Stillbirths Associated with Particle Pollution are Disproportionally Contributed by Sand Dust: Findings from 52 Low- and Middle-Income Countries.

Whether maternal exposure to dust-sourced particulate matter (hereafter, dust PM2.5) is associated with stillbirth remains unknown. We adopted a sibling-matched case-control design to analyze 9332 stillbirths and 17,421 live births. We associated the risk of stillbirth simultaneously with dust and nondust components of PM2.5 and developed a nonlinear joint exposure-response function. Next, we estimated the burden of stillbirths attributable to the PM2.5 mixture. The concentration index was used to evaluate whether the burden of PM2.5-related stillbirths was disproportionally distributed among pregnancies exposed to dust-rich particles. Each 10 µg/m3 increase in dust PM2.5 was associated with a 14.5% (95% confidence interval: 5.5, 24.2%) increase in the odds of stillbirth. Based on the risk assessment across 137 countries, sand dust contributed to about 15% of the PM2.5 exposure but to about 45% of the PM2.5-related stillbirths during 2003-2019. In 2015, 30% of the PM2.5-related stillbirths were concentrated within 15% of pregnancies exposed to the dust-richest PM2.5. The index increased in subregions, such as South Asia, suggesting the growth of health inequality due to exposure to dust PM2.5. Based on our findings, land management, such as halting desertification, will help prevent stillbirths and reduce global maternal health inequality.

Gestational exposure to wildfire PM2.5 and its specific components and the risk of gestational hypertension and eclampsia in the southwestern United States.

In the southwestern United States, the frequency of summer wildfires has elevated ambient PM2.5 concentrations and rates of adverse birth outcomes. Notably, hypertensive disorders in pregnancy (HDP) constitute a significant determinant associated with maternal mortality and adverse birth outcomes. Despite the accumulating body of evidence, scant research has delved into the correlation between chemical components of wildfire PM2.5 and the risk of HDP. Derived from data provided by the National Center for Health Statistics, singleton births from >2.68 million pregnant women were selected across 8 states (Arizona, AZ; California, CA, Idaho, ID, Montana, MT; Nevada, NV; Oregon, OR; Utah, UT, and Wyoming, WY) in the southwestern US from 2001 to 2004. A spatiotemporal model and a Goddard Earth Observing System chemical transport model were employed to forecast daily concentrations of total and wildfire PM2.5-derived exposure. Various modeling techniques including unadjusted analyses, covariate-adjusted models, propensity-score matching, and double robust typical logit models were applied to assess the relationship between wildfire PM2.5 exposure and gestational hypertension and eclampsia. Exposure to fire PM2.5, fire-sourced black carbon (BC) and organic carbon (OC) were associated with an augmented risk of gestational hypertension (ORPM2.5 = 1.125, 95 % CI: 1.109,1.141; ORBC = 1.247, 95 % CI: 1.214,1.281; OROC = 1.153, 95 % CI: 1.132, 1.174) and eclampsia (ORPM2.5 = 1.217, 95 % CI: 1.145,1.293; ORBC = 1.458, 95 % CI: 1.291,1.646; OROC = 1.309, 95 % CI: 1.208,1.418) during the pregnancy exposure window with the strongest effect. The associations were stronger that the observed effects of ambient PM2.5 in which the sources primarily came from urban emissions. Social vulnerability index (SVI), education years, pre-pregnancy diabetes, and hypertension acted as effect modifiers. Gestational exposure to wildfire PM2.5 and specific chemical components (BC and OC) increased gestational hypertension and eclampsia risk in the southwestern United States.

Burden of Child Anemia Attributable to Fine Particulate Matters Brought by Sand Dusts in Low- and Middle-Income Countries.

Addressing environmental factors has recently been recommended to curb the growing trend of anemia in low- and middle-income countries (LMICs). Fine particulate matter (PM2.5) generated by dust storms were concentrated in place with a high prevalence of anemia. In a multicounty, multicenter study, we analyzed the association between anemia and life-course averaged exposure to dust PM2.5 among children aged <5 years based on 0.65 million records from 47 LMICs. In the fully adjusted mixed effects model, each 10 µg/m3 increase in life-course averaged exposure to dust PM2.5 was associated with a 9.3% increase in the odds of anemia. The estimated exposure-response association was nonlinear, with a greater effect of dust PM2.5 exposure seen at low concentrations. Applying this association, we found that, in 2017, among all children aged <5 years in the 125 LMICs, dust PM2.5 contributed to 37.98 million cases of anemia. Results indicated that dust PM2.5 contributed a heavier burden than all of the well-identified risk factors did, except for iron deficiency. Our study revealed that long-term exposure to dust PM2.5 can be a novel risk factor, pronouncedly contributed to the burden of child anemia in LMICs, affected by land degradations or arid climate.

Reduced human fecundity attributable to ambient fine particles in low- and middle-income countries.

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.

Association between electrocardiographic abnormalities and flood exposure among middle-aged and elderly people: A national longitudinal study in China.

BACKGROUND: Flooding has become more frequent and intensive due to climate change, particularly in Asian countries. However, evidence on the long-term health effects of floods from large-scale studies on the vulnerable aged population in China is insufficient. This study analyzed the long-term effects of exposure to flood on electrocardiographic (ECG) abnormalities, a commonly used indicator of cardiovascular disease (CVD) screening, in middle-aged and elderly people. METHOD: We evaluated the Chinese National Stroke Screening Survey data of 80,711 follow-up records from 38,375 participants aged > 40 years with two or more visits between 2013 and 2018 in this longitudinal study. Flood exposure was assessed as the presence of a satellite-detected flooded area within 500 m of the residence within 5 years before the survey date. The association between ECG abnormalities and flood exposure was analyzed using a random effects model with multiple adjustments. As age is an important CVD risk factor, a varying-coefficient function was derived to estimate the nonlinear modifying effect of age on the association between ECG abnormalities and flood exposure. The strata-specific associations between ECG abnormalities and flood exposure were applied to characterize vulnerability to flood. RESULTS: The fully adjusted model suggested that flood exposure was associated with an increased risk for ECG abnormalities among the middle-aged and elderly population (odds ratio [OR] 1.74, 95 % confidence interval [CI] 1.49, 2.03). The ORs of flood exposure for ECG suggesting atrial fibrillation, ST depression, and left ventricular hypertrophy were 1.85 (95 % CI 1.16, 2.94), 6.92 (95 % CI 5.23, 9.16), and 1.55 (95 % CI 0.66, 3.65), respectively. These associations were generally robust in various subpopulations, while a sublinear curve for the negative modifying effect of age was observed on the population vulnerability to flood. CONCLUSION: Flood exposure was associated with an increased long-term risk for an ECG abnormality. The need for effective measures to mitigate vulnerability to flood is not negligible in China.

Health benefits from the rapid reduction in ambient exposure to air pollutants after China's clean air actions: progress in efficacy and geographic equality.

Clean air actions (CAAs) in China have been linked to considerable benefits in public health. However, whether the beneficial effects of CAAs are equally distributed geographically is unknown. Using high-resolution maps of the distributions of major air pollutants (fine particulate matter [PM2.5] and ozone [O3]) and population, we aimed to track spatiotemporal changes in health impacts from, and geographic inequality embedded in, the reduced exposures to PM2.5 and O3 from 2013 to 2020. We used a method established by the Global Burden of Diseases Study. By analyzing the changes in loss of life expectancy (LLE) attributable to PM2.5 and O3, we calculated the gain of life expectancy (GLE) to quantify the health benefits of the air-quality improvement. Finally, we assessed the geographic inequality embedded in the GLE using the Gini index (GI). Based on risk assessments of PM2.5 and O3, during the first stage of CAAs (2013 to 2017), the mean GLE was 1.87 months. Half of the sum of the GLE was disproportionally distributed in about one quarter of the population exposed (GI 0.44). During the second stage of CAAs (2017 to 2020), the mean GLE increased to 3.94 months and geographic inequality decreased (GI 0.18). According to our assessments, CAAs were enhanced, from the first to second stages, in terms of not only preventing premature mortality but also ameliorating health inequalities. The enhancements were related to increased sensitivity to the health effects of air pollution and synergic control of PM2.5 and O3 levels. Our findings will contribute to optimizing future CAAs.

Estimating birthweight reduction attributable to maternal ozone exposure in low- and middle-income countries.

The effect of O3 on birthweight in low- and middle-income countries (LMICs) remains unknown. A multicenter epidemiological study was conducted to evaluate the association between maternal peak-season O3 exposure and birthweight, using 697,148 singleton newborns obtained in 54 LMICs between 2003 and 2019. We estimated the birthweight reduction attributable to peak-season O3 exposure in 123 LMICs based on a nonlinear exposure-response function (ERF). With every 10-part per billion increment in O3 concentration, we found a reduction in birthweight of 19.9 g [95% confidence interval (CI): 14.8 to 24.9 g]. The nonlinear ERF had a monotonic decreasing curve, and no safe O3 exposure threshold was identified. The mean reduction in birthweight reduction attributable to O3 across the 123 LMICs was 43.8 g (95% CI: 30.5 to 54.3 g) in 2019. The reduction in O3-related birthweight was greatest in countries in South Asia, the Middle East, and North Africa. Effective O3 pollution control policies have the potential to substantially improve infant health.

Estimating the exposure-response function between long-term ozone exposure and under-5 mortality in 55 low-income and middle-income countries: a retrospective, multicentre, epidemiological study.

BACKGROUND: In 2021, WHO suggested new target concentration limits for long-term exposure to ambient ozone. However, the harmful effects of ozone on vulnerable children have not been sufficiently studied. We aimed to evaluate the association between long-term ozone exposure and mortality in children younger than 5 years (hereafter denoted under-5 mortality) in low-income and middle-income countries (LMICs) and to estimate this mortality burden for 97 LMICs. METHODS: By combining information from 128 Demographic and Health Surveys, we evaluated the association between the survival status of more than 1·2 million children younger than 5 years from 2457 sampling strata in 55 LMICs and the average peak-season ozone concentration during the life course, using a fixed-effects Cox model. A non-linear exposure-response function was developed by integrating the marginal effects of within-strata variation in exposure. We extrapolated the function obtained from the 55 LMICs to estimate the under-5 mortality burden attributable to ozone exposure in 97 LMICs, in which more than 95% of global deaths in this age group occur. FINDINGS: The fixed-effects model showed a robust association between ozone and under-5 mortality. According to the fully adjusted linear model, an increment of 10 ppb in the life-course average peak-season ozone concentration was associated with a 6·4% (95% CI 2·4-10·7) increase in the risk of under-5 mortality. The non-linear exposure-response function showed a sublinear curvature with a threshold, suggesting that the effect of ozone exposure was non-significant at concentrations lower than the first-stage interim target (100 µg/m3) recommended by WHO. Using this function, we estimate that, in 2010, long-term ozone exposure contributed to 153 361 (95% CI 17 077-276 768; 2·3% [0·3-4·1]) deaths of children younger than 5 years in 97 LMICs, which is equivalent to 56·8% of all ozone-related deaths in adults (269 785) in these countries. From 2003 to 2017, the ozone-related under-5 mortality burden decreased in most of the 97 LMICs. INTERPRETATION: Long-term exposure to ozone concentrations higher than the WHO first-stage interim target is a risk factor for under-5 mortality, and ozone exposure contributes substantially to mortality in this age group in LMICs. Increased efforts should be made to control ambient ozone pollution as this will lead to positive health benefits. FUNDING: Ministry of Science and Technology of the People's Republic of China and China National Natural Science Foundation.

Gestational age modifies the association between exposure to fine particles and fetal death: findings from a nationwide epidemiological study in the contiguous United States.

BACKGROUNDS: The vulnerability of fetuses differs at different developmental stages, in response to environmental stressors such as fine particulate matter (PM2.5), a ubiquitous air pollutant. Whether gestational age (GA) modifies the association between prenatal fine particulate matter (PM2.5) exposure and fetal death remains unclear. METHODS: We selected approximately 47.8 million eligible United States (US) livebirth and fetal death (defined as a termination at a GA of 20-43 weeks) records from 1989 to 2004. For each record, we took the level of prenatal exposure to PM2.5 as the average concentration in the mother's residential county during the entire gestational period, or a specific trimester (i.e., GA-specific exposure), according to well-established estimates of monthly levels across the contiguous US. First, we evaluated the associations between PM2.5 exposure and fetal death at a specific GA (i.e., GA-specific outcome) using five different logit models (unadjusted, covariate-adjusted, propensity-score, double robust, and diagnostic-score models). Double robust model was selected as the main model due to its advantages in causal inference. Then, we conducted meta-analyses to pool the estimated GA-specific associations, and explored how the pooled estimates varied with GA. RESULTS: According to the meta-analysis, all models suggested gestational PM2.5 exposure was associated with fetal death. However, there was slight heterogeneity in the estimated effects, as different models revealed a range of 3.6-10.7% increase in the odds of fetal death per 5-µg/m3 increment of PM2.5. Each 5-µg/m3 increase in PM2.5 exposure during the entire gestation period significantly increased the odds of fetal death, by 8.1% (95% confidence interval [CI]: 5.1-11.2%). In terms of GA-specific outcomes, the odds of fetal death at a GA of 20-27, 28-36, or ≥ 37 weeks increased by 11.0% (5.9-16.4%), 5.2% (0.4-10.1%), and 8.3% (2.5-14.5%), respectively. In terms of GA-specific exposure, the odds of fetal death increased by 6.0% (3.9-8.2%), 4.1% (3.9-8.2%), and 4.3% (0.5-8.2%) with 5-µg/m3 increases in PM2.5 exposure during the first, second, and third trimester, respectively. The association had the largest effect size (odds ratio = 1.098, 95% CI: 1.061-1.137) between PM2.5 exposure during early gestation (i.e., first trimester) and early fetal death (i.e., 20-27 weeks). CONCLUSIONS: Prenatal exposure to PM2.5 was significantly associated with an increased risk of fetal death. The association was varied by gestational-age-specific exposures or outcomes, suggesting gestation age as a potential modifier on the effect of PM2.5. The fetus was most vulnerable during the early stage of development to death associated with PM2.5 exposure.

Long-term exposure to the components of fine particulate matters and disability after stroke: Findings from the China National Stroke Screening Surveys.

BACKGROUND: Long-term exposure to ambient fine particulate matter (PM2.5) has been linked to an increased risk of stroke. However, the effect of long-term exposure to PM2.5 and its major components on the functional disability of stroke patients remains unclear. METHODS: Based on China National Stroke Screening Survey data obtained from 2013 to 2019, we conducted a national multicenter longitudinal study of the associations of long-term exposure to PM2.5 and its components with the risk of disability after stroke in China. Post-stroke disability was assessed using the modified Rankin scale (mRS), which ranges from 0 to 5, with higher scores indicating greater disability. Long-term exposure to PM2.5 and its five components [sulfate (SO42-), nitrate (NO3-), ammonium salt (NH4+), organic matter (OM), and black carbon (BC)] was determined based on average concentrations during the 3 years preceding mRS administration according to the geographic coordinates of residential communities, using state-of-the-art estimates from multiple sources. We used a fixed-effect model to evaluate the associations between mRS scores and PM2.5 exposure, with adjustment for multiple covariates. RESULTS: Every 10 µg/m3 increase in PM2.5 was associated with a 0.019 (95% confidence interval, 0.003, 0.036) increase in mRS score, but the effect was not significant after adjusting for all covariates [0.016 (95% CI, -0.003, 0.032)]. For PM2.5 components, each IQR (7.92 µg/m3) increment in OM exposure was associated significantly with 0.062 (95% CI, 0.013, 0.111) increment in the mRS score. A significant association was observed between SO42- exposure and the mRS score [0.057 (95% CI, 0.003, 0.112), per IQR: 6.28 µg/m3]. However, no significant association was found with BC, NO3-, or NH4+ exposure. Furthermore, the nonlinear curves were observed for the exposure-response relationship between PM2.5 exposure and the mRS score. CONCLUSION: Greater PM2.5 exposure increased the mRS score and was associated with post-stroke functional disability among stroke patients. However, different chemical components showed unequal neurotoxic effects, and long-term exposure to OM and SO42- may play a more important role. SYNOPSIS: This study reports fine particulate matter at higher concentrations damages the functional ability among specific stroke patients, and PM2.5 components have different neurotoxicities.

The short-term effect of ozone on pregnancy loss modified by temperature: Findings from a nationwide epidemiological study in the contiguous United States.

BACKGROUND: Pregnancy loss, a major health issue that affects human sustainability, has been linked to short-term exposure to ground-surface ozone (O3). However, the association is inconsistent, possibly because of the co-occurrence of O3 and heat episodes, as increased temperature is a risk factor for pregnancy loss. To explain this inconsistency, the effect of O3 on pregnancy loss needs to be examined jointly with that of high temperature. METHODS: A total of 247,305 pregnancy losses during the warm season were extracted from fetal death certificates from the 386 counties in contiguous United States from 1989 to 2005. We assessed environmental exposure based on the daily maximum 8 h average of O3 from Air Quality System monitors and the 24 h average temperature from the North American Regional Reanalysis product. We conducted a bidirectional, time-stratified case-crossover study of the association between pregnancy loss and exposures to O3 and temperature and their multiplicative interaction. The main time window for the exposure assessment was the day of case occurrence and the preceding 3 days. To estimate the association, we used conditional logistic regression with adjustment for relative humidity, height of the planetary boundary layer, and holidays. Sensitivity analyses were performed on the lagged structure, nonlinearity, and between-subpopulation heterogeneity of the estimated joint effect. RESULTS: The joint effect was first estimated by the regression against categorical exposure by tertile. Compared to the low-low exposure group (O3 ≤ 78 µg/m3 and temperature ≤ 18 °C), the odds of pregnancy loss was significantly higher by 6.0 % (95 % confidence interval [CI] 2.4-9.7 %), 9.8 % (6.1-13.8 %), and 7.5 % (4.7-10.3 %) in the high-low (>104 µg/m3 and ≤18 °C), low-high (≤78 µg/m3 and >23 °C), and high-high (>104 µg/m3 and >23 °C) groups. The model of linear exposure and the multiplicative interaction yielded similar results. Each increment of 10 µg/m3 in O3 and 1 °C in temperature was associated with a 3.0 % (2.0 %-4.0 %) and 3.9 % (3.5 %-4.3 %), respectively, increase in the odds of pregnancy loss. A decrease in odds of 0.2 % (0.1 %-0.2 %) was associated with the temperature × O3 interaction. The finding of an antagonistic interaction between temperature and O3 was confirmed by models parametrizing the joint exposure as alternative nonlinear terms (i.e., a two-dimensional spline term or a varying-coefficient term) and was robust to a variety of exposure lags and stratifications. Therefore, the marginal effect of O3 was estimated to vary by climate zone. A significant association between O3 and pregnancy loss was observed in the northern, but not southern, United States. CONCLUSION: Joint exposure to O3 and high temperature can increase the risk for pregnancy loss. The adverse effect of O3 is potentially modified by ambient temperature. In high-latitude cities, controlling for O3 pollution could protect maternal health.

Stillbirths attributable to open fires and their geographic disparities in non-Western countries.

Due to global warming, an increased number of open fires is becoming a major contributor to PM2.5 pollution and thus a threat to public health. However, the burden of stillbirths attributable to fire-sourced PM2.5 is unknown. In low- and middle-income countries (LMICs), there is a co-occurrence of high baseline stillbirth rates and frequent firestorms, which may lead to a geographic disparity. Across 54 LMICs, we conducted a self-matched case-control study, making stillbirths comparable to the corresponding livebirths in terms of time-invariant characteristics (e.g., genetics) and duration of gestational exposure. We established a joint-exposure-response function (JERF) by simultaneously associating stillbirth with fire- and non-fire-sourced PM2.5 concentrations, which were estimated by fusing multi-source data, such as chemical transport model simulations and satellite observations. During 2000-2014, 35,590 pregnancies were selected from multiple Demographic and Health Surveys. In each mother, a case of stillbirth was compared to her livebirth(s) based on gestational exposure to fire-sourced PM2.5. We further applied the JERF to assess stillbirths attributable to fire-sourced PM2.5 in 136 non-Western countries. The disparity was evaluated using the Gini index. The risk of stillbirth increased by 17.4% (95% confidence interval [CI]: 1.6-35.7%) per 10 µg/m3 increase in fire-sourced PM2.5. In 2014, referring to a minimum-risk exposure level of 10 µg/m3, total and fire-sourced PM2.5 contributed to 922,860 (95% CI: 578,451-1,183,720) and 49,951 (95% CI: 3,634-92,629) stillbirths, of which 10% were clustered within the 6.4% and 0.6% highest-exposure pregnancies, respectively. The Gini index of stillbirths attributable to fire-sourced PM2.5 was 0.65, much higher than for total PM2.5 (0.28). Protecting pregnant women against PM2.5 exposure during wildfires is critical to avoid stillbirths, as the burden of fire-associated stillbirths leads to a geographic disparity in maternal health.

Associations between hemoglobin levels and source-specific exposure to ambient fine particles among children aged <5 years in low- and middle-income countries.

OBJECTIVE: We investigated associations between source-specific fine particulate matter (PM2.5) exposure and hemoglobin levels among children in low- and middle-income countries (LMICs). METHOD: 36,675 children aged < 5 years were collected in 11 LMICs during 2017. We associated child hemoglobin with 20 source-specific PM2.5, and calculated changes in hemoglobin that could be attributed to different PM2.5-mixture scenarios, established using real-world data from 88 Asian and African LMICs (AA-LMICs). RESULTS: Multiple-source analysis revealed PM2.5 produced by solvents (change in hemoglobin for 1-µg/m3 increment in PM2.5: -10.34 g/L, 95% CI -14.88 to -5.91), industrial coal combustion (-0.51 g/L, 95% CI -9.25 to -0.08), road transportation (-0.50 g/L, 95% CI -6.96 to -0.29), or waste handling and disposal (-0.34 g/L, 95% CI -4.38 to -0.23) was significantly associated with a decrease in hemoglobin level. Decreases in hemoglobin attributable to the PM2.5 mixtures were co-determined by the concentrations and their source profiles. The largest PM2.5-related change in hemoglobin was -10.25 g/L (95% CI -15.54 to -5.27) for a mean exposure of 61.01 µg/m3 in India. CONCLUSION: Association between PM2.5 and a decrease in hemoglobin was affected by variations in PM2.5 source profiles. Source-oriented interventions are warranted to protect children in LMICs from air pollution.

The association of birthweight with fine particle exposure is modifiable by source sector: Findings from a cross-sectional study of 17 low- and middle-income 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.

Health Impacts of Long-Term NO2 Exposure and Inequalities among the Chinese Population from 2013 to 2020.

Nitrogen dioxide (NO2) is associated with mortality and many other adverse health outcomes. In 2021, the World Health Organization established a new NO2 air quality guideline (AQG) (annual average <10 µg/m3). However, the burden of diseases attributable to long-term NO2 exposure above the AQG is unknown in China. Nitrogen oxide is a major air pollutant in populous cities, which are disproportionately impacted by NO2; this represents a form of environmental inequality. We conducted a nationwide risk assessment of premature deaths attributable to long-term NO2 exposure from 2013 to 2020 based on the exposure-response relationship, high-resolution annual NO2 concentrations, and gridded population data (considering sex, age, and residence [urban vs rural]). We calculated health metrics including attributable deaths, years of life lost (YLL), and loss of life expectancy (LLE). Inequality in the distribution of attributable deaths and YLLs was evaluated by the Lorenz curve and Gini index. According to the health impact assessments, in 2013, long-term NO2 exposure contributed to 315,847 (95% confidence interval [CI]: 306,709-319,269) premature deaths, 7.90 (7.68-7.99) million YLLs, and an LLE of 0.51 (0.50-0.52) years. The high-risk subgroup (top 20%) accounted for 85.7% of all NO2-related deaths and 85.2% of YLLs, resulting in Gini index values of 0.81 and 0.67, respectively. From 2013 to 2020, the estimated health impact from NO2 exposure was significantly reduced, but inequality displayed a slightly increasing trend. Our study revealed a considerable burden of NO2-related deaths in China, which were disproportionally frequent in a small high-risk subgroup. Future clean air initiatives should focus not only on reducing the average level of NO2 exposure but also minimizing inequality.

Probability of chronic kidney disease and associated risk factors in Chinese adults: a cross-sectional study of 9 million Chinese adults in the Meinian Onehealth screening survey.

Background: Chronic kidney disease (CKD) is an increasing global health problem, but little is known about the age- and sex-specific prevalence of CKD and the associated risk factors in low- and middle-income populations. We examined the age- and sex-specific prevalence of CKD and the associated risk factors in a population-based study of 9 million Chinese adults. Methods: The study involved a cross-sectional survey of 9 461 631 adults, >18 years of age, who were recruited in 2017 from 31 provinces in the Meinian Onehealth screening survey. All participants had plasma creatinine measured by standard methods and CKD was defined if the estimated glomerular filtration rate (eGFR) was <60 ml/min/1.73 m2. Results: Overall, among 9.5 million adults [mean age 41 years (standard deviation 13.1)], 88 271 (1.26%) had CKD. The prevalence rate of CKD was 1.20%, 0.04% and 0.02% for stage 3, 4 and 5, respectively. After adjustment for the proportion and prevalence of urban and rural areas, the overall prevalence rate of CKD was 1.07%, indicating that ∼14 million Chinese adults have CKD. The prevalence of CKD increased 3-fold for each 10-year increment in age (1.15%, 3.05% and 13.02% at age 50-59, 60-69 and >70 years, respectively) and was 1.8-fold higher in women than men. The prevalence of CKD was higher in the Southwest region {1.68% [95% confidence interval (CI) 1.12-2.24]} but lower in the Northwest region [0.84% (95% CI 0.61-1.07)] than other regions. If proteinuria is also used as a diagnostic criterion, the prevalence rate increased to 2.16%. Stepwise logistic regression analysis demonstrated that body mass index; history of hypertension, cardiovascular disease or diabetes; and levels of systolic blood pressure, triglycerides, fasting glucose and uric acid were independent risk factors for CKD. Conclusion: CKD is an important public health problem in Chinese adults and this study highlights the need for public health strategies to detect and reduce modifiable risk factors for prevention of CKD.

Estimation of stillbirths attributable to ambient fine particles in 137 countries.

Gestational exposure to ambient fine particles (PM2.5) increases the risk of stillbirth, but the related disease burden is unknown, particularly in low- and middle-income countries (LMICs). We combine state-of-the-art estimates on stillbirths, and multiple exposure-response functions obtained from previous meta-analyses or derived by a self-matched case-control study in 54 LMICs. 13,870 stillbirths and 32,449 livebirths are extracted from 113 geocoded surveys from the Demographic and Health Surveys. Each stillbirth is compared to livebirth(s) of the same mother using a conditional logit regression. We find that 10-µg/m3 increase of PM2.5 is associated with an 11.0% (95% confidence interval [CI] 6.4, 15.7) increase in the risk of stillbirth, and the association is significantly enhanced by maternal age. Based on age-specific nonlinear PM2.5-stillbirth curves, we evaluate the PM2.5-related stillbirths in 137 countries. In 2015, of 2.09 (95% CI: 1.98, 2.20) million stillbirths, 0.83 (0.54, 1.08) million or 39.7% (26.1, 50.8) are attributable to PM2.5 exposure exceeding the reference level of 10 µg/m3. In LMICs, preventing pregnant women from being exposed to PM2.5 can improve maternal health.

Greenspace exposure and poststroke disability: A nationwide longitudinal study.

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.

Deaths attributable to anomalous temperature: A generalizable metric for the health impact of global warming.

The U-shaped association between health outcomes and ambient temperatures has been extensively investigated. However, such analyses cannot fully estimate the mortality burden of climate change because the features of the association (e.g., minimum mortality temperature) vary with human adaptation; thus, they are not generalizable to different locations. In this study, we assumed that humans could adapt to regular temperature variations; and thus examined the all-cause mortality attributable to temperature anomaly (TA), an indicator widely utilized in climate science to measure irregular temperature fluctuations, across 115 cities in the United States (US). We first used quasi-Poisson regressions to obtain the city-specific TA-mortality associations, then used meta-regression to pool these city-specific estimates. Finally, we calculated the number of TA-related deaths using the uniform pooled association, then compared it to the estimates from city-specific associations, which had been controlled for adaptation. Meta-regression showed a U-shaped TA-mortality association, centered at a TA near 0. According to the pooled association, 0.579 % (95 % confidence interval [CI]: 0.465-0.681 %), 0.394 % (95 % CI: 0.332-0.451 %), and 0.185 % (95 % CI: 0.107-0.254 %) of all-cause deaths were attributable to all anomalous temperatures (TA ≠ 0), anomalous heat (TA > 0), and anomalous cold (TA < 0), respectively. At the city level, heat-related deaths estimated from the pooled association were in good agreement with heat-related deaths estimated from the city-specific associations (R2 = 0.84). However, the cold-related deaths estimated from the two methods showed a weaker correlation (R2 = 0.07). Our findings suggest that TA constitutes a generalizable indicator that can uniformly evaluate deaths attributable to anomalous heat in distinct geographical locations.

Long-Term Exposure to Ozone Increases Neurological Disability after Stroke: Findings from a Nationwide Longitudinal Study in China.

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.