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1.
Am J Epidemiol ; 188(1): 102-109, 2019 01 01.
Article in English | MEDLINE | ID: mdl-30325407

ABSTRACT

Social isolation is associated with higher mortality in studies comprising mostly white adults, yet associations among black adults are unclear. In this prospective cohort study, we evaluated whether associations of social isolation with all-cause, cardiovascular disease, and cancer mortality differed by race and sex. Adults enrolled in Cancer Prevention Study II in 1982/1983 were followed for mortality through 2012 (n = 580,182). Sex- and race-specific multivariable-adjusted hazard ratios and 95% confidence intervals were estimated for associations of a 5-point social isolation score with risk of death. Social isolation was associated with all-cause mortality in all subgroups (P for trend ≤ 0.005); for the most isolated versus the least isolated, the hazard ratios were 2.34 (95% confidence interval (CI): 1.58, 3.46) and 1.60 (95% CI: 1.41, 1.82) among black men and white men, respectively (P for interaction = 0.40) and 2.13 (95% CI: 1.44, 3.15) and 1.84 (95% CI: 1.68, 2.01) among black women and white women, respectively (P for interaction = 0.89). The association did not differ between black men and black women (P for interaction = 0.33) but was slightly stronger in white women than in white men (P for interaction = 0.01). Social isolation was associated with cardiovascular disease mortality in each subgroup (P for trend < 0.03) but with cancer mortality only among whites (P for trend < 0.0001). Subgroup differences in the influence of specific social isolation components were identified. Identifying and intervening with socially isolated adults could improve health outcomes.


Subject(s)
Black or African American/statistics & numerical data , Cardiovascular Diseases/mortality , Neoplasms/mortality , Social Isolation , White People/statistics & numerical data , Adult , Aged , Cardiovascular Diseases/ethnology , Female , Humans , Male , Middle Aged , Neoplasms/ethnology , Proportional Hazards Models , Prospective Studies , Race Factors , Risk Factors , Sex Factors , Social Participation , Socioeconomic Factors , United States/epidemiology
2.
Pediatr Infect Dis J ; 37(6): 526-530, 2018 06.
Article in English | MEDLINE | ID: mdl-29140936

ABSTRACT

BACKGROUND: Kawasaki disease (KD) is an acute febrile vasculitis, which primarily affects children. The etiology of KD is unknown; while certain characteristics of the disease suggest an infectious origin, genetic or environmental factors may also be important. Seasonal patterns of KD incidence are well documented, but it is unclear whether these patterns are caused by changes in climate or by other unknown seasonal effects. METHODS: The relationship between KD incidence and deviations from expected temperature and precipitation were analyzed using KD incidence data from Japanese nationwide epidemiologic surveys (1991-2004) and climate data from 136 weather stations of the Japan Meteorological Agency. Seven separate Poisson-distributed generalized linear regression models were run to examine the effects of temperature and precipitation on KD incidence in the same month as KD onset and the previous 1, 2, 3, 4, 5 and 6 months, controlling for geography as well as seasonal and long-term trends in KD incidence. RESULTS: KD incidence was negatively associated with temperature in the previous 2, 3, 4 and 5 months and positively associated with precipitation in the previous 1 and 2 months. The model that best predicted variations in KD incidence used climate data from the previous 2 months. An increase in total monthly precipitation by 100 mm was associated with increased KD incidence (rate ratio [RR] 1.012, 95% confidence interval [CI]: 1.005-1.019), and an increase of monthly mean temperature by 1°C was associated with decreased KD incidence (RR 0.984, 95% CI: 0.978-0.990). CONCLUSIONS: KD incidence was significantly affected by temperature and precipitation in previous months independent of other unknown seasonal factors. Climate data from the previous 2 months best predicted the variations in KD incidence. Although fairly minor, the effect of temperature and precipitation independent of season may provide additional clues to the etiology of KD.


Subject(s)
Climate , Mucocutaneous Lymph Node Syndrome/epidemiology , Rain , Seasons , Temperature , Child, Preschool , Epidemiological Monitoring , Humans , Incidence , Infant , Japan/epidemiology , Linear Models , Risk Factors
3.
Helicobacter ; 21(6): 488-492, 2016 Dec.
Article in English | MEDLINE | ID: mdl-27006167

ABSTRACT

BACKGROUND: Study results on overall seroprevalence of Helicobacter pylori and colorectal cancer risk have been inconsistent. However, one study found positive associations with antibodies to specific H. pylori proteins. To follow up on those findings, we assessed associations of 15 H. pylori specific proteins with colorectal cancer incidence in the prospective Cancer Prevention Study-II Nutrition Cohort. MATERIALS AND METHODS: Participants in this nested case-control study included 392 cases and 774 controls who were predominantly elderly (median age at blood draw: 71 years) and Caucasian (98%). Seroreactivity against 15 H. pylori proteins was assessed by fluorescent bead-based multiplex serology and associations with colorectal cancer were estimated using conditional logistic regression. RESULTS: Helicobacter pylori serostatus was not associated with colorectal cancer incidence (odds ratio (OR), 1.17, 95% confidence interval (95% CI), 0.91-1.50). Among individual antigens, GroEl serostatus was associated with colorectal cancer risk (OR, 1.32, 95% CI: 1.03-1.70), whereas CagM was associated with colon cancer risk only (OR, 1.35, 95% CI: 1.01-1.80). No dose-response relationships were observed for any of the antigens, including GroEl and CagM. CONCLUSIONS: The results of our study do not support an association between H. pylori infection and colorectal cancer risk in this elderly, mostly Caucasian population.


Subject(s)
Antibodies, Bacterial/blood , Colorectal Neoplasms/epidemiology , Helicobacter Infections/complications , Helicobacter Infections/diagnosis , Helicobacter pylori/immunology , Aged , Aged, 80 and over , Bacterial Proteins/immunology , Case-Control Studies , Female , Humans , Male , Middle Aged , Prospective Studies , Risk Assessment , White People
4.
5.
Am J Epidemiol ; 182(1): 41-8, 2015 Jul 01.
Article in English | MEDLINE | ID: mdl-25964260

ABSTRACT

The proportion of parents aged ≥35 years at the birth of their child continues to increase, but long-term health consequences for these children are not fully understood. A recent prospective study of 110,999 adult women showed an association between paternal-but not maternal-age at birth and sporadic hematological cancer risk. To further investigate this topic, we examined these associations in women and men in the American Cancer Society Cancer Prevention Study-II Nutrition Cohort. Among 138,003 Cancer Prevention Study-II participants, 2,532 incident hematological cancers were identified between 1992 and 2009. Multivariable-adjusted hazard ratios and 95% confidence intervals were computed by using Cox proportional hazards regression. There was no clear linear trend in the risk of hematological malignancies by either paternal or maternal age. However, there was a strong, positive association with paternal age among participants without siblings. In that group, the hazard ratio for fathers aged ≥35 years compared with <25 years at birth was 1.63 (95% confidence interval: 1.19, 2.23), and a linear dose-response association was suggested (Pspline = 0.002).There were no differences by subtype of hematological cancer. Results of this study support the need for further research to better understand the association between paternal age at birth and hematological malignancies.


Subject(s)
Hematologic Neoplasms/epidemiology , Maternal Age , Paternal Age , Adult , Aged , Cohort Studies , Fathers/statistics & numerical data , Female , Humans , Male , Middle Aged , Mothers/statistics & numerical data , United States/epidemiology , Young Adult
6.
Cancer Epidemiol Biomarkers Prev ; 24(2): 477-80, 2015 Feb.
Article in English | MEDLINE | ID: mdl-25488906

ABSTRACT

BACKGROUND: Three human polyomaviruses have been classified as probable (Merkel cell polyomavirus) or possible (BK and JC polyomaviruses) carcinogens, but few epidemiologic studies have examined associations between this growing class of viruses and risk of non-Hodgkin lymphoma (NHL). METHODS: Associations between polyomavirus antibodies and NHL incidence were examined using data from the American Cancer Society Cancer Prevention Study-II. This nested case-control study included 279 NHL cases and 557 controls. Prediagnostic antibodies to the major capsid protein of polyomaviruses BKV, JCV, MCV, TSV, WUV, KIV, HPy6, and HPy7 were measured by fluorescent bead-based multiplex serology, and associations with NHL were estimated using conditional logistic regression (NHL overall) and unconditional polytomous logistic regression (NHL subtypes). RESULTS: Although an inverse trend was suggested for TSV antibody levels and NHL risk, the HRs were not statistically significant. There were no other observed associations between polyomaviruses and NHL risk. For NHL subtypes, TSV antibody level above the median was associated with a lower risk of CLL/SLL; however, this association was based on 19 cases in the high antibody group and may be due to chance. CONCLUSIONS: Our results do not support associations of polyomaviruses BKV, JCV, WUV, KIV, HPyV6, HPyv7, MCV, or TSV with risk of NHL. IMPACT: Human polyomavirus antibody levels do not appear to predict a higher NHL risk in immunocompetent individuals.


Subject(s)
Antibodies, Viral/blood , Lymphoma, Non-Hodgkin/virology , Polyomavirus Infections/virology , Polyomavirus/immunology , Aged , Aged, 80 and over , Case-Control Studies , Female , Humans , Lymphoma, Non-Hodgkin/epidemiology , Lymphoma, Non-Hodgkin/immunology , Male , Middle Aged , Polyomavirus Infections/epidemiology , Polyomavirus Infections/immunology , Prospective Studies , Risk Factors
7.
Int J Cancer ; 136(1): 108-16, 2015 Jan 01.
Article in English | MEDLINE | ID: mdl-24831943

ABSTRACT

Epstein-Barr virus (EBV) causes rare, malignant lymphomas. The role of EBV in other non-Hodgkin lymphomas (NHLs) remains unclear, but mildly reduced immune function could lead to reactivation of EBV and subsequent NHL. We examined the association between prospectively-collected plasma EBV antibodies and NHL risk in the Cancer Prevention Study-II (CPS-II) Nutrition Cohort and conducted a meta-analysis of our and published results. The CPS-II study included 225 NHL cases and 2:1 matched controls. No associations were observed between EBV serostatus or antibody levels and risk of NHL overall. However, when including only the three most common types of NHL (diffuse large B-cell lymphoma, follicular lymphoma, chronic lymphocytic leukemia/small lymphocytic lymphoma), high compared to low early antigen (EA-D) diffuse and BZLF1-encoded replication activator antibodies were associated with approximately 60% higher risk of NHL. Odds ratios (ORs) for EBV nuclear antigen-1 and viral capsid antigen (VCA)-p18 were elevated but not statistically significant. In the meta-analysis, both EA (summary OR = 1.52, 95% confidence interval (CI): 1.16-2.00) and VCA (summary OR = 1.20, 95% CI: 1.00-1.44) were positively associated with NHL risk. These results suggest EBV may be associated with a wider spectrum of NHL subtypes, but further study is needed to confirm and fully understand these associations.


Subject(s)
Epstein-Barr Virus Infections/virology , Herpesvirus 4, Human/immunology , Lymphoma, Non-Hodgkin/virology , Antibodies, Viral/blood , Antigens, Viral/immunology , Case-Control Studies , Epstein-Barr Virus Infections/blood , Epstein-Barr Virus Infections/immunology , Epstein-Barr Virus Infections/prevention & control , Humans , Lymphoma, Non-Hodgkin/blood , Lymphoma, Non-Hodgkin/immunology , Lymphoma, Non-Hodgkin/prevention & control , Risk
8.
Pediatrics ; 133(3): e766-70, 2014 Mar.
Article in English | MEDLINE | ID: mdl-24488737

ABSTRACT

The occurrence of sporadic prion disease among adolescents is extremely rare. A prion disease was confirmed in an adolescent with disease onset at 13 years of age. Genetic, neuropathologic, and biochemical analyses of the patient's autopsy brain tissue were consistent with sporadic fatal insomnia, a type of sporadic prion disease. There was no evidence of an environmental source of infection, and this patient represents the youngest documented case of sporadic prion disease. Although rare, a prion disease diagnosis should not be discounted in adolescents exhibiting neurologic signs. Brain tissue testing is necessary for disease confirmation and is particularly beneficial in cases with an unusual clinical presentation.


Subject(s)
Brain/pathology , Insomnia, Fatal Familial/diagnosis , Adolescent , Fatal Outcome , Humans , Insomnia, Fatal Familial/complications , Male
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