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Abstrct A composite Air Health Index (AHI) is helpful for separately emphasizing the health risks of multiple stimuli and communicating the overall risks of an adverse atmospheric environment to the public. We aimed to establish a new AHI by integrating daily mortality risks due to air pollution with those due to non-optimum temperature in China. Based on the exposure-response (E-R) coefficients obtained from time-series models, the new AHI was constructed as the sum of excess mortality risk associated with air pollutants and non-optimum temperature in 272 Chinese cities from 2013 to 2015. We examined the association between the “total AHI” (based on total mortality) and total mortality, and further compared the ability of the “total AHI” to predict specific cardiopulmonary mortality with that of “specific AHIs” (based on specific mortalities). On average, air pollution and non-optimum temperature were associated with 28.23% of daily excess mortality, of which 23.47% was associated with non-optimum temperature while the remainder was associated with fine particulate matter (PM2.5) (1.12%), NO2 (2.29%,), and O3 (2.29%). The new AHI uses a 10-point scale and shows an average across all 272 cities of 6 points. The E-R curve for AHI and mortality is approximately linear, without any thresholds. Each one unit increase in “total AHI” is associated with a 0.84% increase in all-cause mortality and 1.01%, 0.98%, 1.02%, 1.66%, and 1.71% increases in cardiovascular disease, coronary heart disease, stroke, respiratory diseases, and chronic obstructive pulmonary disease mortality, respectively. Cause-specific mortality risk estimates using the “total AHI” are similar to those predicted by “specific AHIs”. In conclusion, the “total AHI” proposed herein could be a promising tool for communicating health risks related to exposure to the ambient environment to the public.

It remains unclear whether carbon content in airway macrophages (AM) can predict personal short-term exposure to fine particulate matter (PM2.5) air pollution and its respiratory health effects. We aimed to evaluate the pathway from personal PM2.5 exposure to adverse respiratory outcomes through AM carbon content. We designed a longitudinal panel study with 3 scheduled follow-ups among 113 non-smoking patients of chronic obstructive pulmonary disease in Shanghai, China, from April 2017 to January 2019. We quantified AM carbon content from induced sputum by image analysis, tested lung function and measured sputum levels of 4 pro-inflammatory cytokines and 2 anti-inflammatory cytokines. We applied the “meet in the middle” approach incorporating linear mixed-effect models to evaluate the associations from external PM2.5 exposure to respiratory outcomes through AM carbon content. Our results indicated that personal exposure to PM2.5 within 24 h was significantly associated with decreased forced expiratory volume in 1s and anti-inflammatory cytokines, as well as increased macrophages and pro-inflammatory cytokines. These changes were accompanied by increased areas of AM carbon and higher percentage of AM area occupied by carbon, both of which were associated with increased levels of pro-inflammatory cytokines and decreased levels of anti-inflammatory cytokines. Exposure to ambient black carbon and organic carbon in PM2.5 within 2 days was significantly associated with increased AM carbon area and percentage of AM area occupied by carbon. Our findings reinforced the causality in respiratory health effects of PM2.5 in which increased AM carbon content might serve as a valid exposure biomarker.

Background Previous studies have suggested acute effects of ambient fine particulate matter (PM2.5) air pollution on respiratory health among children, but evidence for PM2.5 constituents and respiratory health were still limited. Objectives To investigate associations of short-term exposure to PM2.5 and its constituents with airway inflammation, lung function, and airway microbiota in children. Methods We conducted a longitudinal panel study with 3 repeated health measurements among 62 children in Shanghai, China from November 2018 to June 2019. Respiratory health was measured by fractional exhaled nitric oxide (FeNO), saliva tumor necrosis factor-α (TNF-α), lung function (forced vital capacity and forced exhaled volume in 1 s), and microbiota diversity in buccal mucosa samples. Based on the linear mixed-effect models, we applied the single-constituent models and the constituent-PM2.5 adjustment models to examine the associations between PM2.5 constituents and health outcomes. Result Short-term exposure to PM2.5 was associated with higher TNF-α, FeNO levels and reduced lung function. Among all constituents, organic carbon, elemental carbon, NO3− and NH4+ had the consistent and strongest associations with airway inflammation biomarkers and lung function parameters, followed by metallic elements. We also found short-term PM2.5 exposure was associated with decreased diversity in buccal mucosa bacterial community and two bacterial phyla, Fusobacteria and Proteobacteria, were identified as differential microbes with PM2.5 exposure. Conclusion Short-term exposure to PM2.5 may impair children's respiratory health represented by higher airway inflammation, lower lung function and altered buccal mucosa microbial colonization. Organic carbon, elemental carbon, NO3− and NH4+ may dominate these effects.

Background Combined atmospheric oxidant capacity (Ox), represented by the sum of nitrogen dioxide (NO2) and ozone (O3), is an important hazardous property of outdoor air pollution mixture. It remains unknown whether its adverse effects can be ameliorated by dietary fish-oil supplementation. Objective To assess the effects of fish-oil supplementation against oxidative stress induced by acute Ox exposure. Methods We conducted a randomized, double-blinded and placebo-controlled study among 65 young adults in Shanghai, China between September 2017 and January 2018. We randomly assigned participants to receive either 2.5 g/day of fish oil or placebo, and conducted four repeated physical examinations during the last two months of treatments. Ox concentrations were calculated as the sum of hourly measurements of NO2 and O3. We measured six biomarkers on systemic oxidative stress and antioxidant activity. Linear mixed-effect models were used to assess the short-term effects of Ox on biomarkers in each group. Results During our study period, the 72-h average Ox concentration was 93.6 μg/m3. Short-term exposure to Ox led to weaker changes in all biomarkers in the fish oil group than in the placebo group. Compared with the placebo group, for a 10-μg/m3 increase in Ox, there were smaller decrements in myeloperoxidase (MPO, difference = 5.92%, lag = 0–2 d, p = 0.03) and malondialdehyde (MDA, difference = 5.00%, lag = 1 d, p = 0.04) in the fish-oil group; there were also larger increments in total antioxidant capacity (TAC, difference = 16.33%, lag = 2 d, p = 0.02) and in glutathione peroxidase (GSH-Px, difference = 8.89%, lag = 0–2 d, p = 0.03) in the fish-oil group. The estimated differences for MPO were robust to adjustment for all co-pollutants and the differences for other biomarkers remained for some co-pollutants. Conclusions This trial provides first-hand evidence that dietary fish-oil supplementation may alleviate the systemic oxidative stress induced by Ox.

Particulate matter (PM) is the most important air pollution problem that leads to substantial health effects. However, very few studies focused on the effects of ultrafine particles (UFPs, particles0.1 μm) on children respiratory health. We performed a panel study with 3 rounds of follow-up among 65 pupils at the Elementary School Affiliated to Shanghai Normal University in China from November 2018 to June 2019. Real-time concentrations of UFPs were measured in the campus. In each visit, we detected biomarkers in saliva and microflora in buccal mucosa, fractional exhaled nitric oxide (FeNO) and lung function. We applied a linear mixed-effect (LME) model to examine the associations of UFPs and each health outcome. We found increased levels of FeNO and tumor necrosis factor-α (TNF-α) and reduced lung function in association with higher UFP exposure. For each interquartile range increase of UFPs, the largest changes were found in lag 0-72 h for forced vital capacity [-69.02 ml (95% CI: -114.20, -23.84)], TNF-α [13.41 pg/ml (95% CI: 7.08, 19.73)], and FeNO [26.85% (95% CI: 11.84%, 43.88%)]. UFP exposure was associated with reduced diversity in buccal microflora with largest reduction in lag 0-72 h [12.24 (95% CI: 7.76, 16.71) for Ace index; 8.78 (95% CI: 2.96, 14.60) for Chao1 index]. UFP exposure was also associated with increased Streptococcus, Gemella, and decreased Actinomyces. Short-term UFP exposures may impair the respiratory system by inducing inflammation, decreasing lung function and attenuating buccal microbe diversity in children.

Background Few studies have investigated respiratory effects of particulate matter air pollution using a full range of particle size distribution. Objectives To explore the short-term associations between size-fractionated particle number concentration (PNC) and chronic obstructive pulmonary disease (COPD) mortality. Methods We conducted a time-series study to explore the associations between size-fractionated PNC and daily COPD mortality in the Pudong New Area of Shanghai, China, from 2014 to 2016. We evaluated particle size distribution from 0.01 μm to 10 μm, which was segregated into 7 ranges to better explore the size-dependent associations. We used over-dispersed generalized additive models to estimate the associations after controlling for time trends, temperature, humidity, day of the week and holidays. Results A total of 5430 deaths due to COPD were identified during the study period. For size ranges from 2.5 – 10 μm, 1–2.5 μm to 0.3–1 μm, there were stronger associations between PNC and COPD mortality, but the associations were statistically insignificant. However, for the smaller size ranges from 0.3 to 0.01 μm, the associations became statistically significant and the magnitude of association remained stable. An interquartile range increase in PNC at lag 0–1 day for size ranges 0.01–0.03 μm, 0.03–0.05 μm, 0.05–0.1 μm and 0.1–0.3 μm was associated with increments of 4.44% (95% CI: 1.16%, 7.73%), 4.31% (95% CI: 1.16%, 7.47%), 4.22% (95% CI: 1.05%, 7.40%), and 4.28% (95% CI: 0.48%, 8.09%) in COPD mortality, respectively. Conclusion This study suggested that particles below 0.3 μm in diameter might be mainly responsible for the adverse effect of particulate air pollution on CDPD mortality in Shanghai, China.