Exploring the impact of prenatal perfluoroalkyl and polyfluoroalkyl substances exposure on blood pressure in early childhood: A longitudinal analysis.

Previous research investigating the correlation between prenatal exposure to per- and polyfluoroalkyl substances (PFAS) and subsequent blood pressure (BP) in offspring has yielded limited and contradictory findings. This study was conducted to investigate the potential relationship between maternal PFAS levels during pregnancy and subsequent BP in early childhood. A total of 129 expectant mothers from the Shanghai Birth Cohort were included in the study. Using high-performance liquid chromatography/tandem mass spectrometry, we measured ten PFAS compounds in maternal plasma throughout the pregnancy. When the children reached the age of 4, we examined their systolic BP (SBP) and diastolic BP (DBP), along with mean arterial pressure (MAP) and pulse pressure (PP). Data interpretation employed multiple linear and logistic regression models, complemented by Bayesian kernel machine regression (BKMR).We found that the majority of PFAS concentrations remained stable during pregnancy. The linear and BKMR models indicated a positive relationship between the PFAS mixture in maternal plasma and offspring's DBP and MAP, with perfluorohexanesulphonic acid (PFHxS) having the most significant influence (PFHxS and DBP [first trimester:ß=3.03, 95%CI: (1.01,5.05); second trimester: ß=2.35, 95%CI: (0.94,3.75); third trimester: ß=2.57, 95%CI:(0.80,4.34)]; MAP [first trimester:ß=2.55, 95%CI: (0.64,4.45); second trimester: ß=2.28, 95%CI: (0.95,3.61); third trimester: ß=2.35, 95%CI:(0.68,4.01)]). Logistic regression highlighted an increased risk of prehypertension and hypertension in offspring with higher maternal PFHxS concentrations during all three trimesters [first trimester: OR=2.53, 95%CI:(1.11,5.79), second trimester: OR=2.05, 95%CI:(1.11,3.78), third trimester: OR=3.08, 95%CI:(1.40,6.79)]. A positive correlation was identified between the half-lives of PFAS and the odds ratio (OR) of prehypertension and hypertension in childhood (ß=0.139, P=0.010). In conclusion, this research found maternal plasma PFAS concentrations to be positively associated with BP in offspring, with PFHxS showing the most significant influence. This correlation remained consistent throughout pregnancy, and this effect was proportional to the half-lives of PFAS.

Association between environmental chemical exposure and albumin-to-creatinine ratio is modified by hypertension status in women of reproductive age.

Chemicals have been identified as a potential risk factor of renal dysfunction. However, studies that consider both multiple chemicals and non-chemical risk factors, such as hypertension, are rare. In this study, we assessed the associations between exposure to several chemicals, including major metals, phthalates, and phenolic compounds, and the albumin-to-creatinine ratio (ACR). A group of Korean adult women in reproductive age (n = 438, aged between 20 and 49 years), who had previously been studied for association of several organic chemicals, was chosen for this purpose. We constructed multivariable linear regression models for individual chemicals and weighted-quantile sum (WQS) mixtures, by hypertension status. Among the study population, approximately 8.5% of the participants exhibited micro/macro-albuminuria (ACR ≥30 mg/g), and 18.5% and 3.9% exhibited prehypertension and hypertension, respectively. Blood cadmium and lead levels showed a stronger association with ACR only among women with prehypertension or hypertension. Among organic chemicals, depending on the statistial model, benzophenone-1 (BP-1) and mono(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP) showed a significant association regardless of hypertension status, but most associations disappeared in the (pre)hypertensive group. These findings clearly indicate that hypertension status can modify and may potentiate the association of environmental chemicals with ACR. Our observations suggest that low-level environmental pollutant exposure may have potential adverse effects on kidney function among general adult women. Considering the prevalence of prehypertension in the general population, efforts to reduce exposure to cadmium and lead are necessary among adult women to minimize the risk of adverse kidney function.

High-normal blood pressure (prehypertension) is associated with PM2.5 exposure in young adults.

We aimed to examine PM2.5 exposure, blood pressure (SBP and DBP) measurement, and hypertension risk factors and to assess the association between PM2.5 exposure and hypertension among young adults. The mean SBP was 117.78 mmHg, with 11.22% high-normal blood pressure (prehypertension) and 2.51% hypertension (≥ 140 mmHg). DBP was 75.48 mmHg with 26.37% prehypertension and 4.53% hypertension (≥ 90 mmHg). The median PM2.5 in the past year was 31.79 µg/m3, with highest in winter (49.33 µg/m3), followed by spring (37.34 µg/m3), autumn (29.64 µg/m3), and summer (24.33 µg/m3). Blood pressure was positively correlated with age, height, weight, BMI, daily smoking, alcohol consumption, mental stress, and staying up in the past 1 year, and negatively with season-specific temperature. After adjustment for the covariates, each 10 µg/m3 increase in PM2.5 was associated with SBP (day 1 = 1.07 mmHg, day 3 = 1.25 mmHg, day 5 = 1.01 mmHg) and DBP (day 1 = 1.06 mmHg, day 3 = 1.28 mmHg, day 5 = 1.29 mmHg, day 15 = 0.87 mmHg, day 30 = 0.56 mmHg). Exposure in winter and the past year was associated with 1.21 mmHg and 0.95 increase mmHg in SBP, respectively. Logistic models showed for every 1 µg/m3 increase of PM2.5, SBP in day 1 and day 5 was increased by 6% and 4%, and DPB by 3% and 16%, respectively. SBP was increased by 8% in spring and 19% in winter, and DBP was increased by 7% in winter. Our data suggest a certain prevalence of pre- or hypertension among young population, which is associated with short-term fluctuation and season-specific exposure of PM2.5.

The association between low blood lead levels and the prevalence of prehypertension among nonhypertensive adults in Korea.

OBJECTIVES: Low-level lead exposure has been associated with increases in blood pressure (BP) and impairment of the cardiovascular system. Prehypertension is not categorized as a disease currently; however, individuals with untreated prehypertension are known to be at increased risk of progression to hypertension and mortality caused by cardiovascular disease. We investigated the association between blood lead levels below the threshold for the harmful effects of lead and the prevalence of prehypertension in Korean adults. METHODS: A total of 8,493 participants (3,945 men and 4,548 women) were included in the current analysis, using data from the fourth, fifth, and sixth Korean National Health and Nutrition Examination Survey (KNHANES) in 2007-2013. Blood analysis, self-report questionnaires, and physical examinations were used to assess blood lead levels, BP, and medical history. Odds ratios (OR) and 95% confidence intervals (95% CI) for prehypertension were calculated using multiple logistic regression models. RESULTS: Compared to the first quartile (Q1) blood lead level (0.206-1.539 µg/dl), the ORs (95% CI) were 1.24 (1.04-1.48) in Q2, (1.540-2.056 µg/dl), 1.27 (1.06-1.52) in Q3, (2.057-2.716 µg/dl), and 1.30 (1.07-1.60) in Q4 (2.717-24.532 µg/dl) for the prevalence of prehypertension after adjusting for age, sex, morbidity status, socioeconomic status, and health behavioral variables. CONCLUSIONS: Our large, cross-sectional, nationwide study revealed that blood lead levels below the threshold for the harmful effects of lead were significantly associated with prehypertension. Am. J. Hum. Biol. 28:729-735, 2016. © 2016 Wiley Periodicals, Inc.

Urinary phthalates are associated with higher blood pressure in childhood.

OBJECTIVE: To examine associations of urinary phthalate levels with blood pressure (BP) and serum triglyceride and lipoprotein levels in children. STUDY DESIGN: We performed a cross-sectional analysis of a subsample of US children aged 6-19 years who participated in the National Health and Nutrition Examination Survey between 2003 and 2008. We quantified exposure to 3 families of phthalates--low molecular weight, high molecular weight and di-2-ethylhexylphthalate (DEHP)--based on molar concentration of urinary metabolites. We assessed descriptive, bivariate, and multivariate associations with BP and lipid levels. RESULTS: Controlling for an array of sociodemographic and behavioral factors, as well as diet and body mass index, levels of metabolites of DEHP, a phthalate commonly found in processed foods, were associated with higher age-, sex-, and height-standardized BP. For each log unit (roughly 3-fold) increase in DEHP metabolites, a 0.041 SD unit increase in systolic BP z-score was identified (P = .047). Metabolites of low molecular weight phthalates commonly found in cosmetics and personal care products were not associated with BP. Phthalate metabolites were not associated with triglyceride levels, high-density lipoprotein level, or prehypertension. CONCLUSIONS: Dietary phthalate exposure is associated with higher systolic BP in children and adolescents. Further work is needed to confirm these associations, as well as to evaluate opportunities for intervention.

Risk of methylphenidate-induced prehypertension in normotensive adult smokers with attention deficit hyperactivity disorder.

The authors studied predictors of methylphenidate-induced increases in blood pressure (BP). In this secondary analysis of a randomized, double-blind, placebo-controlled smoking cessation trial, nonhypertensive adult smokers with attention deficit hyperactivity disorder randomized to osmotic-release oral system methylphenidate (OROS-MPH) (n=115) were matched one-to-one on baseline systolic BP (SBP) (±5 mm Hg) with participants randomized to placebo (n=115) and followed for 10 weeks. In adjusted mixed linear models of SBP and diastolic BP (DBP), baseline normal SBP (P<.0001) and DBP (P<.0001) were associated with significant OROS-MPH-induced increases compared with placebo, whereas significant increases were not observed in participants with baseline prehypertensive SBP (P=.27) and DBP (P=.79). Participants randomized to OROS-MPH with baseline normal BP had increased odds of developing either systolic (odds ratio [OR], 3.32; 95% confidence interval [CI], 1.41-8.37; P=.006) or diastolic prehypertension (OR, 4.32; 95% CI, 1.56-14.0; P=.004) compared with placebo using simple logistic regression. The authors demonstrated an augmented OROS-MPH-induced BP elevation and risk of prehypertension in adults with baseline normal BP. Significantly increased BP was not observed in adults with baseline prehypertension.

Upregulation of junctional adhesion molecule-A is a putative prognostic marker of hypertension.

AIMS: Establishing biochemical markers of pre-hypertension and early hypertension could help earlier diagnostics and therapeutic intervention. We assess dynamics of junctional adhesion molecule-A (JAM-A) expression in rat models of hypertension and test whether JAM-A expression could be driven by angiotensin (ANG) II and whether JAM-A contributes to the progression of hypertension. We also compare JAM-A expression in normo- and hypertensive humans. METHODS AND RESULTS: In pre-hypertensive and spontaneously hypertensive rats (SHRs), JAM-A protein was overexpressed in the brainstem microvasculature, lung, liver, kidney, spleen, and heart. JAM-A upregulation at early and late stages was even greater in the stroke-prone SHR. However, JAM-A was not upregulated in leucocytes and platelets of SHRs. In Goldblatt 2K-1C hypertensive rats, JAM-A expression was augmented before any increase in blood pressure, and similarly JAM-A upregulation preceded hypertension caused by peripheral and central ANG II infusions. In SHRs, ANG II type 1 (AT(1)) receptor antagonism reduced JAM-A expression, but the vasodilator hydralazine did not. Body-wide downregulation of JAM-A with Vivo-morpholinos in juvenile SHRs delayed the progression of hypertension. In the human saphenous vein, JAM-A mRNA was elevated in hypertensive patients with untreated hypertension compared with normotensive patients but reduced in patients treated with renin-angiotensin system antagonists. CONCLUSION: Body-wide upregulation of JAM-A in genetic and induced models of hypertension in the rat precedes the stable elevation of arterial pressure. JAM-A upregulation may be triggered by AT(1) receptor-mediated signalling. An association of JAM-A with hypertension and sensitivity to blockers of ANG II signalling were also evident in humans. We suggest a prognostic and possibly a pathogenic role of JAM-A in arterial hypertension.