Background

Hospitalized patients are at increased risk for acquisition of methicillin-resistant Staphylococcus aureus (MRSA). As hospital length of stay shortens, hospital-acquired MRSA events may be more likely to be detected after discharge.

Objective

We assessed the impact of attributing MRSA cases discovered within 30 days after discharge to the most recent hospitalization and identified patient characteristics associated with MRSA detection after discharge.

Design

Retrospective cohort study.

Setting

Twenty-seven acute care hospitals in Orange County, California.

Participants

Adult acute care admissions (2002-2007).

Methods

Using a countywide hospital data set containing diagnostic codes with present-on-admission (POA) indicators, we identified the first admission with a MRSA code for each patient. This incident MRSA admission was defined as predischarge-detected (pre-DD) hospital-onset MRSA (HO-MRSA) when MRSA was not POA. If MRSA was POA and a prior admission occurred within 30 days, this prior admission was assigned postdischarge-detected (post-DD) HO-MRSA. We evaluated the impact of including post-DD HO-MRSA in the calculation of hospital HO-MRSA incidence using signed-rank tests and reviewed changes in hospital rankings. We conducted multivariate comparisons of patient characteristics of pre-DD versus post-DD HO-MRSA patients.

Results

Among 1,217,253 at-risk hospitalizations, the inclusion of post-DD HO-MRSA tripled the median hospital HO-MRSA incidence, from 12.2 to 35.7 cases per 10,000 at-risk admissions (P < .0001). Hospital ranking changed substantially when including post-DD HO-MRSA. Patients with shorter stays were more likely to have post-DD MRSA.

Conclusions

On the basis of administrative claims data, the inclusion of post-DD HO-MRSA significantly increased the estimated HO-MRSA incidence and altered hospital rankings. This finding underscores the limitations of single-facility data when deriving HO-MRSA incidence and rank.

Background

Several per- and polyfluoroalkyl substances (PFAS) are ubiquitous anthropogenic pollutants almost universally detected in humans. Experimental evidence indicates that PFAS alter glucose metabolism and insulin secretion. However, epidemiological studies have yielded inconsistent results.

Objective

We sought to examine associations between plasma PFAS concentrations, glycemic indicators, and diabetes incidence among high-risk adults.

Methods

Within the Diabetes Prevention Program (DPP), a trial for the prevention of type 2 diabetes among high-risk individuals, we quantified baseline plasma concentrations of nine PFAS among 957 participants randomized to a lifestyle intervention or placebo. We evaluated adjusted associations for plasma PFAS concentrations with diabetes incidence and key glycemic indicators measured at baseline and annually over up to 4.6 y.

Results

Plasma PFAS concentrations were similar to those reported in the U.S. population in 1999-2000. At baseline, in cross-sectional analysis, a doubling in plasma perfluorooctanesulfonic acid (PFOS) and perfluorooctanoic acid (PFOA) concentrations was associated with higher homeostatic model assessment of insulin resistance (HOMA-IR) [β_PFOS=0.39; 95% confidence interval (CI): 0.13, 0.66; β_PFOA=0.64; 95% CI: 0.34, 0.94], β-cell function (HOMA-β) (β_PFOS=9.62; 95% CI: 1.55, 17.70; β_PFOA=15.93; 95% CI: 6.78, 25.08), fasting proinsulin (β_PFOS=1.37 pM; 95% CI: 0.50, 2.25; β_PFOA=1.71 pM; 95% CI: 0.72, 2.71), and glycated hemoglobin (HbA_1c) (β_PFOS=0.03%; 95% CI: 0.002, 0.07; β_PFOA=0.04%; 95% CI: 0.001, 0.07). There was no strong evidence of associations between plasma PFAS concentrations and diabetes incidence or prospective changes in glycemic indicators during the follow-up period.

Conclusions

At baseline, several PFAS were cross-sectionally associated with small differences in markers of insulin secretion and β-cell function. However, there was limited evidence suggesting that PFAS concentrations are associated with diabetes incidence or changes in glycemic indicators during the follow-up period. https://doi.org/10.1289/EHP1612.

Background

Per- and polyfluoroalkyl substances (PFAS) are endocrine disrupting chemicals that have been associated with cardiovascular risk factors including elevated body weight and hypercholesterolemia. Therefore, PFAS may contribute to the development of atherosclerosis and cardiovascular disease (CVD). However, no previous study has evaluated associations between PFAS exposure and arterial calcification.

Methods and results

This study used data from 666 prediabetic adults enrolled in the Diabetes Prevention Program trial who had six PFAS quantified in plasma at baseline and two years after randomization, as well as measurements of coronary artery calcium (CAC) and ascending (AsAC) and descending (DAC) thoracic aortic calcification 13-14 years after baseline. We performed multinomial regression to test associations between PFAS and CAC categorized according to Agatston score [low (<10), moderate (11-400) and severe (>400)]. We used logistic regression to assess associations between PFAS and presence of AsAC and DAC. We adjusted models for baseline sex, age, BMI, race/ethnicity, cigarette smoking, education, treatment assignment (placebo or lifestyle intervention), and statin use. PFAS concentrations were similar to national means; 53.9% of participants had CAC > 11, 7.7% had AsAC, and 42.6% had DAC. Each doubling of the mean sum of plasma concentrations of linear and branched isomers of perfluorooctane sulfonic acid (PFOS) was associated with 1.49-fold greater odds (95% CI: 1.01, 2.21) of severe versus low CAC. This association was driven mainly by the linear (n-PFOS) isomer [1.54 (95% CI: 1.05, 2.25) greater odds of severe versus low CAC]. Each doubling of mean plasma N-ethyl-perfluorooctane sulfonamido acetic acid concentration was associated with greater odds of CAC in a dose-dependent manner [OR = 1.26 (95% CI:1.08, 1.47) for moderate CAC and OR = 1.37 (95% CI:1.07, 1.74) for severe CAC, compared to low CAC)]. Mean plasma PFOS and n-PFOS were also associated with greater odds of AsAC [OR = 1.67 (95% CI:1.10, 2.54) and OR = 1.70 (95% CI:1.13, 2.56), respectively], but not DAC. Other PFAS were not associated with outcomes.

Conclusions

Prediabetic adults with higher plasma concentrations of select PFAS had higher risk of coronary and thoracic aorta calcification. PFAS exposure may be a risk factor for adverse cardiovascular health among high-risk populations.