Associations between ABO non-identical platelet transfusions and patient outcomes-A multicenter retrospective analysis.

BACKGROUND: Due to platelet availability limitations, platelet units ABO mismatched to recipients are often transfused. However, since platelets express ABO antigens and are collected in plasma which may contain ABO isohemagglutinins, it remains controversial as to whether ABO non-identical platelet transfusions could potentially pose harm and/or have reduced efficacy. STUDY DESIGN AND METHODS: The large 4-year publicly available Recipient Epidemiology and Donor Evaluation Study-III (REDS-III) database was used to investigate patient outcomes associated with ABO non-identical platelet transfusions. Outcomes included mortality, sepsis, and subsequent platelet transfusion requirements. RESULTS: Following adjustment for possible confounding factors, no statistically significant association between ABO non-identical platelet transfusion and increased risk of mortality was observed in the overall cohort of 21,176 recipients. However, when analyzed by diagnostic category and recipient ABO group, associations with increased mortality for major mismatched transfusions were noted in two of eight subpopulations. Hematology/Oncology blood group A and B recipients (but not group O) showed a Hazard Ratio (HR) of 1.29 (95%CI: 1.03-1.62) and intracerebral hemorrhage group O recipients (but not groups A and B) showed a HR of 1.75 (95%CI: 1.10-2.80). Major mismatched transfusions were associated with increased odds of receiving additional platelet transfusion each post-transfusion day (through day 5) regardless of the recipient blood group. DISCUSSION: We suggest that prospective studies are needed to determine if specific patient populations would benefit from receiving ABO identical platelet units. Our findings indicate that ABO-identical platelet products minimize patient exposure to additional platelet doses.

Outdoor air pollution exposure and uterine cancer incidence in the Sister Study.

BACKGROUND: Outdoor air pollution is a ubiquitous exposure that includes endocrine-disrupting and carcinogenic compounds that may contribute to the risk of hormone-sensitive outcomes such as uterine cancer. However, there is limited evidence about the relationship between outdoor air pollution and uterine cancer incidence. METHODS: We investigated the associations of residential exposure to particulate matter less than 2.5 µm in aerodynamic diameter (PM2.5) and nitrogen dioxide (NO2) with uterine cancer among 33 417 Sister Study participants with an intact uterus at baseline (2003-2009). Annual average air pollutant concentrations were estimated at participants' geocoded primary residential addresses using validated spatiotemporal models. Cox proportional hazards models were used to estimate hazard ratios and 95% confidence intervals for the association between time-varying 12-month PM2.5 (µg/m3) and NO2 (parts per billion; ppb) averages and uterine cancer incidence. RESULTS: Over a median follow-up period of 9.8 years, 319 incident uterine cancer cases were identified. A 5-ppb increase in NO2 was associated with a 23% higher incidence of uterine cancer (hazard ratio = 1.23, 95% confidence interval = 1.04 to 1.46), especially among participants living in urban areas (hazard ratio = 1.53, 95% confidence interval = 1.13 to 2.07), but  PM2.5 was not associated with increased uterine cancer incidence. CONCLUSION: In this large US cohort, NO2, a marker of vehicular traffic exposure, was associated with a higher incidence of uterine cancer. These findings expand the scope of health effects associated with air pollution, supporting the need for policy and other interventions designed to reduce air pollutant exposure.

Early life socioeconomic position contributes to adult obesity independent of adult socioeconomic factors: Findings from the sister study cohort.

Low socioeconomic position (SEP) has been associated with obesity within life stages; however, life course SEP may also alter downstream obesity risk. Research is needed to understand the impact of childhood SEP, independent of adult SEP, as well as SEP trajectories over the life course on adult obesity risk. We use data from the Sister Study, a prospective U.S. cohort of women aged 35-74 years (N = 50,884; enrollment: 2003-2009). Relative risks (RR) for adult obesity associated with childhood SEP (latent variable) and five latent life course SEP profiles were estimated in overall and race and ethnicity-stratified log binomial regression models. We estimated the direct effect of childhood SEP on adult obesity and mediation by adult SEP. Lower childhood SEP was associated with greater obesity risk (RR = 1.16, 95% CI: 1.15-1.17). In stratified models, RRs were elevated across groups though lower for Black and Hispanic/Latina participants, despite greater prevalence of obesity among Black participants. The direct effect of childhood SEP on adult obesity persisted in mediation models independent of adult SEP (RR = 1.10, 95% CI: 1.08-1.12) with adult SEP mediating approximately 40% of the total effect of childhood SEP on adult obesity. Furthermore, adult obesity risk was elevated for all life course SEP profiles compared to persistent high advantage. Life course SEP profiles indicating greater advantage in adulthood than childhood were not associated with reduced adult obesity risk among those experiencing less than high advantage in childhood. In conclusion, lower childhood SEP, independent of adult SEP, may be an important risk factor for adult obesity.

Air Pollution and Breast Cancer: An Examination of Modification By Underlying Familial Breast Cancer Risk.

BACKGROUND: An increased familial risk of breast cancer may be due to both shared genetics and environment. Women with a breast cancer family history may have a higher prevalence of breast cancer-related gene variants and thus increased susceptibility to environmental exposures. We evaluated whether air pollutant and breast cancer associations varied by familial risk. METHODS: Sister Study participants living in the contiguous United States at enrollment (2003-2009; N = 48,453), all of whom had at least one first-degree relative with breast cancer, were followed for breast cancer. Annual NO2 and PM2.5 concentrations were estimated at the enrollment addresses. We predicted 1-year familial breast cancer risk using the Breast and Ovarian Analysis of Disease Incidence and Carrier Estimation Algorithm (BOADICEA). Using Cox regression, we estimated HRs and 95% confidence intervals (CI) for associations between each pollutant dichotomized at the median and breast cancer with interaction terms to examine modification by BOADICEA score. RESULTS: NO2 was associated with a higher breast cancer risk among those with BOADICEA score >90th percentile (HR, 1.28; 95% CI, 1.05-1.56) but not among those with BOADICEA score ≤90th percentile (HR, 0.98; 95% CI, 0.90-1.06; P interaction = 0.01). In contrast to NO2, associations between PM2.5 and breast cancer did not vary between individuals with BOADICEA score >90th percentile and ≤90th percentile (P interaction = 0.26). CONCLUSIONS: Our results provide additional evidence that air pollution may be implicated in breast cancer, particularly among women with a higher familial risk. IMPACT: Women at higher underlying breast cancer risk may benefit more from interventions to reduce exposure to NO2.