Background: Malnutrition and tuberculosis (TB) tend to interact with each other. TB may lead to nutrition deficiencies that will conversely delay recovery by depressing immune functions. Nutrition support can promote recovery in the subject being treated for TB. The aim of this study was to evaluate the effectiveness of nutrition support on promoting the recovery of adult pulmonary TB patients with anti-TB drug therapy. Methods: English database of the Cochrane Controlled Trials Register, PubMed, EMBASE, and Chinese database of CBM, CNKI, VIP, and WANFANG were searched. Randomized controlled trials comparing nutrition support (given for more than 2 weeks) with no nutrition intervention, nutrition advice only, or placebo-control for TB patients being anti-TB treated were included. Two reviewers conducted data extraction, assessed the quality of the studies independently, and any discrepancies were solved by the third reviewer. Data were entered and analyzed by RevMan 5.2 software, and meta-analysis was done using risk ratios (RR s) for dichotomous variables and mean differences (MDs) for continuous variables with 95% confidence intervals (CI s). Results: A total of 19 studies (3681 participants) were included. In nutritional support for TB patients, pooled RR and its 95% CI of sputum smears- or culture-negative conversion rate and chest X-ray (CXR) absorption rate were 1.10 (1.04, 1.17) and 1.22 (1.08, 1.39), respectively, the pooled MD and its 95% CI of body mass index (BMI) and time of sputum smears or culture negativity were 0.59 (0.16, 1.2) and − 5.42 (−7.93, −2.92), respectively, compared with the control group. The differences in outcomes of CXR zone affected, TB score, serum albumin, and hemoglobin were not statistically significant (P = 0.76, 0.24, 0.28, and 0.20, respectively) between the intervention group and the control group. No systemic adverse events were recorded. Conclusions: During anti-TB course, nutrition support may be helpful in treatment of TB patients by improving both sputum smears- or culture-negative conversion rate and BMI, shortening the time of sputum conversion negative. Whether it can improve the final clinical effect, there still needs high-level quality studies to confirm in the future.

Objective Our aim was to elucidate the polycyclic aromatic hydrocarbon (PAH) metabolites exposure levels of pregnant women in the underdeveloped region of Zunyi, southwest China. Methods Sociodemographic information was collected via questionnaires, and urine samples were collected at the same time. A total of 3047 pregnant women participated in the study. Gas chromatography/mass spectrometry was used to detect the urine concentrations of 10 PAH metabolites. A generalised linear model (GLM) was used to identify predictive factors of PAH metabolites. Results All PAH metabolites had a detection rate greater than 60% (67.21%–90.57%) except for 4-OH-PHE at 55.54%. The median concentrations were 0.02–0.11 µg/g Cre except for 1-OH-NAP, 2-OH-NAP, 2-OH-FLU and 9-OH-FLU (0.36–0.50 µg/g Cre). The cluster analysis identified the phenanthrene and fluorene metabolite clusters (containing no other metabolites), while naphthalene metabolites (1-OH-NAP, 2-OH-NAP) could not be clustered without other metabolites. GLM analysis identified that pregnant women with the following characteristics have high urinary concentration of PAH metabolites: overweight, in the last trimester of pregnancy, distance between their house and main traffic lines as <5 m, use fuel for cooking, passive smoking, renovated their residence for less than 3 years, middle family income and office workers. Conclusion The results clarified pregnant women from the economically underdeveloped area could be the victims of PAHs. In addition, PAHs present a demographic and seasonal differential distribution, which will aid in the development of targeted interventions and reduce exposure to PAHs during pregnancy.

Studies have shown that exposure to phthalates can affect neonatal birth weight. However, epidemiological evidence on the mediating role of maternal thyroid hormones is limited. Therefore, this study, based on the Compliance Birth Cohort, aimed to reveal the potential mediating function of maternal thyroid hormones during pregnancy between phthalic acid ester (PAE) exposure and neonatal birth weight. The study included 1274 mother-infant pairs. Linear regression analysis revealed a negative association between MIBP and neonatal birth weight (β = -62.236; 95% CI: -118.842, -5.631). Bayesian kernel-machine regression (BKMR) indicated a nonlinear negative association between PAE metabolites (PAEs) and birth weight. Linear regression analysis revealed a positive association between neonatal birth weight and FT3 (β = 41.605; 95% CI: 2.631, 80.380). The BKMR model also found a positive association between thyroid hormones and birth weight but in a nonlinear manner. Additionally, linear regression analyses showed that TSH, TT3, TT4, FT3, and FT4 were associated with PAEs. The BKMR model revealed an inverted U-shaped association of PAEs with TT3 and FT3 and a nonlinear association with TSH, TT4, and FT4. Structural equation modeling revealed that MMP, MIBP, MBP, MEHP, MOP, MBZP, and MEOHP contributed to a net reduction in neonatal birth weight of 32 g through the TT3, FT3, TT4, and FT4 pathways. The findings suggest that exposure to PAEs during pregnancy leads to a reduction in neonatal birth weight, possibly due to the involvement of maternal thyroid hormones as mediators. Controlling maternal thyroid hormone levels during pregnancy may be a viable method to reduce the harmful effects of phthalate exposure on the developing fetus.

Cumulative evidence has demonstrated that exposure to polycyclic aromatic hydrocarbons (PAHs) or phthalates (PAEs) contributes to a variety of adverse health effects. However, the association of PAHs and PAEs co-exposure with blood cell-based inflammatory indicators during early pregnancy is still unclear. We aimed to investigate the single and mixed associations of exposure to PAHs and PAEs with blood cell-based inflammatory indicators among early pregnant women. A total of 318 early pregnant women were included in this study. General linear regressions were used to estimate the relationships of individual OH-PAHs and mPAEs with blood cell-based inflammatory indicators. The key pollutants were selected by an adapted least absolute shrinkage and selection operator (LASSO) penalized regression model and wasemployed to build the Bayesian kernel machine regression (BKMR) and quantile g-computation (Q-g) models, which can assess the joint association of OH-PAHs and mPAEs with blood cell-based inflammatory indicators. General linear regression indicated that each 1% increase in MOP was associated with a 4.92% (95% CI: 2.12%, 7.68%), 3.25% (95% CI: 0.50%, 6.18%), 5.87% (95% CI: 2.22%, 9.64%), and 6.50% (95% CI: 3.46%, 9.64%) increase in WBC, lymphocytes, neutrophils, and monocytes, respectively. BKMR and Q-g analysis showed that the mixture of OH-PAHs and mPAEs was linked with increased levels of white blood cells (WBC), neutrophils, monocytes, and lymphocytes, and MOP was identified as the dominant contributor. OH-PAHs and mPAEs co-exposure in early pregnancy was associated with elevated blood cell-based inflammatory indicators reactions. More attention should be paid to the inflammation induced by environmental pollution for perinatal women, especially early pregnant women.