Fluctuating risk of acute kidney injury-related mortality for four weeks after exposure to air pollution: A multi-country time-series study in 6 countries.

BACKGROUND: Recent studies have reported that air pollution is related to kidney diseases. However, the global evidence on the risk of death from acute kidney injury (AKI) owing to air pollution is limited. Therefore, we investigated the association between short-term exposure to air pollution-particulate matter ≤ 2.5 µm (PM2.5), ozone (O3), and nitrogen dioxide (NO2)-and AKI-related mortality using a multi-country dataset. METHODS: This study included 41,379 AKI-related deaths in 136 locations in six countries during 1987-2018. A novel case time-series design was applied to each air pollutant during 0-28 lag days to estimate the association between air pollution and AKI-related deaths. Moreover, we calculated AKI deaths attributable to non-compliance with the World Health Organization (WHO) air quality guidelines. RESULTS: The relative risks (95% confidence interval) of AKI-related deaths are 1.052 (1.003, 1.103), 1.022 (0.994, 1.050), and 1.022 (0.982, 1.063) for 5, 10, and 10 µg/m3 increase in lag 0-28 days of PM2.5, warm-season O3, and NO2, respectively. The lag-distributed association showed that the risk appeared immediately on the day of exposure to air pollution, gradually decreased, and then increased again reaching the peak approximately 20 days after exposure to PM2.5 and O3. We also found that 1.9%, 6.3%, and 5.2% of AKI deaths were attributed to PM2.5, warm-season O3, and NO2 concentrations above the WHO guidelines. CONCLUSIONS: This study provides evidence that public health policies to reduce air pollution may alleviate the burden of death from AKI and suggests the need to investigate the several pathways between air pollution and AKI death.

Joint effect of heat and air pollution on mortality in 620 cities of 36 countries.

BACKGROUND: The epidemiological evidence on the interaction between heat and ambient air pollution on mortality is still inconsistent. OBJECTIVES: To investigate the interaction between heat and ambient air pollution on daily mortality in a large dataset of 620 cities from 36 countries. METHODS: We used daily data on all-cause mortality, air temperature, particulate matter ≤ 10 µm (PM10), PM ≤ 2.5 µm (PM2.5), nitrogen dioxide (NO2), and ozone (O3) from 620 cities in 36 countries in the period 1995-2020. We restricted the analysis to the six consecutive warmest months in each city. City-specific data were analysed with over-dispersed Poisson regression models, followed by a multilevel random-effects meta-analysis. The joint association between air temperature and air pollutants was modelled with product terms between non-linear functions for air temperature and linear functions for air pollutants. RESULTS: We analyzed 22,630,598 deaths. An increase in mean temperature from the 75th to the 99th percentile of city-specific distributions was associated with an average 8.9 % (95 % confidence interval: 7.1 %, 10.7 %) mortality increment, ranging between 5.3 % (3.8 %, 6.9 %) and 12.8 % (8.7 %, 17.0 %), when daily PM10 was equal to 10 or 90 µg/m3, respectively. Corresponding estimates when daily O3 concentrations were 40 or 160 µg/m3 were 2.9 % (1.1 %, 4.7 %) and 12.5 % (6.9 %, 18.5 %), respectively. Similarly, a 10 µg/m3 increment in PM10 was associated with a 0.54 % (0.10 %, 0.98 %) and 1.21 % (0.69 %, 1.72 %) increase in mortality when daily air temperature was set to the 1st and 99th city-specific percentiles, respectively. Corresponding mortality estimate for O3 across these temperature percentiles were 0.00 % (-0.44 %, 0.44 %) and 0.53 % (0.38 %, 0.68 %). Similar effect modification results, although slightly weaker, were found for PM2.5 and NO2. CONCLUSIONS: Suggestive evidence of effect modification between air temperature and air pollutants on mortality during the warm period was found in a global dataset of 620 cities.

Heat-related cardiorespiratory mortality: Effect modification by air pollution across 482 cities from 24 countries.

BACKGROUND: Evidence on the potential interactive effects of heat and ambient air pollution on cause-specific mortality is inconclusive and limited to selected locations. OBJECTIVES: We investigated the effects of heat on cardiovascular and respiratory mortality and its modification by air pollution during summer months (six consecutive hottest months) in 482 locations across 24 countries. METHODS: Location-specific daily death counts and exposure data (e.g., particulate matter with diameters ≤ 2.5 µm [PM2.5]) were obtained from 2000 to 2018. We used location-specific confounder-adjusted Quasi-Poisson regression with a tensor product between air temperature and the air pollutant. We extracted heat effects at low, medium, and high levels of pollutants, defined as the 5th, 50th, and 95th percentile of the location-specific pollutant concentrations. Country-specific and overall estimates were derived using a random-effects multilevel meta-analytical model. RESULTS: Heat was associated with increased cardiorespiratory mortality. Moreover, the heat effects were modified by elevated levels of all air pollutants in most locations, with stronger effects for respiratory than cardiovascular mortality. For example, the percent increase in respiratory mortality per increase in the 2-day average summer temperature from the 75th to the 99th percentile was 7.7% (95% Confidence Interval [CI] 7.6-7.7), 11.3% (95%CI 11.2-11.3), and 14.3% (95% CI 14.1-14.5) at low, medium, and high levels of PM2.5, respectively. Similarly, cardiovascular mortality increased by 1.6 (95%CI 1.5-1.6), 5.1 (95%CI 5.1-5.2), and 8.7 (95%CI 8.7-8.8) at low, medium, and high levels of O3, respectively. DISCUSSION: We observed considerable modification of the heat effects on cardiovascular and respiratory mortality by elevated levels of air pollutants. Therefore, mitigation measures following the new WHO Air Quality Guidelines are crucial to enhance better health and promote sustainable development.

Role of oxides of nitrogen in the ozone-cardiorespiratory visit association.

Ozone (O3)-induced health effects vary in terms of severity, from deterioration of lung function and hospitalization to death. Several studies have reported a linear increase in health risks after O3 exposure. However, current evidence suggests a non-linear U- and J-shaped concentration-response (C-R) function. The potential increasing risks with decreasing O3 concentrations may seem counterintuitive from the traditional standpoint that decreasing exposure should lead to decreasing health risks. Tus, the question of whether the increasing risks with decreasing concentrations are truly O3-induced or might be from other C-R mechanisms. If these potential risks were not accounted for, this may have contributed to the risks observed at the low ozone concentration range. In this study, we examined the short-term effects of photochemical oxidant (Ox, parts per billiion) on outpatient cardiorespiratory visits in 21 Japanese cities after adjusting for other air pollutant-specific C-R functions. Daily cardiorespiratory visits from January 1, 2014 to December 31, 2016 were obtained from the Japanese Medical Data Center Co. Ltd. Similar period of meteorological and air pollution variables were obtained from relevant data sources. We utilized a time-stratified case crossover design coupled with the generalized additive mixed model (TSCC-GAMM) to estimate the association between Ox and cardiorespiratory outpatient visits, after adjusting for several covariates. A total of 2,588,930 visits were recorded across the study period, with a mean of 111.87 and a standard deviation of 138.75. The results revealed that crude Ox-cardiorespiratory visits exhibited a U-shaped pattern. However, adjustment of the oxides of nitrogen, particularly nitrogen monoxide (NO), attenuated the lower risk curve and subsequently altered the shape of the C-R function, with a substantial reduction observed during winter. NO- and nitrogen dioxide (NO2)-adjusted Ox-cardiorespiratory associations increased nearly linearly, without an apparent threshold. Current evidence suggests the importance of adjusting the oxides of nitrogen in estimating the Ox C-R risk functions.

Early life exposure to indoor air pollutants and the risk of neurodevelopmental delays: The Japan Environment and Children's Study.

Air pollution has been associated with childhood neurodevelopment. However, the role of indoor air pollution, especially volatile organic compounds (VOCs), on childhood neurodevelopment has been poorly explored to date. We investigated the association between indoor air pollutants and childhood neurodevelopment in 5,017 randomly selected children from the Japan Environment and Children's Study. When the participants reached 1.5 and 3 years of age, they were followed up with home visits and neurodevelopmental tests using the Ages and Stages Questionnaire (ASQ). At both ages, we collected indoor air samples for 1 week and measured 13 indoor air pollutants: particulate matter with an aerodynamic diameter of ≤2.5 µm, ozone, nitrogen dioxide, sulfur dioxide, and nine VOCs. The associations between air pollutants and ASQ scores were estimated using linear mixed effects models and weighted quantile sum regressions (WQS) at each age separately. Stratified analysis by sex was conducted. Exposure to m,p-xylene at the age of 3 was associated with lower communication, fine motor, and overall ASQ scores (coefficients: -0.18 [99% confidence intervals (CI): -0.35, -0.02], -0.23 [99 %CI: -0.43, -0.03], and - 0.72 [99 %CI: -1.41, -0.04] per 1 µg/m3 increase, respectively). Exposure to o-xylene at the age of 3 was associated with lower communication, gross motor, fine motor, and overall ASQ scores (coefficients: -0.48 [99 %CI: -0.90, -0.07], -0.45 [99 %CI: -0.78, -0.13], -0.65 [99 %CI: -1.14, -0.16], and -2.15 [99 %CI: -3.83, -0.47] per 1 µg/m3 increase, respectively). The WQS index was associated with lower gross motor ASQ scores at the age of 3 (coefficient: -0.27 [95 %CI: -0.51, -0.03] for one-unit WQS index increases), which was attributed to benzene (33.96%), toluene (26.02%), o-xylene (13.62%), and ethylbenzene (9.83%). Stratified analysis showed similar results. Although further investigations are required, our results suggest an association of neurodevelopmental delays with indoor low-level exposure to m,p-xylene and o-xylene in early life.

Changing Susceptibility to Non-Optimum Temperatures in Japan, 1972-2012: The Role of Climate, Demographic, and Socioeconomic Factors.

BACKGROUND: Previous studies have shown that population susceptibility to non-optimum temperatures has changed over time, but little is known about the related time-varying factors that underlie the changes. OBJECTIVE: Our objective was to investigate the changing population susceptibility to non-optimum temperatures in 47 prefectures of Japan over four decades from 1972 to 2012, addressing three aspects: minimum mortality temperature (MMT) and heat- and cold-related mortality risks. In addition, we aimed to examine how these aspects of susceptibility were associated with climate, demographic, and socioeconomic variables. METHODS: We first used a two-stage time-series design with a time-varying distributed lag nonlinear model and multivariate meta-analysis to estimate the time-varying MMT, heat- and cold-related mortality risks. We then applied linear mixed effects models to investigate the association between each of the three time-varying aspects of susceptibility and various time-varying factors. RESULTS: MMT increased from 23.2 [95% confidence interval (CI): 23, 23.6] to 28.7 (27.0, 29.7) °C. Heat-related mortality risk [relative risk (RR) for the 99th percentile of temperature vs. the MMT] decreased from 1.18 (1.15, 1.21) to 1.01 (0.98, 1.04). Cold-related mortality risk (RR for the first percentile vs. the MMT) generally decreased from 1.48 (1.41, 1.54) to 1.35 (1.32, 1.40), with the exception of a few eastern prefectures that showed increased risk. The changing patterns in all three aspects differed by region, sex, and causes of death. Higher mean temperature was associated (p<0.01) with lower heat risk, whereas higher humidity was associated with higher cold risk. A higher percentage of elderly people was associated with a higher cold risk, whereas higher economic strength of the prefecture was related to lower cold risk. CONCLUSIONS: Population susceptibility to heat has decreased over the last four decades in Japan. Susceptibility to cold has decreased overall except for several eastern prefectures where it has either increased or remained unchanged. Certain climate, demographic, and socioeconomic factors explored in the current study might underlie this changing susceptibility. https://doi.org/10.1289/EHP2546.