Associations between cooking fuels and hypertension prevalence in Chinese adults: A prospective cohort analysis focusing on fuel transitioning.

BACKGROUND: Using polluting cooking fuels is a suggested risk factor for hypertension. Transitioning to clean cooking fuels has occurred widely in China in the past 30 years. This provides an opportunity to examine whether the transition could reduce hypertension risk and to ascertain the inconsistent literature on the relationship between cooking fuels and hypertension prevalence. METHODS: Initiated in 1989, the China Health and Nutrition Survey (CHNS) enrolled participants from 12 provinces in China. By 2015, nine waves of follow-up have been conducted. Based on self-reported cooking fuels, participants were classified into persistent clean fuel users, persistent polluting fuel users and those who transitioned from polluting fuels to clean fuels. Hypertension was defined as having systolic blood pressure (SBP) ≥ 140 mmHg, diastolic blood pressure (DBP) ≥ 90 mmHg, or self-reported current use of antihypertension medication. FINDINGS: Among 12,668 participants, 3963 (31.28%) were persistent polluting fuel users; 4299 (33.94%) transitioned to clean fuels; and 4406 (34.78%) were persistent clean fuel users. During the period of follow-up (7.8 ± 6.1 years), hypertension was diagnosed in 4428 participants. Compared to persistent clean fuel users, persistent polluting fuel users had a higher risk for hypertension (hazard ratio [HR] 1.69, 95%CI 1.55-1.85), while those transitioned to clean fuels did not. The effects were consistent by gender and urbanicity, respectively. The HRs for hypertension were 1.99 (95%CI 1.75-2.25), 1.55 (95%CI 1.32-1.81) and 1.36 (95%CI 1.13-1.65) among those persistent polluting fuel users aged 18-44, 45-59 and ≥60 years old, respectively. INTERPRETATION: Transitioning from using polluting fuels to clean fuels prevented an increase in hypertension risk. The finding highlights the importance of promoting the fuel transition as a risk-reduction strategy for reducing the disease burden from hypertension.

Impacts of implementing Healthy Building guidelines for daily PM2.5 limit on premature deaths and economic losses in urban China: A population-based modeling study.

Given a large fraction of people's exposure to urban PM2.5 occur indoors, reducing indoor PM2.5 levels may offer a more feasible and immediate way to save substantial lives and economic losses attributable to PM2.5 exposure. We aimed to estimate the premature mortality and economic loss reductions associated with achieving the newly established Chinese indoor air guideline and a few hypothetical indoor PM2.5 guideline values. We used outdoor PM2.5 concentrations from 1497 monitoring sites in 339 Chinese cities in 2015, coupled with a steady-state mass balance model, to estimate indoor concentrations of outdoor-infiltrated PM2.5. Using province-specific time-activity patterns for urban residents, we estimated outdoor and indoor exposures to PM2.5 of outdoor origin. We then proceeded to use localized census-based concentration-response models and the value of statistical life estimates to calculate premature deaths and economic losses attributable to PM2.5 exposure across urban China. Finally, we estimated potentially avoidable mortality and corresponding economic losses by meeting the current 24-hour based guideline and various hypothetical indoor limits for PM2.5. In 2015 in urban areas of mainland China, the city-specific annual mean outdoor and indoor PM2.5 concentrations ranged 9-108 µg/m3 and 5-56 µg/m3, respectively. Indoor exposures contributed 62%-91% daily and 68%-83% annually to the total time-weighted exposures. The potential reductions in total deaths and economic losses for the scenario in which daily indoor concentrations met the current guideline of 75 µg/m3, 37.5 µg/m3, and 25 µg/m3 were 16.9 (95% CI: 0.7-62.1) thousand, 87.7 (95% CI: 9.7-197.7) thousand, and 165.5 (95% CI: 30.8-304.0) thousand, respectively. The corresponding reductions in economic losses were 5.7 (95% CI: 0.2-34.8) billion, 29.4 (95% CI: 2.4-109.6) billion, and 55.2 (95% CI: 7.7-168.0) billion US Dollars, respectively. Deaths and economic losses would be reduced exponentially within the range of 0-75 µg/m3 for hypothetical indoor PM2.5 limits. The findings demonstrate the effectiveness of reducing indoor concentrations of outdoor-originated PM2.5 in saving substantial lives and economic losses in China. The analysis provides quantitative evidence to support the implementation of an indoor air quality guideline or standard for PM2.5.

Responses of serum chemokines to dramatic changes of air pollution levels, a panel study.

Background: Despite the in vitro and in vivo evidence, studies are limited in evaluating whether chemokines are potential inflammatory mediators in response to air pollution exposure in humans. Methods: We conducted a panel study coinciding with the Beijing Olympics, when temporary air pollution controls were implemented. We measured a suite of serum chemokines among healthy adults before, during and after the Olympics, respectively. Linear mixed-effect models were used to evaluate changes in chemokine levels over the three time periods. Results: In response to the 50% drop in air pollution levels during the games, levels of RANTES, MCP-2, and TARC decreased by 25.8%, 20.9% and 35.3%, respectively (p < 0.001) from pre-Olympics, and then increased by 45.8%, 34.9% and 61.5%, respectively (p < 0.001) after the games when air pollution levels went up again. Similar patterns were observed in subgroup analyses by sex, age, smoking and body mass index. GRO-α and IL-8 decreased significantly during the games (22.5% and 30.4%), and increased non-significantly after the games. Eotaxin-1 only increased significantly from during- to post-games. Conclusions: The strongest associations with air pollution levels were observed among RANTES, TARC and MCP-2. Those chemokines may play important roles in the air pollution-induced inflammatory pathway.

Self-reported prenatal tobacco smoke exposure, AXL gene-body methylation, and childhood asthma phenotypes.

BACKGROUND: Epigenetic modifications, including DNA methylation, act as one potential mechanism underlying the detrimental effects associated with prenatal tobacco smoke (PTS) exposure. Methylation in a gene called AXL was previously reported to differ in response to PTS. METHODS: We investigated the association between PTS and epigenetic changes in AXL and how this was related to childhood asthma phenotypes. We tested the association between PTS and DNA methylation at multiple CpG loci of AXL at birth using Pyrosequencing in two separate study populations, the Children's Health Study (CHS, n = 799) and the Newborn Epigenetic Study (NEST, n = 592). Plasma cotinine concentration was used to validate findings with self-reported smoking status. The inter-relationships among AXL mRNA and miR-199a1 expression, PTS, and AXL methylation were examined. Lastly, we evaluated the joint effects of AXL methylation and PTS on the risk of asthma and related symptoms at age 10 years old. RESULTS: PTS was associated with higher methylation level in the AXL gene body in both CHS and NEST subjects. In the pooled analysis, exposed subjects had a 0.51% higher methylation level in this region compared to unexposed subjects (95% CI 0.29, 0.74; p < 0.0001). PTS was also associated with 21.2% lower expression of miR-199a1 (95% CI - 37.9, - 0.1; p = 0.05), a microRNA known to regulate AXL expression. Furthermore, the combination of higher AXL methylation and PTS exposure at birth increased the risk of recent episodes of bronchitic symptoms in childhood. CONCLUSIONS: PTS was associated with methylation level of AXL and the combination altered the risk of childhood bronchitic symptoms.