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RESEARCH AND PRACTICE |
Geraldine M. McQuillan, Deanna Kruszon-Moran, Benny J. Kottiri, and Lester R. Curtin are with the Division of Health Examination Surveys, and Jacqueline B. Lucas is with the Division of Health Interview Statistics, National Center for Health Statistics, Hyattsville, Md. Raynard S. Kington is with the National Institutes of Health, Bethesda, Md.
Correspondence: Requests for reprints should be sent to Geraldine M. McQuillan, PhD, National Center for Health Statistics, 3311 Toledo Rd, Room 4204, Hyattsville, MD 20782 (e-mail: gmm2{at}cdc.gov).
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMETHODSRESULTSDISCUSSIONReferences |
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Objectives. We examined racial/ethnic differences in the seroprevalence of selected infectious agents in analyses stratified according to risk categories to identify patterns and to determine whether demographic, socioeconomic, and behavioral characteristics explain these differences.
Methods. We analyzed data from the third National Health and Nutrition Examination Survey, comparing differences among groups in regard to the prevalence of infection with hepatitis A, B, and C viruses, Toxoplasma gondii, Helicobacter pylori, and herpes simplex virus type 2.
Results. Racial/ethnic differences were greater among those in the low-risk category. In the case of most infectious agents, odds associated with race/ethnicity were almost 2 times greater in that category than in the high-risk category.
Conclusions. Stratification and adjustment for socioeconomic factors reduced or eliminated racial/ethnic differences in the prevalence of infection in the high-risk but not the low-risk group, wherein race/ethnicity remained significant and might have been a surrogate for unmeasured risk factors.
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONReferences |
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The objectives of this study were to examine racial/ethnic differences in the seroprevalence of 6 infectious diseases and to assess the extent to which demographic, socioeconomic, and behavioral characteristics explain these differences. Data collected during NHANES III, a nationally representative survey of the US population, were analyzed to assess differences in seroprevalence of 3 enteric pathogens, hepatitis A virus (HAV), Toxoplasma gondii, and Helicobacter pylori, and 3 blood-borne/sexually transmissible diseases, hepatitis B virus (HBV), hepatitis C virus (HCV), and herpes simplex virus type 2 (HSV-2).
Serologic measurements of the prevalence of these infectious agents were included in the survey because either the agents are not reportable (in the case of T gondii, H pylori, and HSV-2) or only clinical cases are reportable (in the case of the hepatitis viruses) and the majority of infections are asymptomatic. Thus, there was a need for population-based serologic studies designed to estimate the extent of the infection burden and to develop and evaluate prevention efforts.
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METHODS |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONReferences |
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The survey was divided into two 3-year components so that national estimates could be produced for each 3-year period as well as for the overall 6-year interval. NHANES III was based on a complex, stratified, multistage probability cluster sample design.12 Children aged younger than 5 years and adults aged older than 59 years, along with Black Americans and Mexican Americans, were sampled at higher frequencies than other groups.
Interviews conducted in respondents’ homes and examination centers collected information on a wide range of demographic, socioeconomic, and behavioral characteristics. Data on race/ethnicity (non-Hispanic White, non-Hispanic Black, or Mexican American) were obtained via self-report. Individuals who did not identify themselves as belonging to 1 of the categories just mentioned were not assessed separately but were included in the overall analysis.
Individuals aged 20 years or older who were examined and provided a blood sample for the laboratory assays were included in the present analyses. Only participants examined in the first phase (1988–1991) of the study were tested for H pylori antibody. Sexual behavior and drug use data were obtained from individuals aged 20 to 59 years, and thus analyses focusing on sexually transmissible and blood-borne infections were restricted to this age range.
Rates of availability of serum for testing of the 3 enteric infections were consistent across all racial/ethnic groups and outcomes (85%–94% of those examined) but were lower among respondents in the oldest age group (80%–82% among those aged 70 years or older vs 88%–95% among all other age groups). Availability of serum was also consistent across all racial/ethnic groups for the 3 sexually transmitted infections (91%–96% of those examined for HBV and HCV and 71%–77% of those examined for HSV-2) and across all age groups for both HBV and HCV (93%–95% of those examined). In the case of HSV-2 testing, availability was lowest among those aged 50 to 59 years (47% vs 77%–80% in the 20- to 49-year age group). More detailed information on serum availability and response rates can be found in previous reports.7–11
Laboratory Analyses
Details on the serologic methods used have been published in previous reports.7–13 Briefly, anti-HAV IgG enzyme immunoassay (HAVAB, Abbott Laboratories, Abbott Park, Ill) was used in screening for HAV; for T gondii antibody, IgG enzyme immunoassay (Sanofi Diagnostics Pasteur, BioRad, Hercules, Calif) was used; and for H pylori antibody, IgG enzyme immunoassay (Wampole Laboratories, Cranbury, NJ) was used. Antibody to hepatitis core antigen (anti-HBc) enzyme-linked immunoassay (CORAB, Abbott Laboratories) was used in screening for HBV; anti-HCV with a second-generation enzyme immunoassay (EIA 2.0, Abbott Laboratories) was used in screening for HCV; and a type-specific immunodot assay was used in screening for HSV-2.13
Statistical Analysis
Prevalence estimates were weighted to represent the overall US population and to account for oversampling and nonresponse to the household interview and physical examination. Standard errors were calculated with SUDAAN,14 a family of statistical procedures used in analyses of data derived from complex sample surveys. All estimates were age adjusted, via the direct method, to the 1980 US population.15
As a means of better interpreting racial/ethnic differences in seropositivity, a core group of socioeconomic and demographic factors were evaluated without correction for multiple comparisons; a univariate t statistic derived from a general linear contrast procedure included in SUDAAN was used in these analyses. Factors shown to be significant in the univariate analysis, along with additional cofactors and possible interaction terms identified from previous modeling of these data,7–11 were entered into the logistic models. Models were reduced through a backward stepwise approach to include variables shown to be significant in the case of the overall sample or any of the racial/ethnic groups.
Main effects models were constructed to control for the influence of various cofactors on race/ethnicity-specific odds of infection. These models, presented to illustrate the influence of the cofactors on the effect of race/ethnicity in comparison with age adjustment alone, should be interpreted cautiously because they did not evaluate interactions within the data. Interactions between race/ethnicity and each of the variables included in the final logistic model were evaluated to determine whether racial/ethnic differences varied according to levels of socioeconomic or risk behavior predictors. Several variables interacted with race/ethnicity; therefore, for ease of interpretation, and because the aim of the analyses was to determine the effects of these cofactors on the odds of infection associated with race/ethnicity, interactions were specified in terms of a stratified modeling scheme.
High- and low-risk strata were formed for each disease outcome by grouping individuals at the lowest and highest levels of risk for each of the variables interacting with race/ethnicity. Individuals who did not fall into these strata were evaluated (data not shown), and results showed that they exhibited odds ratios for race/ethnicity similar to those revealed in the main effects models. The small sample sizes in some of the variable categories limited our ability to stratify groups on all possible interaction terms. Variables in these categories and all remaining factors from the main effects models were included in the stratified logistic models as control variables (Table 1
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In the case of the 3 sexually transmissible/blood-borne infections, prevalence estimates are presented for individuals aged 20 to 59 years, because the sexual behavior and drug use variables used in stratifying groups according to risk were collected only among this age group. The procedure used in defining risk groups and creating models for these pathogens was similar to that used for enteric pathogens. In addition to a core group of socioeconomic and demographic variables (age [coded as 20–29, 30–39, or 40–59 years], gender, poverty index, crowding, foreign country of birth, education [coded as less than high school, high school, or some college], and marital status (divorced or separated vs all others), the models also included behavioral risk factors associated with disease outcomes such as age at first sexual intercourse (less than 18 years vs 18 years or greater), lifetime number of sexual partners (0–9 vs 10 or more), and illegal drug use.
The drug use variables were limited to cocaine (including crack; coded as ever vs never used) and marijuana (coded into the following categories of use: 0–2 times, 3–99 times, and 100 or more times) and did not include information on mode of administration or injection history. Table 1
provides a description of the variables entered into the high- and low-risk models for each type of infection. Prevalence estimates and models were also stratified according to gender in the case of HSV-2, because gender exhibited a significant interaction with race/ethnicity. Interactions between gender and the other infectious diseases were not significant, so estimates are provided for men and women combined.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONReferences |
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presents race/ethnicity-specific, age-adjusted seroprevalence for each of the infectious agents in the overall study population and among members of each risk stratum. In these analyses, non-Hispanic Blacks and Mexican Americans were compared with non-Hispanic Whites. Tables 3 and 4 present, for each pathogen, comparisons of age-adjusted and fully adjusted odds ratios according to race/ethnicity for the overall sample and for the low-risk and high-risk strata. We present results from the main effects models to allow comparisons with the models that adjusted for age only and those that stratified groups according to risk. Since race/ethnicity interacted with many of the other variables, estimates based on the main effects models should be interpreted cautiously.
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Race/ethnicity was highly significant in the logistic regression model controlling for age, and it remained significant in the main effects model (Table 3). Adjustment in the main effects model for sociodemographic factors, including foreign country of birth, did not eliminate the significantly greater odds of infection among both non-Hispanic Blacks and Mexican Americans in comparison with non-Hispanic Whites, although the difference between Mexican Americans and Whites was greatly reduced.
The extent of differences between Mexican Americans and non-Hispanic Whites did not vary significantly across the risk strata, probably because the small sample size did not allow stratification by foreign birth. Foreign birth was the strongest predictor, although its effect varied by race/ethnicity. There were no significant differences in the risk of infection between non-Hispanic Whites and non-Hispanic Blacks in the high-risk stratum, but significant differences were still observed in the low-risk stratum.
Toxoplasma gondii.
The overall age-adjusted prevalence of T gondii antibody among adults aged 20 years or older was 25.4% (95% CI= 23.9%, 27.0%), with few differences between race/ethnicity groups in either the overall population or the 2 risk strata (Table 2). Summary statistics derived from the age-adjusted model demonstrated significantly greater odds of infection among non-Hispanic Blacks and Mexican Americans than among non-Hispanic Whites. When sociodemographic variables were included, the difference between non-Hispanic Blacks and non-Hispanic Whites was eliminated in the main effects model and in the low-risk stratum. In the high-risk stratum, both non-Hispanic Blacks and Mexican Americans were significantly less likely than non-Hispanic Whites to be seropositive (Table 3).
Helicobacter pylori. Analysis of adults aged 20 years or older from the first phase of the survey demonstrated an overall age-adjusted prevalence of 34.6% (95% CI = 31.5%, 37.6%) for H pylori antibody, and the pattern of racial/ethnic differences was similar to that seen with HAV. Non-Hispanic Blacks were almost twice as likely as non-Hispanic Whites to be seropositive, and Mexican Americans were 2.2 times more likely to be seropositive than non-Hispanic Whites. The age-adjusted model revealed significant racial/ethnic differences. The odds ratio for Mexican Americans was reduced in the main effects model, but differences were still significant. Racial/ethnic differences were further reduced in the high-risk model but exhibited slight increases for non-Hispanic Blacks and Mexican Americans in the low-risk model.
Sexually Transmissible/Blood-Borne Pathogens
Hepatitis B virus.
The overall age-adjusted prevalence of HBV antibody among adults aged 20 to 59 years was 5.6% (95% CI = 4.8%, 6.5%; Table 2). Non-Hispanic Blacks exhibited odds 4.6 times higher than those of non-Hispanic Whites, and Mexican Americans exhibited 1.8 times higher odds. Higher prevalences of infection were observed among non-Hispanic Blacks than among non-Hispanic Whites in both risk groups, but Mexican Americans exhibited a significantly higher prevalence than non-Hispanic Whites only in the low-risk group.
The age-adjusted model showed that both non-Hispanic Blacks and Mexican Americans had significantly higher odds of infection than non-Hispanic Whites (Table 4). In the main effects model controlling for socioeconomic and behavioral variables, the difference between non-Hispanic Blacks and non-Hispanic Whites was reduced but remained significant; however, the difference between Mexican Americans and non-Hispanic Whites became nonsignificant. In the model for the low-risk group, the odds for both non-Hispanic Blacks and Mexican Americans were significantly higher than those for non-Hispanic Whites and higher than those revealed in the age-adjusted model. In the high-risk group, the odds for non-Hispanic Blacks were further reduced but remained statistically significant. The difference between non-Hispanic Whites and Mexican Americans became nonsignificant in the high-risk model.
Hepatitis C virus.
The overall age-adjusted prevalence of HCV antibody was 2.4% (95% CI = 1.9%, 3.1%; Table 2). In comparison with non-Hispanic Whites, prevalence estimates were twice as high among non-Hispanic Blacks and 1.7 times higher among Mexican Americans. Racial/ethnic differences remained significant only in the low-risk group. Non-Hispanic Black race/ethnicity was a significant predictor in the age-adjusted model but not in the full main effects model. The difference in seroprevalence associated with Mexican American ethnicity was significant only in the full model (P=.04). Race/ethnicity became nonsignificant after stratification according to both low and high risk and adjustment for the remaining cofactors in the main effects model.
Herpes simplex 2.
The overall age-adjusted prevalence of HSV-2 antibody was 25.1% (95% CI = 22.7%, 27.5%; Table 2). Women exhibited a significantly higher prevalence of infection than men, and this difference varied among the different racial/ethnic groups; therefore, all analyses were stratified according to gender. Among men, race/ethnicity differences were significant both overall and in the low-risk group. In the high-risk group, only the estimate for non-Hispanic Blacks remained significantly higher than that for non-Hispanic Whites. Among women, race/ethnicity differences were significant regardless of risk stratification.
In the case of men, non-Hispanic Black race/ethnicity was associated with an increase in the odds of HSV-2 infection in all models, despite adjustment or stratification; however, the odds ratio in the high-risk group, while remaining significant, was lower than in the other models. Mexican American ethnicity was no longer significant in any of the models other than the age-adjusted model. Among women, non-Hispanic Black race/ethnicity was significantly associated with greater odds of infection than those observed in non-Hispanic Whites in all models, although the odds ratio was highest in the low-risk stratum. With the exception of the high-risk group, Mexican American women also exhibited significantly higher odds of infection than non-Hispanic White women.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONReferences |
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In the case of the enteric pathogens HAV and H pylori, racial/ethnic differences were reduced, but not always eliminated, by statistical modeling and risk group stratification. Such findings suggest that the socioeconomic variables used in the present analyses are important predictors of risk but that they can account only partially for racial/ethnic disparities in the prevalence of infection with these enteric diseases.
Significantly higher odds of T gondii infection among non-Hispanic Blacks and Mexican Americans were observed only in the age-adjusted model. These differences became nonsignificant in the low-risk strata and were reversed in the high-risk strata, wherein non-Hispanic Blacks and Mexican Americans had lower odds of infection than non-Hispanic Whites. T gondii is transmitted through consumption of raw or uncooked meat or ingestion of oocysts from the soil. Information on frequency and type of meat consumption and soil exposure not available in this survey may better explain why racial/ethnic differences were shown to reverse after risk group stratification.
Stratification according to risk, based on reported behaviors and after controlling for socioeconomic and demographic variables, had a greater impact on the prevalence of the sexually transmissible/blood-borne infections than on that of the enteric pathogens. Within the high-risk group, seroprevalence estimates for the 3 sexually transmissible/blood-borne infections were no longer significantly higher among Mexican Americans than among non-Hispanic Whites. Statistical modeling and stratification into high- and low-risk groups eliminated the difference in the prevalence of infection between non-Hispanic Whites and non-Hispanic Blacks only in the case of HCV antibody. This finding was primarily attributable to the influence of reported cocaine use as a predictor of infection, regardless of other characteristics.
In the case of HBV, the effect of race/ethnicity was reduced in the high-risk group, but the difference between non-Hispanic Whites and non-Hispanic Blacks remained significant. In the low-risk group, the effect of race/ethnicity increased slightly relative to the effects observed in the age-adjusted and main effects models. A similar pattern was seen with HSV-2. Modeling or stratification on risk behaviors that interacted with race (drug use and number of sexual partners) had no effect on HSV-2 seropositivity in comparisons of non-Hispanic Whites and non-Hispanic Blacks. Sample sizes within the 0–9-lifetime-partners group were not adequate to allow further explorations of risk based on this exposure category.
The socioeconomic characteristics of a given population (e.g., crowding, income, education) and individual sexual or drug use behaviors affect infection risks, regardless of race/ethnicity. However, the background prevalence of an infection in a population with which an individual interacts may have an equally important impact on infection potential. Even in communities heterogeneous in terms of race/ethnicity, individuals live and interact predominantly with people of their own racial background,6,17 and this situation may increase within-group spread of infection and limit transmission across race/ethnicity boundaries.
Classification of the sample into risk groups reduced but did not consistently remove all racial/ethnic differences. Mexican Americans still exhibited higher odds of infection for the enteric pathogens (other than T gondii) than did non-Hispanic Whites, and non-Hispanic Blacks exhibited higher odds of sexually transmissible/blood-borne infections. A reduction was observed only in the case of HCV, which has such a low prevalence that any adjustment or stratification removes the effect of race/ethnicity.
NHANES selects a population-based sample that is representative of the overall US population. We assessed infectious disease prevalence in this population along with information on socioeconomic factors and risk behaviors to help clarify racial/ethnic differences in the prevalence of selected pathogens. As expected, racial/ethnic differences were greatly reduced or even eliminated in the high-risk stratum. It is these high-risk factors, rather than race/ethnicity, that have the greatest effects on the prevalence of infection. Since the majority of infections occur among members of these risk groups, and such individuals can transmit infections to others regardless of risk profile, prevention programs that target these factors or behaviors will have the greatest impact in terms of reducing prevalence of infection.
However, in our study, racial and ethnic disparities were greatest among individuals who did not fit the usual risk profile for these infectious diseases. Thus, race/ethnicity may be a surrogate for other characteristics or behaviors that place these individuals at increased risk. More research is needed among low-risk populations to determine the additional factors (e.g., condom use, sexual network characteristics, or cultural differences) that may determine infection risks in these populations. Until these factors are identified, race/ethnicity remains a factor that, when assessed appropriately, may be of value in guiding decisions regarding the targeting of prevention strategies. Our data suggest that unless individuals who might be considered to be at low risk are brought into the prevention spectrum as well, the Healthy People 201018 goal to eliminate racial/ethnic disparities in the prevalence of infectious diseases in the United States will not be met.
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Acknowledgments |
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Human Participant Protection
Informed consent was obtained from survey participants before their participation, and the institutional review board of the National Center for Health Statistics approved the study protocol.
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Footnotes |
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Contributors
G. M. McQuillan and R. S. Kington contributed to the conception and design of the analysis and to the writing of the article. D. Kruszon-Moran and L. R. Curtin contributed to the data analysis, and B. J. Kottiri and J. B. Lucas contributed to interpretation of the data and to the writing of the article.
Accepted for publication November 2, 2003.
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References |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONReferences |
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