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Background: Exposure to ambient fine particulate matter (PM2.5) has been associated with reduced human fecundity. However, the attributable burden has not been estimated for low- and middle-income countries (LMICs), where the exposure–response function between PM2.5 and the infertility rate has been insufficiently studied. Objective: This study examined the associations between long-term exposure to PM2.5 and human fecundity indicators, namely the expected time to pregnancy (TTP) and 12-month infertility rate (IR), and then estimated PM2.5-attributable burden of infertility in LMICs. Methods: We analyzed 164,593 eligible women from 100 Demographic and Health Surveys conducted in 49 LMICs between 1999 and 2021. We assessed PM2.5 exposures during the 12 months before a pregnancy attempt using the global satellite-derived PM2.5 estimates produced by Atmospheric Composition Analysis Group (ACAG). First, we created a series of pseudo-populations with balanced covariates, given different levels of PM2.5 exposure, using a matching approach based on the generalized propensity score. For each pseudo-population, we used 2-stage generalized Gamma models to derive TTP or IR from the probability distribution of the questionnaire-based duration time for the pregnancy attempt before the interview. Second, we used spline regressions to generate nonlinear PM2.5 exposure–response functions for each of the two fecundity indicators. Finally, we applied the exposure–response functions to estimate number of infertile couples attributable to PM2.5 exposure in 118 LMICs. Results: Based on the Gamma models, each 10 µg/m3 increment in PM2.5 exposure was associated with a TTP increase by 1.7 % (95 % confidence interval [CI]: -2.3 %–6.0 %) and an IR increase by 2.3 % (95 %CI: 0.6 %–3.9 %). The nonlinear exposure–response function suggested a robust effect of an increased IR for high-concentration PM2.5 exposure (>75 µg/m3). Based on the PM2.5-IR function, across the 118 LMICs, the number of infertile couples attributable to PM2.5 exposure exceeding 35 µg/m3 (the first-stage interim target recommended by the World Health Organization global air quality guidelines) was 0.66 million (95 %CI: 0.061–1.43), accounting for 2.25 % (95 %CI: 0.20 %–4.84 %) of all couples affected by infertility. Among the 0.66 million, 66.5 % were within the top 10 % high-exposure infertile couples, mainly from South Asia, East Asia, and West Africa. Conclusion: PM2.5 contributes significantly to human infertility in places with high levels of air pollution. PM2.5-pollution control is imperative to protect human fecundity in LMICs.

Background: In the 21st century, China experienced a rapid increase in urbanization, which has enhanced medical service availability, but has also increased exposure to adverse environmental and socioeconomic factors. Urbanization-related factors can affect the prognosis of stroke patients, particularly the progression of neurological disabilities. However, the overall association between urbanization and post-stroke disability remains unknown. Method: A total of 21,678 stroke patients were selected from the China National Stroke Screening Survey (2013–2018); all included patients had at least one follow-up record. The modified Rankin Scale (mRS), a clinician-reported functional outcome measure for recovery from stroke, was utilized to assess post-disability at each visit. A larger mRS score means severer disability. The urbanization level before each visit was evaluated based on 5-year average satellite measurements of night-time light (NTL) or urban land cover (i.e., proportion of impervious surface). We used a fixed-effects model to estimate the association between urbanization level and risk of disability (i.e., mRS score). The non-linear relationship was modelled by penalized spline functions. Results: According to linear models with multivariate adjustment, every 10 digital number (DN) increment in NTL was associated with a 0.050 (95% confidence interval [CI]: 0.026, 0.074) increase in mRS score, and every 10% increment in impervious surface was associated with a 0.052 (95% CI: 0.034, 0.070) increase in mRS score. The association was stronger in patients diagnosed with atrial fibrillation, dyslipidemia, hypertension, or diabetes compared with the corresponding reference group. Non-linear analysis showed a U-shaped relationship between urbanization and the mRS score, which indicates that high and low urbanization levels were both associated with an increased risk of post-stroke disability. Conclusions: Our study revealed a complex association between urbanization and post-stroke disability. The optimal level of urbanization to prevent neurological disabilities in stroke patients could be inferred from the U-shaped curve. The reasons for the complex association between urbanization and post-stroke disability should be further explored to establish causality.

Gestational exposure to ambient fine particles increases the risk of stillbirth, but the related disease burden is unknown, particularly in low- and middle-income countries (LMICs). Here, the authors combine state-of-the-art estimates on stillbirths, and multiple exposure–response functions to evaluate the burden in 137 countries.

Background: Low birthweight attributable to fine particulate matter (PM2.5) exposure is a global issue affecting infant health, especially in low- and middle-income countries (LMICs). However, large-population studies of multiple LMICs are lacking, and little is known about whether the source of PM2.5 is a determinant of the toxic effect on birthweight. Objective: We examined the effect on birthweight of long-term exposure to PM2.5 from different sources in LMICs. Methods: The birthweights of 53,449 infants born between September 16, 2017 and September 15, 2018 in 17 LMICs were collected from demographic and health surveys. Long-term exposure to PM2.5 in 2017 produced by 20 different sources was estimated by combining chemical transport model simulations with satellite-based concentrations of total mass. Generalized linear regression models were used to investigate the associations between birthweight and each source-specific PM2.5 exposure. A multiple-pollutant model with a ridge penalty on the coefficients of all 20-source-specific components was employed to develop a joint exposure–response function (JERF) of the PM2.5 mixtures. The estimated JERF was then used to quantify the global burden of birthweight reduction attributable to PM2.5 mixtures and to PM2.5 from specific sources. Results: The fully adjusted single-pollutant model indicated that exposure to a 10 μg/m3 increase in total PM2.5 was significantly associated with a −6.6 g (95% CI –11.0 to –2.3) reduction in birthweight. In single- and multiple-pollutant models, significant birthweight changes were associated with exposure to PM2.5 produced by international shipping (SHP), solvents (SLV), agricultural waste burning (GFEDagburn), road transportation (ROAD), waste handling and disposal (WST), and windblown dust (WDUST). Based on the global average exposure to PM2.5 mixtures, the JERF showed that the overall change in birthweight could mostly be attributed to PM2.5 produced by ROAD (–37.7 g [95% CI –49.2 to –24.4] for a global average exposure of 2.2 μg/m3), followed by WST (–27.5 g [95% CI –42.6 to –10.7] for a 1.6-μg/m3 exposure), WDUST (–19.5 g [95% CI –26.7 to –12.6] for a 8.6-μg/m3 exposure), and SHP (–19.0 g [95% CI –32.3 to –5.7] for a 0.2-μg/m3 exposure), which, with the exception of WDUST, are anthropogenic sources. The changes in birthweight varied geographically and were co-determined by the concentration as well as the source profile of the PM2.5 mixture. Conclusion: PM2.5 exposure is associated with a reduction in birthweight, but our study shows that the magnitude of the association differs depending on the PM2.5 source. A source-targeted emission-control strategy that considers local features is therefore critical to maximize the health benefits of air quality improvement, especially with respect to promoting maternal and child health.

Background: Fine particulate matter (PM2.5) produced by landscape fires is thought to be more toxic than that from non-fire sources. However, the effects of “fire-sourced” PM2.5 on acute respiratory infection (ARI) are unknown. Methods: We combined Demographic and Health Survey (DHS) data from 48 countries with gridded global estimates of PM2.5 concentrations from 2003 to 2014. The proportions of fire-sourced PM2.5 were assessed by a chemical transport model using a variety of PM2.5 source data. We tested for associations between ARI and short-term exposure to fire- and “non-fire-sourced” PM2.5 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 PM2.5 and ARI using a two-dimensional spline function. Results: The study included 36,432 children under 5 years who reported ARI symptoms. Each 1 µg/m3 increment of fire-sourced PM2.5 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 PM2.5 from non-fire sources (3.1 %; 95 % CI 2.4, 3.7). The association between ARI and total PM2.5 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 PM2.5, but especially by the former. Conclusions: PM2.5 produced by landscape fire was more strongly associated to ARI among children under 5 years than that from non-fire sources.

Introduction: Exposure to greenspace has been reported to reduce stroke mortality, but there is a lack of evidence regarding poststroke disability. This study aimed to investigate the association between long-term greenspace exposure and the risk of poststroke disability. Methods: Based on the China National Stroke Screening Survey from 2013 to 2019, a total of 65,892 visits from 28,085 stroke survivors with ≥ 2 visits were included in this longitudinal study. Long-term greenspace exposure was assessed by a 3-year average of the Normalized Difference Vegetation Index (NDVI) and the proportion of green land cover according to participants’ residential communities. Poststroke functional status was assessed with the modified Ranking Score (mRS) at each visit; a cutoff score > 2 indicated disability. Fixed effects regressions were used to examine the association of greenspace exposure with continuous mRS scores or binary indicators for disability. Results: The annual mean NDVI value was 0.369 (standard deviation = 0.120) for all visits among stroke survivors. With full adjustments, each 0.05 increase in NDVI was associated with a 0.056-unit (95 % confidence interval (CI): 0.034, 0.079) decrease in the mRS score and a 46.6 % (95 % CI: 10.0 %, 68.3 %) lower risk of poststroke disability. An L-shaped curve was observed for the nonlinear associations between NDVI and mRS score or disability. Additionally, each 1 % increase in grasslands, savannas, forest, and croplands was associated with 0.008- (95 % CI: 0.002, 0.014), 0.003- (95 % CI: 0.001, 0.005), 0.001- (95 % CI: −0.015, 0.018), and 0.002-unit (95 % CI: −0.003, 0.007) decreases in the mRS score, respectively. Conclusions: Increasing greenspace was inversely associated with mRS score. Greenspace planning can be a potential intervention to prevent poststroke disability.

Background: 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. Method: 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 (PM2.5) attributable to landscape fires, estimated using a global atmospheric model. Three pairwise associations between fire-sourced PM2.5, 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. Results: After adjustments for multiple confounders, each 1-µg/m3 increase in gestational exposure to fire-sourced PM2.5 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 PM2.5 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 PM2.5 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. Conclusion: In low- and middle-income countries, gestational exposure to LFS can increase mortality during infancy; appropriate interventions are needed to promote health in childhood.

Open fires can increase heavy exposure to hazardous particulate matters, and thus harm human health, particularly among the vulnerable individuals, such as pregnant women. Here, the authors show an association between maternal exposure to fire smoke and increased risk of pregnancy loss in South Asia.

Background. Increasing evidence from human studies has revealed the adverse impact of ambient fine particles (PM2.5) on health outcomes related to metabolic disorders and distant organs. Whether exposure to ambient PM2.5 leads to kidney impairment remains unclear. The rapid air quality improvement driven by the clean air actions in China since 2013 provides an opportunity for a quasiexperiment to investigate the beneficial effect of PM2.5 reduction on kidney function. Methods. Based on two repeated nationwide surveys of the same population of 5115 adults in 2011 and 2015, we conducted a difference-in-difference study. Variations in long-term exposure to ambient PM2.5 were associated with changes in kidney function biomarkers, including estimated glomerular filtration rate by serum creatinine (GFRscr) or cystatin C (GFRcys), blood urea nitrogen (BUN), and uric acid (UA). Results. For a 10 μg/m3 reduction in PM2.5, a significant improvement was observed for multiple kidney functional biomarkers, including GFRscr, BUN and UA, with a change of 0.42 (95% confidence interval [CI]: 0.06, 0.78) mL/min/1.73m2, -0.38 (-0.64, -0.12) mg/dL, and -0.06 (-0.12, -0.00) mg/dL, respectively. A lower socioeconomic status, indicated by rural residence or low educational level, enhanced the adverse effect of PM2.5 on kidney function. Conclusions. These results support a significant nephrotoxicity of PM2.5 based on multiple serum biomarkers and indicate a beneficial effect of improved air quality on kidney function.

Background: Maternal exposure to ambient fine particulate matter (PM2.5) is a potential risk factor for pregnancy loss, but the extant findings are inconsistent. One reason for the inconsistency is the difficulty of distinguishing spontaneous from induced pregnancy losses, particularly in countries with planning policies. Objective: To examine the association between maternal PM2.5 exposure and spontaneous incident pregnancy loss in China. Methods: A total of 18,513 women of reproductive age was recruited from Jiangsu Province, China, in 2007. Among them, 2451 women reported 2613 valid records of incident pregnancies from 2007 to 2010. We used Cox regression to link the outcomes (live birth, spontaneous pregnancy loss, or induced abortion) of those incident pregnancies with maternal PM2.5 exposures, assessed using well-developed estimates of historical concentrations at the county level. Results: Among the 2613 incident pregnancies, 69 spontaneous pregnancy losses, 596 induced abortions, and 1948 live births occurred. According to the adjusted model, each 10-μg/m3 increment in the average PM2.5 concentration during pregnancy was associated with a 43.3% (95% confidence interval, 6.6–92.5%) increased probability of spontaneous pregnancy loss. Advanced maternal age, a potential competing risk factor, weakened the association between PM2.5 and spontaneous pregnancy loss. The association was nonsignificant for unintended pregnancies. Conclusion: Maternal PM2.5 exposure was associated significantly with incident spontaneous pregnancy loss. Our findings provide insight into the harmful effect of air pollution on human reproduction.

Background: Landscape fire smoke (LFS) has been associated with reduced birthweight, but evidence from low- and middle-income countries (LMICs) is rare. Methods: Here, we present a sibling-matched case–control study of 227,948 newborns to identify an association between fire-sourced fine particulate matter (PM2.5) and birthweight in 54 LMICs from 2000 to 2014. We selected mothers from the geocoded Demographic and Health Survey with at least two children and valid birthweight records. Newborns affiliated with the same mother were defined as a family group. Gestational exposure to LFS was assessed in each newborn using the concentration of fire-sourced PM2.5. We determined the associations of the within-group variations in LFS exposure with birthweight differences between matched siblings using a fixed-effects regression model. Additionally, we analyzed the binary outcomes of low birthweight (LBW) or very low birthweight (VLBW). Results: According to fully adjusted models, a 1 µg/m3 increase in the concentration of fire-sourced PM2.5 was significantly associated with a 2.17 g (95% confidence interval [CI] 0.56–3.77) reduction in birthweight, a 2.80% (95% CI 0.97–4.66) increase in LBW risk, and an 11.68% (95% CI 3.59–20.40) increase in VLBW risk. Conclusions: Our findings indicate that gestational exposure to LFS harms fetal health. Funding: PKU-Baidu Fund, National Natural Science Foundation of China, Peking University Health Science Centre, and CAMS Innovation Fund for Medical Sciences.

Background: Although epidemiological studies on the effect of chronic fine particulate matter (PM2.5) exposure on lipid disorders have been conducted, it is unclear if improved air quality is associated with beneficial changes in the blood lipid profile. In China, clean air actions introduced in 2013 have rapidly reduced the concentration of ambient PM2.5. Methods: We conducted a change-by-change study, based on two waves (2011 and 2015) of a national survey of the same 5111 Chinese adults before and after implementation of the clean air actions. Long-term PM2.5 exposure was assessed using a state-of-the-art estimator at the city level. Based on the within-individual differences between the two waves, we associated PM2.5 changes with the variations of four lipid biomarkers—triglycerides (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C)—using a mixed-effects regression model. The robustness and homogeneity of the association were tested via sensitivity analyses. Results: For each 10 μg/m3 reduction in PM2.5, LDL-C, and TC decreased by 2.71 (95% confidence interval [CI] 0.10–5.32) and 4.16 (95% CI 1.24–7.08) mg/dL, respectively. There was no significant association with HDL-C or TG. The results were robust among models adjusted for different covariates. PM2.5 was a significant risk factor for dyslipidemia with an adjusted relative risk of 1.21 (95% CI 1.09–1.34). The association between PM2.5 and LDL-C was stronger in the elderly or adults who did not take medications. Conclusions: The results suggest that PM2.5 exert a cardiotoxic effect by increasing the risk of lipid disorders. Improvement of air quality could prevent dyslipidemia by reducing LDL-C and TC levels. Clean air policies should be implemented as public health measures in countries with aging societies, especially developing ones with a high air pollution burden.

Exposure to ozone (O3) is associated with stroke incidence and mortality. However, whether long-term exposure to O3 is associated with post-stroke neurological disability remains unknown. This study investigated the relationship based on the longitudinal analysis of China National Stroke Screening Survey (CNSSS), which included 65,778 records of stroke patients. All of the analyzed patients were followed-up at least twice. Stroke disability was assessed using the modified Rankin scale (mRS). Long-term exposure was assessed by the peak-season or annual mean of maximum 8-h O3 concentrations for 365 days before the mRS measurement. We used fixed-effect models to evaluate the associations between O3 and mRS score, with adjustment for multiple confounders, and found a 10 µg/m3 increase in peak-season O3 concentration was associated with a 0.0186 (95% confidence interval [CI] 0.0115–0.0256) increment in the mRS score. The association was robust in various subpopulations. For secondary outcomes, for each 10 µg/m3 increment in peak-season O3, the odds ratio of an increased mRS score (vs. unchanged or decreased mRS score) increased by 23% (95% CI 9–37%). A nonlinear analysis showed a sublinear association between O3 exposure and risk for post-stroke disability. A saturation effect was observed at an O3 concentration of more than ~120 μg/m3. Our study adds to evidence that long-term exposure to O3 increases the risk of neurological disability after stroke.