Personal PM2.5 Elemental Components, Decline of Lung Function, and the Role of DNA Methylation on Inflammation-Related Genes in Older Adults: Results and Implications of the BAPE Study.

Epidemiological evidence of the effects of PM2.5 elements on lung function and DNA methylation is limited. We conducted a longitudinal panel study of 76 healthy older adults aged 60-69 years in Jinan, China, from September 2018 to January 2019. We periodically measured individual 72 h PM2.5 and element concentrations, lung function, and DNA methylation levels of eight inflammation-related genes. We used linear mixed-effect models to investigate the effects of exposure to personal PM2.5 elements on the lung function and DNA methylation. Mediation analysis was used to investigate the underlying effect mechanism. Negative changes in the ratio of forced expiratory volume in 1 s to forced vital capacity, ranging from -1.23% [95% confidence interval (CI): -2.11%, -0.35%] to -0.77% (95% CI: -1.49%, -0.04%), were significantly associated with interquartile range (IQR) increases in personal PM2.5 at different lag periods (7-12, 13-24, 25-48, 0-24, 0-48, and 0-72 h). Arsenic (As), nickel, rubidium (Rb), selenium, and vanadium were significantly associated with at least three lung function parameters, and IQR increases in these elements led to 0.12-5.66% reductions in these parameters. PM2.5 elements were significantly associated with DNA methylation levels. DNA methylation mediated 7.28-13.02% of the As- and Rb-related reduced lung function. The findings indicate that exposure to elements in personal PM2.5 contributes to reduced lung function through DNA methylation.

Short-term exposure to ozone and cause-specific mortality risks and thresholds in China: Evidence from nationally representative data, 2013-2018.

BACKGROUND: Ambient ozone pollution is steadily increasing and becoming a major environmental risk factor contributing to the global disease burden. Although the association between short-term ozone exposure and mortality has been widely studied, results are mostly reported on deaths from non-accidental or total cardiopulmonary disease rather than a spectrum of causes. In particular, a knowledge gap still exists for the potential thresholds in mortality risks. METHODS: This nationwide time-series study in China included 323 counties totaling 230,266,168 residents. Daily maximum 8-hour average was calculated as the ozone exposure metric. A two-stage statistical approach was adopted to assess ozone effects on 21 cause-specific deaths for 2013-2018. The subset approach and threshold approach were utilized to explore potential thresholds, and stratification analysis was used to evaluate population susceptibility. RESULTS: On average, the annual mean ozone concentration was 93.4 µg/m3 across 323 counties. A 10-µg/m3 increase in lag 0-1 day of ozone was associated with increases of 0.12 % in mortality risk from non-accidental disease, 0.11 % from circulatory disease, 0.09 % from respiratory disease, 0.29 % from urinary system disease, and 0.20 % from nervous system disease. There may be a "safe" threshold in the ozone-mortality association, which may be between 60 and 100 µg/m3, and vary by cause of death. Women and older adults (especially those over 75) are more affected by short-term ozone exposure. Populations in North China had a higher risk of ozone-related circulatory mortality, while populations in South China had a higher risk of ozone-related respiratory mortality. CONCLUSIONS: National findings link short-term ozone exposure to premature death from circulatory, respiratory, neurological, and urinary diseases, and provide evidence for a potential "safe" threshold in the association of ozone and mortality. These findings have important implications for helping policymakers tighten the relevant air quality standards and developing early warning systems for public health protection in China.

Assessment of the temporal variability and health risk of atmospheric particle-phase polycyclic aromatic hydrocarbons in a northeastern city in China.

In this study, we examined the sources and temporal variability of 16 polycyclic aromatic hydrocarbons (PAHs) found in fine particulate matter (PM2.5) in a typical industrial city in northern China. We also evaluated the incremental lifetime cancer risk (ILCR) from the inhalation of these PAHs. Atmospheric PM2.5 samples were collected for 7 consecutive days each month from 2014 to 2019, and the 16 PAHs were measured using multiplex gas chromatography-tandem mass spectrometry. The carcinogenic risk of PAH exposure was assessed using the inhalation unit risk (IUR) and cancer slope factor (CSF) methods. The annual average concentrations of PM2.5 for each year from 2014 to 2019 were 102.87±55.25, 86.92±60.43, 69.17±37.74, 58.20±59.15, 56.01±34.52, and 52.54±58.15 µg m-3, and the annual average ΣPAH concentrations were 56.03±81.09, 47.99±79.30, 40.41±57.31, 33.57±51.79, 43.23±74.80, and 25.20±50.91 ng m-3, respectively. Source identification, using diagnostic ratio analysis, indicated that the major PAH sources were coal/biomass combustion, fuel combustion, and traffic emissions. A health risk assessment showed that the ILCR from PAH inhalation decreased throughout the study period and varied with age. The IUR and CSF methods both showed that the adult ILCR exceeded 1.0×10-6. These findings demonstrate the importance of addressing the carcinogenic risk of PM2.5-bound PAHs, particularly in adults.