Facemasks are increasingly worn during air pollution episodes in China, but their protective effects are poorly understood. We aimed to evaluate the filtration efficiencies of N95 facemasks and the cardiopulmonary benefits associated with wearing facemasks during episodes of pollution. We measured the filtration efficiencies of particles in ambient air of six types of N95 facemasks with a manikin headform. The most effective one was used in a double-blind, randomized, controlled crossover study, involving 15 healthy young adults, conducted during 2 days of severe pollution in Beijing, China. Subjects were asked to walk along a busy-traffic road for 2 h wearing authentic or sham N95 facemasks. Clinical tests were performed four times to determine changes in the levels of biomarkers of airway inflammation, endothelial dysfunction, and oxidative stress within 24 h after exposure. The facemasks removed 48–75% of number concentrations of ambient air particles between 5.6 and 560 nm in diameter. After adjustments for multiple comparison, the exhaled nitric oxide level and the levels of interleukin-1α, interleukin-1β, and interleukin-6 in exhaled breath condensate increased significantly in all subjects; however, the increases in those wearing authentic facemasks were statistically significantly lower than in the sham group. No significant between-group difference was evident in the urinary creatinine-corrected malondialdehyde level. In arterial stiffness indicators, the ejection duration of subjects wearing authentic facemasks was higher after exposure compared to the sham group; no significant between-group difference was found in augmentation pressure or the augmentation index. In young healthy adults, N95 facemasks partially reduced acute particle-associated airway inflammation, but neither systemic oxidative stress nor endothelial dysfunction improved significantly. The clinical significance of these findings long-term remains to be determined. The trial registration number (TRN) for this study is ChiCTR1800016099 , which was retrospectively registered on May 11, 2018.

Gestational hypertension (GH), preeclampsia (PE), and gestational diabetes mellitus (GDM) are common pregnancy complications and can result in maternal and prenatal morbidity and mortality. Air pollution exposure could adversely impact pregnancy complications; however, evidence remains limited in China, where ambient air pollution is relatively severe. This study aims to examine the associations of GH, PE, and GDM with exposure to six air pollutants (PM_2.5, PM₁₀, SO₂, NO₂, O₃, and CO) during pregnancy. Leveraging a multicenter birth cohort study among pregnant women in 24 hospitals from 15 provinces in China, we obtained data for maternal characteristics and pregnancy outcomes. We generated ambient concentrations of the six air pollutants using a combination of chemical transport model simulations with monitoring data. We used multivariable logistic regression models to estimate the effects on pregnancy complications from exposure to six air pollutants in each trimester and the entire pregnancy. Among the total 3754 pregnant women in this study, the prevalences of GH, GDM, and PE were 2.6 %, 11.2 %, and 0.7 %, respectively. GH risk increased 11.9 % (95 % CI, -8.5 %, 36.8 %) and 13.8 % (1.4 %, 27.8 %) per 10 μg/m³ increases in PM_2.5 and PM₁₀ in the entire pregnancy, respectively. PM_2.5 and PM₁₀ exposures in the first trimester were significantly associated with an increased risk of GDM. Exposure to O₃, SO₂, NO₂, and CO in early pregnancy could be associated with GDM risk. Geographic region and season of conception may influence the associations of GH and PE with air pollution. Ambient particulate matter pollution adversely affects GH, GDM, and PE among Chinese pregnant women. Since most regions of China still suffer from hazardous levels of air pollution, our findings indicate importance of better protecting pregnant women from the risk of air pollution.

Fine particulate matter (PM_2.5) produced by landscape fires is thought to be more toxic than that from non-fire sources. However, the effects of "fire-sourced" PM_2.5 on acute respiratory infection (ARI) are unknown. We combined Demographic and Health Survey (DHS) data from 48 countries with gridded global estimates of PM_2.5 concentrations from 2003 to 2014. The proportions of fire-sourced PM_2.5 were assessed by a chemical transport model using a variety of PM_2.5 source data. We tested for associations between ARI and short-term exposure to fire- and "non-fire-sourced" PM_2.5 using a bidirectional case-crossover analysis. The robustness and homogeneity of the associations were examined by sensitivity analyses. We also established a nonlinear exposure-response relationship between fire- and non-fire-sourced PM_2.5 and ARI using a two-dimensional spline function. The study included 36,432 children under 5 years who reported ARI symptoms. Each 1 µg/m³ increment of fire-sourced PM_2.5 was associated with a 3.2 % (95 % confidence interval [CI] 0.2, 6.2) increment in the risk of ARI. This effect was comparable to that of each ∼5 µg/m³ increment in PM_2.5 from non-fire sources (3.1 %; 95 % CI 2.4, 3.7). The association between ARI and total PM_2.5 concentration was significantly mediated by the proportion of fire-sourced particles. Nonlinear analysis showed that the risk of ARI was increased by both fire- and non-fire-sourced PM_2.5, but especially by the former. PM_2.5 produced by landscape fire was more strongly associated to ARI among children under 5 years than that from non-fire sources.

Exposure to landscape fire smoke (LFS) is linked to child mortality and birthweight. It is unknown whether gestational exposure to LFS affects child survival rate. We aimed to link under-five death (U5D) to gestational LFS exposure by performing a causal mediation analysis based on birthweight. We conducted a sibling-matched case-control study of children under 5 years of age who were affiliated with the same mothers from Demographic and Health Surveys in 54 low- and middle-income countries, during the period from 2000 to 2014. LFS exposure was quantified as the surface concentration of fine particulate matter (PM_2.5) attributable to landscape fires, estimated using a global atmospheric model. Three pairwise associations between fire-sourced PM_2.5, birthweight, and U5D were assessed using fixed-effects regressions. We used a bootstrap-based mediation test of regression coefficients to examine whether the LFS-birthweight-U5D pathway was statistically significant. We also conducted three pairwise exposure-response functions using nonlinear models and used them to estimate the pathway-specific disease burden from 2000 to 2014. After adjustments for multiple confounders, each 1-µg/m³ increase in gestational exposure to fire-sourced PM_2.5 was associated with a reduction of 2.179 (95% confidence interval [CI]: -3.777, -0.580) g in birthweight. Each 1-g birthweight reduction was associated with a 0.072% (95% CI: 0.065%, 0.078%) increase in U5D. Furthermore, each increase in exposure to fire-sourced PM_2.5 was associated with a 2.853% (95% CI: 0.835%, 4.911%) increase in U5D; 7.294% (95% CI: 0.710%, 24.254%) of the linkage was explained by LFS-attributable birthweight reduction. Based on the estimated exposure-response functions, from 2000 to 2014, global exposure to fire-sourced PM_2.5 contributed a mean birthweight reduction of 10.30 (95% CI: 2.93, 19.47) g, contributing to 60,350 (18,111, 106,619) premature U5Ds annually. In low- and middle-income countries, gestational exposure to LFS can increase mortality during infancy; appropriate interventions are needed to promote health in childhood.