of human disease. In addition, because arbovirus infections are endemic in the continental United States, states should have a comprehensive plan and a functional arbovirus surveillance and response capacity that includes trained personnel with suitable laboratory support for identifying arbovirus activity, including WNV.5

Lanciotti RS, Roehrig JT, Deubel V.  et al.  Origin of the West Nile virus responsible for an outbreak of encephalitis in the Northeastern United States.  Science.1999;286:2333-7.
CDC.  National West Nile virus surveillance system, 2000: final plan, May 26, 2000. Available at http://www.cdc.gov/ncidod/dvbid/westnile. Accessed November 2000.
Komar N. West Nile viral encephalitis.  Rev Sci Tech Off Int Epiz.2000;19:166-76.
Reinert JF. New classification for the composite genus Aedes (Diptera: Culicidae: Aedini), elevation of subgenus Ochlerotatus to generic rank, reclassification of other subgenera, and notes on certain subgenera and species.  J Am Mosq Control Assoc.2000;16:175-88.
CDC.  Guidelines for surveillance, prevention, and control of West Nile virus infection—United States.  MMWR Morb Mortal Wkly Rep.2000;49:25-8.
Hubalek Z, Halouzka J. West Nile fever—a reemerging mosquito-borne viral disease in Europe.  Emerg Infect Dis.1999;5:643-50.
Animal and Plant Health Inspection Service, US Department of Agriculture.  Summary of West Nile virus in the United States, 1999. Available at http://www.aphis.usda.gov/vs/ep/WNV/summary.html. Accessed November 2000.
Outbreak of Poliomyelitis—Cape Verde, 2000

MMWR. 2000;49:1070

During August 16-October 17, 2000, 33 cases of acute flaccid paralysis (AFP), including seven (21%) deaths, were reported in Cape Verde, an archipelago of 10 islands west of Senegal and Mauritania. Preliminary laboratory results identified wild type 1 poliovirus among eight cases. The first patient was a child aged 2 years from the capital city of Praia; paralysis onset occurred August 16. The child had received one dose of the recommended three doses of oral poliovirus vaccine (OPV). Twenty-two cases were reported from the island of Santiago, seven from Sal, three from San Vincente, and one from Maio. The ages of the AFP patients ranged from 3 months-38 years; 11 (33%) were aged <5 years, 15 (46%) were 5-14 years, and seven (21%) were ≥15 years. No deaths were reported among patients aged <5 years. Three deaths (case fatality rate [CFR]: 20%) occurred among patients aged 5-14 years and four deaths occurred among patients aged ≥15 years (CFR: 57%). Of 33 cases with known vaccination status, 13 (39%) were fully vaccinated.

The estimated population of Cape Verde in 2000 was 437,500 (World Health Organization [WHO], unpublished data, 2000). Reported routine vaccination coverage with three doses of OPV has been <80% every year since 1995. The country has not conducted mass vaccination campaigns against poliomyelitis and has not established AFP surveillance. In response to the outbreak, a mass vaccination campaign was initiated October 16 with the goal of vaccinating every child aged 0-59 months with two OPV doses. Investigations by the Cape Verde Ministry of Health and WHO are under way to determine the circumstances associated with the outbreak, whether the outbreak has spread to other territories such as the neighboring countries of West Africa, and whether additional interventions will be required to control the outbreak, including a mass campaign targeting persons aged 5-14 years.

Travelers to Cape Verde and West Africa who are not vaccinated adequately must be considered at risk for polio. Recommendations for children in the United States include a four-dose vaccination series with inactivated poliovirus vaccine (IPV) at ages 2, 4, and 6-18 months, and 4-6 years. Unvaccinated adults should receive three doses of IPV, the first two doses at 4-8 week intervals and the third dose 6-12 months after the second. If three doses cannot be administered within the recommended intervals before protection is needed, alternative schedules are proposed.1 For incompletely vaccinated persons, additional IPV doses are recommended to complete a series. Booster IPV doses should be considered for persons who have completed a primary series of poliovirus vaccination and who may be traveling to areas where poliomyelitis is endemic.

Reported by:

Ministry of Health, Country Office, Praia, Cape Verde; Intercountry Office for West Africa, Abidjan, Cote d'Ivoire; Intercountry Office for Southern Africa and Regional Office for Africa, Harare, Zimbabwe. Institute Pasteur, Dakar, Senegal. National Institute of Virology, Johannesburg, South Africa. Vaccines and Other Biologicals Dept, World Health Organization, Geneva, Switzerland. Div of Quarantine and Respiratory and Enteric Viruses Br, Div of Viral and Rickettsial Diseases, National Center for Infectious Diseases; Vaccine Preventable Disease Eradication Div, National Immunization Program, CDC.

Reference: 1 available

Declines in Lung Cancer Rates—California, 1988-1997

MMWR. 2000;49:1066-1070

1 table, 1 figure omitted

Cigarette smoking is the leading cause of lung and bronchus cancer.1 During 1988-1997, per capita cigarette smoking in California declined more than twice as rapidly compared with the rest of the country.2 To characterize lung cancer incidence in California, data from the National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) program were compared with data from the population-based California Cancer Registry (CCR). This report summarizes the results of that analysis, which indicated that during 1988-1997, age-adjusted lung cancer incidence rates in California declined significantly compared with stable incidence rates for the combined SEER area of five states and three metropolitan areas.

SEER data used in the analysis were from Connecticut, Hawaii, Iowa, New Mexico, and Utah, and Atlanta, Georgia; Detroit, Michigan; and Seattle-Puget Sound, Washington.3 SEER registries in California were excluded from the SEER analysis and were included with the CCR data. CCR data were statewide; SEER data collected in California included Los Angeles and the San Francisco Bay area only. Data collection standards for SEER and CCR were similar. However, CCR had more data than the SEER California component; therefore, the combined CCR and SEER data provided a more reliable estimate of cancer rates than using the California SEER data alone.

Cancer incidence rates were age-adjusted by the direct method based on estimated 2000 U.S. population data.3 Annual lung and bronchus cancer (International Classification of Diseases, for Oncology, codes C340-C349) incidence rates per 100,000 population during 1988-1997 were reported among men, women, and both sexes combined for California and the eight SEER regions combined. Two measures of change were reported. First, the estimated annual percentage change (EAPC) was calculated using the average percentage increase or decrease in cancer incidence rates per year during 1988-1997, and a regression line was fitted using the assumption that the natural logarithm of cancer rates changed at a constant rate during the 10-year period. Second, the total percentage change was the average of 1988 and 1989 data minus the average of 1996 and 1997 data divided by 1988 and 1989 data and multiplied by 100. Statistical significance was set at alpha = 0.01.

Non-California SEER data did not reveal a consistent pattern in the age-adjusted lung and bronchus cancer incidence rates during 1988-1997. EAPC of −0.4% per year was not significantly different from zero. Comparing the CCR incidence rates with non-California SEER incidence rates, the CCR lung and bronchus cancer incidence rates were slightly higher during 1988-1990. However, during 1991-1997, incidence rates in CCR declined from 68.0 per 100,000 to 60.1. During 1988-1997, overall lung and bronchus cancer CCR incidence rates decreased an average of 1.9% per year (p<0.01). The CCR incidence rates decreased 14.0% during the 10-year period; the rates in non-California SEER regions decreased 2.7%.

The decline in incidence rates among men (all ages combined) in the CCR data was 1.5 times greater than the decline among men in the non-California SEER regions. Among men, lung and bronchus cancer incidence rates declined significantly during 1988-1997 in data from the CCR and the SEER regions; however, the decline was greater in CCR (EAPC = −2.9%; p<0.01) compared with non-California SEER regions (EAPC = −1.8%; p<0.01). Among women (all ages combined) in CCR, lung and bronchus cancer incidence rates declined 4.8% during 1988-1997 (EAPC = −0.6; p<0.01); incidence rates among women in non-California SEER regions increased 13.2% (EAPC = 1.5; p<0.01).

Reported by:

DW Cowling, PhD, SL Kwong, MPH, R Schlag, MS, JC Lloyd, MA, DG Bal, MD, Tobacco Control Section and Cancer Surveillance Section, California Dept of Health Svcs. Office on Smoking and Health, National Center for Chronic Disease Prevention and Health Promotion, CDC.

CDC Editorial Note:

More than 80% of lung and bronchus cancer is caused by cigarette smoking, and former smokers have about half the risk for dying from lung cancer than do current smokers.1 Compared with current smokers, the risk for lung and bronchus cancer among former smokers declines as the duration of abstinence lengthens, with risk reduction becoming evident within 5 years of cessation.1 Reductions in the smoking rate in a state could reduce lung and bronchus cancer rates within 5 years of the decline in smoking rates.1

The difference in the rate of decline in lung and bronchus cancer incidence rates between California and other U.S. regions may be related, in part, to the significant declines in smoking rates as a result of California tobacco control initiatives. The California Tobacco Control Program was created by Proposition 99 and was approved in 1988.2 The program emphasized a comprehensive approach to tobacco control, prevention, and education and included strategies to change social norms related to tobacco use. The decrease in per capita cigarette consumption that began in 1990 has been attributed to the $0.25 increase in the excise tax in 1989.2 During 1988-1996, California had a more rapid decline in per capita cigarette consumption compared with the rest of the country.2,4 This decline has been attributed primarily to a change in the social acceptability of smoking among California residents.2,4 However, smoking rates in California were declining more rapidly than the rest of the country since the late 1980s, before enactment of Proposition 99.

The findings in this study are subject to at least three limitations. First, the SEER cancer incidence rates are based on data from selected geographic areas and may not represent incidence rates nationally; SEER data in this analysis represent 9.5% of the U.S. population (excluding California). Second, although a constant rate of change over the study period is the standard assumption when using EAPC, this assumption has not been tested.3 Third, although decreased population smoking rates in California are probably responsible for reduced rates of lung and bronchus cancer, a cause-and-effort relation cannot be determined through population-based assessments.

Following the California model, aggressive and comprehensive tobacco-control programs have been implemented in other states, including Arizona, Florida, Maine, Massachusetts, and Oregon. Initial results from several states have shown substantial declines in per capita cigarette consumption and/or changes in the prevalence of adult or youth smoking rates.48 The results of this report suggest that a comprehensive tobacco prevention and education program also may reduce rates of lung and bronchus cancer.

On the basis of results from state programs, CDC published Best Practices for Comprehensive Tobacco Control.9 This document, along with the release of Surgeon General's Report, Reducing Tobacco Use: A Report of the Surgeon General,10 provides guidance to states in establishing successful and sustainable tobacco control programs.

US Department of Health and Human Services.  The health benefits of smoking cessation. Washington, DC: US Department of Health and Human Services, Public Health Service, CDC, 1990; US DHHS publication no. 90-8416.
Pierce JP, Gilpin EA, Emery SL, White MM, Rosbrook B, Berry CC. Has the California tobacco control program reduced smoking?  JAMA.1998;280:893-9.
Ries LAG, Eisner MP, Kosary CL. SEER cancer statistics review, 1973-1997. Bethesda, Maryland: National Cancer Institute, 2000.
CDC.  Cigarette smoking before and after an excise tax increase and an antismoking campaign—Massachusetts, 1990-1996.  MMWR.1996;45:966-70.
CDC.  Decline in cigarette consumption following implementation of a comprehensive tobacco prevention and education program—Oregon, 1996-1998.  MMWR Morb Mortal Wkly Rep.1999;48:140-3.
CDC.  Tobacco use among middle and high school students—Florida, 1998 and 1999.  MMWR Morb Mortal Wkly Rep.1999;48:248-53.
Massachusetts Department of Public Health.  Independent evaluation of the Massachusetts tobacco control program. Fifth annual report. Boston, Massachusetts: Massachusetts Department of Public Health, 1998.
Oregon Division of Health.  Oregon tobacco prevention and education program report—1999. Portland, Oregon: Department of Human Resources, Oregon Division of Health, 1999.
CDC.  Best practices of comprehensive tobacco control programs. Atlanta, Georgia: US Department of Health and Human Services, CDC, 1999.
US Department of Health and Human Services.  Reducing tobacco use: a report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, CDC, 2000.