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  • 1
    Online Resource
    Online Resource
    Elsevier BV ; 2020
    In:  Annals of Epidemiology Vol. 49 ( 2020-09), p. 42-49
    In: Annals of Epidemiology, Elsevier BV, Vol. 49 ( 2020-09), p. 42-49
    Type of Medium: Online Resource
    ISSN: 1047-2797
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2020
    detail.hit.zdb_id: 2003468-4
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  • 2
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2023
    In:  Epidemiology Vol. 34, No. 6 ( 2023-11), p. 888-891
    In: Epidemiology, Ovid Technologies (Wolters Kluwer Health), Vol. 34, No. 6 ( 2023-11), p. 888-891
    Abstract: Little is known about the role of air quality in fatal asthma exacerbations among children. Methods: We collected information about 80 deaths that occurred in North Carolina from 2001 through 2016, among children aged 5–17 years, with asthma identified as the primary cause of death. We linked information about each death with county-level estimates of particulate matter ≤2.5 µm (PM 2.5 ) and ozone (O 3 ). Using the linked data, we conducted a case–crossover analysis of associations between PM 2.5 and O 3 lagged by 3–5 days with the odds of fatal asthma exacerbations. Results: In the highest tertile of PM 2.5 lag(3–5) , the odds of a fatal exacerbation of asthma were more than twice the odds in the lowest tertile (odds ratio = 2.2; 95% confidence interval = 1.1, 4.6). Conclusion: These findings from North Carolina provide evidence to support the hypothesis that ambient air pollution increases the risk of fatal exacerbations of asthma among children.
    Type of Medium: Online Resource
    ISSN: 1044-3983
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2023
    detail.hit.zdb_id: 2042095-X
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  • 3
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 30, No. 10 ( 2021-10-01), p. 1956-1964
    Abstract: Cannabis use is increasing, including among smokers, an at-risk population for cancer. Research is equivocal on whether using cannabis inhibits quitting cigarettes. The current longitudinal study investigated associations between smoking cannabis and subsequently quitting cigarettes. Methods: Participants were 4,535 adult cigarette smokers from a cohort enrolled in the American Cancer Society's Cancer Prevention Study-3 in 2009–2013. Cigarette quitting was assessed on a follow-up survey in 2015–2017, an average of 3.1 years later. Rates of quitting cigarettes at follow-up were examined by retrospectively assessed baseline cannabis smoking status (never, former, recent), and by frequency of cannabis smoking among recent cannabis smokers (low: ≤3 days/month; medium: 4–19 days/month; high: ≥20 days/month). Logistic regression models adjusted for sociodemographic factors, smoking- and health-related behaviors, and time between baseline and follow-up. Results: Adjusted cigarette quitting rates at follow-up did not differ significantly by baseline cannabis smoking status [never 36.2%, 95% confidence interval (CI), 34.5–37.8; former 34.1%, CI, 31.4–37.0; recent 33.6%, CI, 30.1–37.3], nor by frequency of cannabis smoking (low 31.4%, CI, 25.6–37.3; moderate 36.7%, CI, 30.7–42.3; high 34.4%, CI, 28.3–40.2) among recent baseline cannabis smokers. In cross-sectional analyses conducted at follow-up, the proportion of cigarette smokers intending to quit smoking cigarettes in the next 30 days did not differ by cannabis smoking status (P = 0.83). Conclusions: Results do not support the hypothesis that cannabis smoking inhibits quitting cigarette smoking among adults. Impact: Future longitudinal research should include follow-ups of & gt;1 year, and assess effects of intensity/frequency of cannabis use and motivation to quit on smoking cessation.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2021
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
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  • 4
    Online Resource
    Online Resource
    MDPI AG ; 2023
    In:  International Journal of Environmental Research and Public Health Vol. 20, No. 4 ( 2023-02-18), p. 3658-
    In: International Journal of Environmental Research and Public Health, MDPI AG, Vol. 20, No. 4 ( 2023-02-18), p. 3658-
    Abstract: Nighttime light exposure may increase cancer risk by disrupting the circadian system. However, there is no well-established survey method for measuring ambient light. In the Cancer Prevention Study-3, 732 men and women answered a light survey based on seven environments. The light environment in the past year was assessed twice, one year apart, and four one-week diaries were collected between the annual surveys. A total of 170 participants wore a meter to measure photopic illuminance and circadian stimulus (CS). Illuminance and CS values were estimated for lighting environments from measured values and evaluated with a cross validation approach. The kappas for self-reported light environment comparing the two annual surveys were 0.61 on workdays and 0.49 on non-workdays. Kappas comparing the annual survey to weekly diaries were 0.71 and 0.57 for work and non-workdays, respectively. Agreement was highest for reporting of darkness (95.3%), non-residential light (86.5%), and household light (75.6%) on workdays. Measured illuminance and CS identified three peaks of light (darkness, indoor lighting, and outdoor daytime light). Estimated illuminance and CS were correlated with the measured values overall (r = 0.77 and r = 0.67, respectively) but were less correlated within each light environment (r = 0.23–0.43). The survey has good validity to assess ambient light for studies of human health.
    Type of Medium: Online Resource
    ISSN: 1660-4601
    Language: English
    Publisher: MDPI AG
    Publication Date: 2023
    detail.hit.zdb_id: 2175195-X
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  • 5
    In: Cancer Prevention Research, American Association for Cancer Research (AACR), Vol. 14, No. 1 ( 2021-01-01), p. 65-76
    Abstract: Increased COX-2 and decreased 15-hydroxyprostaglandin dehydrogenase (15-HPGD) expression promote prostaglandin-mediated inflammation and colorectal carcinogenesis. Experimental studies suggest that vitamin D and calcium may inhibit these pathways, but their effects on colorectal tissue COX-2 and 15-HPGD expression in humans are unknown. We tested the effects of supplemental vitamin D (1,000 IU/day) and/or calcium (1,200 mg/day) on COX-2 and 15-HPGD expression in the morphologically normal rectal mucosa from 62 paients with colorectal adenoma in a placebo-controlled chemoprevention trial. We measured biomarker expression using automated IHC and quantitative image analysis at baseline and 1-year follow-up, and assessed treatment effects using mixed linear models. The primary outcome was the COX-2/15-HPGD expression ratio, because these enzymes function as physiologic antagonists. After 1 year of treatment, the mean COX-2/15-HPGD expression ratio in full-length crypts proportionately decreased 47% in the vitamin D group (P = 0.001), 46% in the calcium group (P = 0.002), and 34% in the calcium + vitamin D group (P = 0.03), relative to the placebo group. Among individuals with the functional vitamin D–binding protein isoform DBP2 (GC rs4588*A), the COX-2/15-HPDG ratio decreased 70% (P = 0.0006), 75% (P = 0.0002), and 60% (P = 0.006) in the vitamin D, calcium, and combined supplementation groups, respectively, relative to placebo. These results show that vitamin D and calcium favorably modulate the balance of expression of COX-2 and 15-HPGD—biomarkers of inflammation that are strongly linked to colorectal carcinogenesis—in the normal-appearing colorectal mucosa of patients with colorectal adenoma (perhaps especially those with the DBP2 isoform). Prevention Relevance: Supplemental calcium and vitamin D reduce indicators of cancer-promoting inflammation in normal colorectal tissue in humans, thus furthering our understanding of how they may help prevent colorectal cancer.
    Type of Medium: Online Resource
    ISSN: 1940-6207 , 1940-6215
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2021
    detail.hit.zdb_id: 2422346-3
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  • 6
    Online Resource
    Online Resource
    Centers for Disease Control and Prevention (CDC) ; 2023
    In:  Preventing Chronic Disease Vol. 20 ( 2023-06-01)
    In: Preventing Chronic Disease, Centers for Disease Control and Prevention (CDC), Vol. 20 ( 2023-06-01)
    Type of Medium: Online Resource
    ISSN: 1545-1151
    Language: English
    Publisher: Centers for Disease Control and Prevention (CDC)
    Publication Date: 2023
    detail.hit.zdb_id: 2135684-1
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  • 7
    In: Journal of the Academy of Nutrition and Dietetics, Elsevier BV, Vol. 122, No. 9 ( 2022-09), p. 1665-1676.e2
    Type of Medium: Online Resource
    ISSN: 2212-2672
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2022
    detail.hit.zdb_id: 2646137-7
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  • 8
    In: British Journal of Nutrition, Cambridge University Press (CUP), Vol. 129, No. 3 ( 2023-02-14), p. 523-534
    Abstract: One potential mechanism by which diet and lifestyle may affect chronic disease risk and subsequent mortality is through chronic systemic inflammation. In this study, we investigated whether the inflammatory potentials of diet and lifestyle, separately and combined, were associated with all-cause, all-CVD and all-cancer mortality risk. We analysed data on 18 484 (of whom 4103 died during follow-up) Black and White men and women aged ≥45 years from the prospective REasons for Geographic and Racial Differences in Stroke study. Using baseline (2003–2007) Block 98 FFQ and lifestyle questionnaire data, we constructed the previously validated inflammation biomarker panel-weighted, 19-component dietary inflammation score (DIS) and 4-component lifestyle inflammation score (LIS) to reflect the overall inflammatory potential of diet and lifestyle. From multivariable Cox proportional hazards models, the hazards ratios (HR) and their 95 % CI for the DIS–all-cause mortality and LIS–all-cause mortality risk associations were 1·32 (95 % CI (1·18, 1·47); P for trend 〈 0·01) and 1·25 (95 % CI (1·12, 1·38); P for trend 〈 0·01), respectively, among those in the highest relative to the lowest quintiles. The findings were similar by sex and race and for all-cancer mortality, but weaker for all-CVD mortality. The joint HR for all-cause mortality among those in the highest relative to the lowest quintiles of both the DIS and LIS was 1·91 (95 % CI 1·57, 2·33) ( P for interaction 〈 0·01). Diet and lifestyle, via their contributions to systemic inflammation, separately, but perhaps especially jointly, may be associated with higher mortality risk among men and women.
    Type of Medium: Online Resource
    ISSN: 0007-1145 , 1475-2662
    Language: English
    Publisher: Cambridge University Press (CUP)
    Publication Date: 2023
    detail.hit.zdb_id: 2016047-1
    SSG: 12
    SSG: 21
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  • 9
    In: JNCI Cancer Spectrum, Oxford University Press (OUP), Vol. 4, No. 3 ( 2020-06-01)
    Abstract: Chronically higher inflammation, likely contributed to by dietary and lifestyle exposures, may increase risk for colorectal cancer (CRC). To address this, we investigated associations of novel dietary (DIS) and lifestyle (LIS) inflammation scores with incident CRC in the prospective National Institutes of Health–American Association of Retired Persons Diet and Health Study (N = 453 465). Methods The components of our previously developed and externally validated 19-component DIS and 4-component LIS were weighted based on their strengths of associations with a panel of circulating inflammation biomarker concentrations in a diverse subset (N = 639) of participants in the REasons for Geographic and Racial Differences in Stroke Study cohort. We calculated the components and applied their weights in the National Institutes of Health-American Association of Retired Persons cohort at baseline, summed the weighted components (higher scores reflect a higher balance of proinflammatory exposures), and investigated associations of the scores with incident CRC using Cox proportional hazards regression. All statistical tests were two-sided. Results Over a mean 13.5 years of follow-up, 10 336 participants were diagnosed with CRC. Among those in the highest relative to the lowest DIS and LIS quintiles, the multivariable-adjusted hazards ratios (HRs) and their 95% confidence intervals (CIs) were HR = 1.27 (95% CI = 1.19 to 1.35; Ptrend & lt; .001) and 1.38 (95% CI = 1.30 to 1.48; Ptrend & lt; .001), respectively. The associations were stronger among men and for colon cancers. The hazards ratio for those in the highest relative to the lowest joint DIS and LIS quintile was HR = 1.83 (95% CI = 1.68 to 1.99; Pinteraction & lt; .001). Conclusions Aggregates of proinflammatory dietary and lifestyle exposures may be associated with higher risk for CRC.
    Type of Medium: Online Resource
    ISSN: 2515-5091
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2020
    detail.hit.zdb_id: 2975772-1
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  • 10
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2023
    In:  Epidemiology Vol. 34, No. 6 ( 2023-11), p. 850-853
    In: Epidemiology, Ovid Technologies (Wolters Kluwer Health), Vol. 34, No. 6 ( 2023-11), p. 850-853
    Abstract: Negative-control exposures can be used to detect and even adjust for confounding that remains after control of measured confounders. A newly described method allows the analyst to reduce residual confounding by unmeasured confounders U by using negative-control exposures to define and select a subcohort wherein the U -distribution among the exposed is similar to that among the unexposed. Here, we show that conventional methods can be used to control for measured confounders in conjunction with the new method to control for unmeasured ones. We also derive an expression for bias that remains after applying this approach. We express remaining bias in terms of a “balancing” parameter and show that this parameter is bounded by a summary variational distance between the U -distribution in the exposed and the unexposed. These measures describe and bound the extent of remaining confounding after using negative controls to adjust for unmeasured confounders with conventional control of measured confounders.
    Type of Medium: Online Resource
    ISSN: 1044-3983
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2023
    detail.hit.zdb_id: 2042095-X
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