Epidemiology最新文献

Background: Early-life trauma (before age of 18 years) is hypothesized to increase the risk for adverse pregnancy outcomes through stress pathways, yet epidemiologic findings are mixed.

Methods: Sister Study participants (US women aged 35-74 years enrolled 2003-2009) completed an adapted Brief Betrayal Trauma Survey at the first follow-up visit. Lifetime history of gestational diabetes mellitus (GDM) or hypertensive disorders of pregnancy (HDP: pregnancy-related high blood pressure, pre-eclampsia/toxemia, or eclampsia) in pregnancies lasting ≥20 weeks was self-reported. We used log-binomial regression to estimate relative risks (RR) and 95% confidence intervals (CIs) for the association between early-life trauma (modeled using conventional measures [e.g., any experience, substantive domains, individual types] and latent classes of co-occurring traumas) and GDM or HDP among 34,879 parous women.

Results: Approximately, 4% of participants reported GDM and 11% reported HDP. Relative to no early-life trauma, the RRs for any were 1.1 (95% CI = 1.0, 1.3) for GDM and 1.2 (95% CI = 1.2, 1.3) for HDP. Women reporting physical trauma had the highest risk of GDM and HDP in comparison to other substantive domains. In analyses using latent classes of early-life trauma, high trauma was associated with an elevated risk of both GDM (RR = 1.9, 95% CI = 1.5, 2.6) and HDP (RR = 1.7, 95% CI = 1.4, 2.0) compared with low trauma.

Conclusions: Women experiencing high levels of trauma in early life were at higher risk of GDM and HDP, adding to a growing evidence base for this association.

Background: Annual influenza epidemics lead to a substantial public health burden, and pregnant people are vulnerable to severe outcomes. Influenza during pregnancy is hypothesized to increase the risk of adverse birth outcomes, but population-based epidemiologic evidence remains limited and inconsistent.

Methods: We conducted a time-series analysis to estimate short-term associations between community-level seasonal influenza activity and daily counts of preterm births in Atlanta, United States from October 17, 2010 to July 10, 2017. We defined weekly influenza exposures four ways: (1) percent test-positive from virologic surveillance, (2) percent of patients with symptoms of influenza-like illness (ILI) in outpatient settings, (3) a composite measure of percent test-positive and ILI, and (4) influenza hospitalization rates. We used Poisson log-linear models to estimate associations, adjusting for time-varying confounders and ongoing at-risk pregnancies. We further examined associations by influenza type and exposure lags and effect modification by maternal characteristics.

Results: We studied a total of 316,253 births. We found consistent positive associations between influenza activity and preterm birth across different exposure measures and exposure lags. An interquartile range increase in a composite measure of ILI activity and percent test-positive was associated with a 1.014 (95% confidence interval: 1.001-1.027) increase in preterm birth during the same week. In stratified analyses, associations were more pronounced among married, non-Black, and Hispanic pregnant people.

Conclusion: Periods of high influenza activity were associated with an increased risk of preterm birth.

Background: Increased lung cancer risks for low socioeconomic status (SES) groups are only partially attributable to smoking habits. Little effort has been made to investigate the persistent risks related to low SES by quantification of potential biases.

Methods: Based on 12 case-control studies, including 18 centers of the international SYNERGY project (16,550 cases, 20,147 controls), we estimated controlled direct effects (CDE) of SES on lung cancer via multiple logistic regression, adjusted for age, study center, and smoking habits and stratified by sex. We conducted mediation analysis by inverse odds ratio weighting to estimate natural direct effects and natural indirect effects via smoking habits. We considered misclassification of smoking status, selection bias, and unmeasured mediator-outcome confounding by genetic risk, both separately and by multiple quantitative bias analyses, using bootstrap to create 95% simulation intervals (SI).

Results: Mediation analysis of lung cancer risks for SES estimated mean proportions of 43% in men and 33% in women attributable to smoking. Bias analyses decreased the direct effects of SES on lung cancer, with selection bias showing the strongest reduction in lung cancer risk in the multiple bias analysis. Lung cancer risks remained increased for lower SES groups, with higher risks in men (fourth vs. first [highest] SES quartile: CDE, 1.50 [SI, 1.32, 1.69]) than women (CDE: 1.20 [SI: 1.01, 1.45]). Natural direct effects were similar to CDE, particularly in men.

Conclusions: Bias adjustment lowered direct lung cancer risk estimates of lower SES groups. However, risks for low SES remained elevated, likely attributable to occupational hazards or other environmental exposures.

Background: Anemia is common among HIV/AIDS patients, impacting prognosis. Particulate matter (PM) exposure is an understudied, potentially modifiable risk factor in this group.

Methods: We gathered 36,266 hemoglobin (Hb) measurements from 6808 HIV/AIDS patients from the HIV/AIDS Comprehensive Response Information Management System from 1 January 2004 to 31 December 2021. We evaluated the relationship between Hb levels and short-term PM exposure using linear mixed-effects models. We used logistic regression to estimate the association of long-term PM exposure with baseline anemia prevalence and time-varying Cox models to estimate the association of long-term PM exposure with follow-up incidence of anemia. Mediation analysis explored the role of chronic kidney disease (CKD) in the association between PM exposure and anemia.

Results: For every 5 µg/m³ increase in 28-day average PM 1 , Hb levels decreased by 0.43 g/l. For a 10 µg/m³ increase in PM 2.5 , Hb decreased by 0.55 g/l; for the same increase in PM 10, Hb decreased by 0.35 g/l. A 5 µg/m³ increase in 1-year average PM 1 corresponded to a 7% higher prevalence of anemia at baseline, a 10 µg/m³ increase in PM 2.5 to 8% higher prevalence, and a 10 µg/m³ increase in PM 10 to 6% higher prevalence. These rises in average PM concentrations during follow-up were associated with increased incident anemia by 54% (PM 1 ), 72% (PM 2.5 ), and 51% (PM 10 ). CKD partially mediated the positive associations between PM exposure and the incidence of anemia.

Conclusion: PM exposure was associated with lower Hb levels and higher incidence of anemia in HIV/AIDS patients and CKD with mediating estimated effects in PM-induced anemia.

Background: Investigations into long-term fine particulate matter (PM 2.5 ) exposure's impact on nonaccidental and cardiovascular (CVD) deaths primarily involve nonrepresentative adult populations at concentrations above the new Environmental Protection Agency annual PM 2.5 standard.

Methods: Using generalized linear models, we studied PM 2.5 exposure on rates of five mortality outcomes (all nonaccidental, CVD, myocardial infarction, stroke, and congestive heart failure) in 12 US states from 2000 to 2016. We aggregated predicted annual PM 2.5 exposures from a validated ensemble exposure model, ambient temperature from Daymet predictions, and mortality rates to all census tract-years within the states. We obtained covariates from the decennial Census and the American Community Surveys and assessed effect measure modification by race and education with stratification.

Results: For each 1-µg/m 3 increase in annual PM 2.5 , we found positive associations with all five mortality outcomes: all nonaccidental (1.08%; 95% confidence interval [CI]: 0.96%, 1.20%), all CVD (1.27%; 95% CI: 1.14%, 1.41%), myocardial infarction (1.89%; 95% CI: 1.67%, 2.11%), stroke (1.08%; 95% CI: 0.87%, 1.30%), and congestive heart failure (2.20%; 95% CI: 1.97%, 2.44%). Positive associations persisted at <8 µg/m 3 PM 2.5 levels and among populations with only under 65. In our study, race, but not education, modifies associations. High-educated Black had a 2.90% larger increased risk of CVD mortality (95% CI: 2.42%, 3.39%) compared with low-educated non-Black.

Conclusion: Long-term PM 2.5 exposure is associated with nonaccidental and CVD mortality in 12 states, below the new Environmental Protection Agency standard, for both low PM 2.5 regions and the general population. Vulnerability to CVD mortality persists among Black individuals regardless of education level.