Previous research has found an association between PM2.5 exposure and worsening depression; however, studies specifically examining the harmful effects of individual PM2.5 components are relatively limited. This national survey enrolled individuals aged 45 and older in mainland China, collecting personal data and assessing depression. Depressive symptoms were assessed using the 10-item Center for Epidemiologic Studies Depression Scale (CES-D-10). Monthly exposure to PM2.5 and its seven components—black carbon (BC), organic matter (OM), nitrate (NO3−), sulfate (SO42−), ammonium (NH4+), soil particles (SOIL), and sea salt (SS)—was matched to each participant’s residence. Linear mixed-effects models (LMEs) assessed the association between single pollutants and depression score, while weighted quantile sum (WQS) regression examined the effect of mixed exposure and identified the contribution of each component. Modifying effects of social activity and green space were also evaluated. A total of 9725 participants were included. In single-exposure models, each interquartile range (IQR) increase in PM2.5 (29.18 μg/m3), BC (2.25 μg/m3), OM (7.18 μg/m3), SOIL (6.04 μg/m3), and SS (0.14 μg/m3) was significantly associated with an increase in depression score of 0.90 (95% CI: 0.59, 1.20), 0.71 (95% CI: 0.42, 1.09), 0.94 (95% CI: 0.61, 1.26), 0.51 (95% CI: 0.38, 0.63), and 0.53 (95% CI: 0.33, 0.73) points, respectively. In mixed-exposure models, each IQR increase in the mixture of all components was associated with a 1.104-point rise in depression score (95% CI: 0.901, 1.307), with BC having the largest weight (33.6%), followed by SOIL (28.59%) and SS (25.05%). The harmful effects of PM2.5 and specific components on depression were lower among those who participated in social activities or lived in areas with higher levels of green space (p < 0.05). These findings suggest that the harmful effects of PM2.5 on depression may be influenced by its components, and that social activity and green space could reduce the risk of depression associated with PM2.5 and its components.

What is already known about this topic?:Severe respiratory infections in early life, particularly lower respiratory tract infections, such as bronchiolitis and pneumonia, may increase the risk of subsequent wheezing and asthma. What is added by this report?:Among the 22,460 children hospitalized for acute respiratory infections in Yichang, 2017-2024, a total of 1,463 subsequently developed wheezing/asthma. Bronchiolitis and pneumonia were associated with the highest subsequent wheezing/asthma risk relative to upper respiratory tract infection or influenza, with excess risk concentrated within the first 2 years after hospitalization; only bronchiolitis remained significantly associated with subsequent wheezing/asthma during the 2 to <4 years period. What are the implications for public health practice?:Children hospitalized with bronchiolitis or pneumonia should undergo systematic post-discharge follow-up and early asthma screening during the first two years after discharge. Extended follow-up for four years after discharge may be warranted for children hospitalized with bronchiolitis.

Environmental noise pollution is increasing, while risks of cardiovascular diseases (CVD) associated with environmental noise in low- and middle-income countries (LMICs) still remain under-recognized. In this study, we utilized land-use regression (LUR) models at high spatial resolution to assess environmental noise and linked the exposure to digital healthcare data from the Yinzhou Regional Health Information Platform (YRHIP) in China to assess the associations of environmental noise with risks of CVD. Among 533,512 participants, mean (SD) age was 53.66 (15.52) years with females constituting 52.8 %. The mean environmental noise level was 59.34 dB[A]. A total of 177,111 (33.20 %), 18,030 (3.38 %), 15,912 (2.98 %), 9,601 (1.80 %), and 161,889 (30.34 %) participants were diagnosed with CVD, cerebrovascular diseases, ischemic heart diseases (IHD), stroke, and hypertension, respectively. Multivariable modified Poisson regression models incorporating community as a random-effect term were used to evaluate associations of environmental noise with the prevalent risk of CVD and its major subtypes. Individual covariates (age, sex, marital status, education, lifestyles), area-level covariates (urbanicity, population density, GDP), and PM2.5 were adjusted. We observed positive associations between residential environmental noise exposure and CVD (prevalence ratio (PR) 1.06, 95 % CI: 1.02-1.09 per 5 dB[A]), IHD (PR 1.14, 95 % CI: 1.07-1.21 per 5 dB[A]), and hypertension (PR 1.06, 95 % CI: 1.03-1.09 per 5 dB[A]), while no association was found for cerebrovascular diseases (PR 1.01, 95 % CI: 0.96-1.07 per 5 dB[A]) and stroke (PR 0.97, 95 % CI: 0.92-1.03 per 5 dB[A]). The risks of CVD and hypertension associated with environmental noise were higher among males and in the 50-60 years age group (P for interaction < 0.001). The associations between environmental noise and IHD were stronger in the ≥ 70 age group and among the participants with lower education levels (P for interaction < 0.05). The study fills the gap of knowledge about the associations between environmental noise, estimated using high spatial resolution LUR models, and CVD prevalent risk in LMICs. The evidence would provide significant implications for policy-making in terms of alleviating the surging disease burden of CVD related to environmental noise in LMICs.

BACKGROUND:Children's respiratory health demonstrates particular sensitivity to air pollution. Existing evidence investigating the association between short-term ozone (O3) exposure and childhood pneumonia remains insufficient and inconsistent, especially in low- and middle-income countries (LMICs). METHOD:To provide more reliable and persuasive evidence, we implemented a multi-city, time-stratified case-crossover design with a large sample size, using data from seven representative children's hospitals across major geographical regions in China. To avoid the impact of the COVID-19 pandemic, individual-level medical records of inpatient children under 6 years of age diagnosed with pneumonia during 2016-2019 were collected. Conditional logistic regression models were fitted for each city, and city-specific estimates were pooled through a meta-analysis using a random-effects model. RESULTS:In total, the study included 137,470 pediatric pneumonia hospital admissions. The highest pooled estimate for O3 occurred at lag0-1, with a 10 µg/m3 increase in O3 associated with a 1.57% (95% CI: 0.67%-2.48%) higher risk of pediatric pneumonia hospital admissions. Stratified analyses indicated that the effects of O3 were robust across different sexes, age groups, and admission seasons. We also observed a statistically significant increase in risk associated with O3 concentrations exceeding the World Health Organization Air Quality Guidelines (WHO-AQGs). CONCLUSIONS:This study revealed a significant positive association between O3 and pediatric pneumonia hospital admissions. Our findings substantially strengthen the evidence base for the adverse health impacts of O3, underscoring the importance of O3 pollution control and management in reducing the public health burden of pediatric pneumonia.

BackgroundAmbient carbon monoxide (CO) exposure has been identified as an emerging environmental risk factor contributing to the progression of pulmonary tuberculosis (PTB). However, the epidemiological evidence remains inconsistent. This study aims to investigate the short-term association between low-level CO exposure and PTB outpatient visits in a developing region.MethodsWe conducted a time-series study utilizing a distributed lag non-linear model (DLNM) combined with mediating effect analysis, based on daily CO and PTB cases from 2011 to 2020 in Ningbo, China.ResultsAmong all patients with PTB, a 0.1 mg/m3 increase in CO concentration was associated with an increased risk of PTB outpatient visits in the single-pollutant model, particularly at lag days 2–6. The maximum relative risk (RR) was 1.091 (95%CI, 1.020–1.168, lag 0–2 days). Similarly, the maximum cumulative lag effect of CO exposure was 1.781 (RR = 1.781, 95%CI: 1.157–2.742, lag 0–15 days). Subgroup analysis revealed a significant effect of CO exposure in males (RR = 1.090, 95%CI: 1.009–1.777, lag 0–3 days), females (RR = 1.101, 95%CI: 1.014–1.195, lag 0–3 days), younger individuals (RR = 1.097, 95%CI: 1.022–1.178, lag 0–2 days), and during the warm season (RR = 1.012, 95%CI: 1.002–1.022, lag 0–4 days). Mediation analysis indicated that temperature had an indirect mediating effect on association between CO and PTB (−0.0065, 95%CI: −0.0130 to −0.0004), while air pressure, visibility, and humidity showed no significant mediating effects.ConclusionOur findings indicate that ambient CO exposure, even at low levels, has a short-term impact on PTB in developing regions. Temperature plays a partial mediating role in this relationship. Consequently, it is critical to enhance environmental monitoring and early warning systems to effectively address the prevalence of PTB and the delays in health-seeking behavior.

The effects of the Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) diet on the risk of neurodegenerative diseases (NDD) associated with air pollution were unclear. We conducted a 11-year cohort study in a population with short/long telomere length (RTL) in the UK Biobank (N = 115 467). Time-varying cox proportional hazard regression models were established. Exposures were PM2.5, PM10, NO2, NOX and their principal component (PC1). The combined effect and modification effect of the MIND diet score and each pollutant on the NDD risk were evaluated. A total of 1201 participants developed NDD. All pollutants were associated with NDD risk in two RTL subgroups. The risk of NDD associated with air pollution was lower in participants with higher MIND scores, especially in the short RTL subgroup (P interaction = 0.083, 0.052, 0.013, 0.007 and 0.017, respectively). The MIND diet may reduce NDD risk caused by air pollution, especially in populations with more severe aging status.

What is already known about this topic?:Urban landscape patterns influence population health and are traditionally measured using landscape indices. However, current indices suffer from a single-dimensional focus, multicollinearity, and limited health relevance. What is added by this report?:Using a two-stage Generalized Weighted Quantile Sum (GWQS) regression, we developed a Landscape Pattern Health Index (LPHI), integrating composition/configuration metrics. This index revealed seasonal protective/hazard effects and represents a holistic tool for assessing urban landscape health impacts. What are the implications for public health practice?:The LPHI identifies high-risk areas and seasonal priorities, thereby guiding targeted interventions to mitigate health risks through landscape optimization.

BACKGROUND:In the UK, an estimated 15% of asthma patients have concurrent chronic obstructive pulmonary disease (COPD), yet the underlying causes and mechanisms remain largely unexplored. This study aimed to investigate the roles of both ambient air pollution and genetic susceptibility in the progression from asthma to COPD. METHODS:46 832 participants with asthma were recruited from the UK Biobank during the baseline period (2006-2010). Particulate matter with a diameter of 2.5 μm (PM2.5) and nitrogen dioxide (NO2) were estimated at baseline address using land-use regression models. Air pollution score reflected joint exposure to air pollution. Polygenic risk score was calculated using novel genetic signals identified for coexistence of asthma+COPD. Cox proportional hazards regression analysis was employed to quantify the risks of both ambient air pollution and genetic scores on incident COPD among asthmatics, adjusting for covariates. RESULTS:Over a median follow-up of 10.84 years, 3759 participants with asthma at baseline developed COPD. For an IQR increase in PM2.5 and NO2, the HR for developing COPD was 1.07 (95% CI: 1.02 to 1.11) and 1.10 (95% CI: 1.04 to 1.15), respectively. Adverse effects could be observed at concentrations as low as 8 µg/m3 for PM2.5 and 12 µg/m3 for NO2. A significant multiplicative interaction was identified between ambient air pollution and genetic susceptibility. Individuals with the highest genetic risk score exhibited the greatest risk, with an HR of 1.13 (95% CI: 1.05 to 1.22) per IQR increase in air pollution score (P interaction <0.05). CONCLUSIONS:Ambient air pollution is strongly associated with progression from asthma to comorbidity COPD, particularly among individuals with high genetic risk.

Residential green space has the potential to benefit cardiometabolic health. However, little is known about its impacts on cardiometabolic multimorbidity (CMM). Furthermore, the capacity of access to green space to reduce health inequalities during the development of CMM is unclear, and longitudinal evidence is urgently needed. Hence, a large prospective study based on the UK Biobank was conducted. CMM was defined as the coexistence of at least two conditions including type 2 diabetes, ischemic heart disease, and stroke. Multi-state models were used to assess the impacts of green space on the transitions of CMM, from free of cardiometabolic disease to first cardiometabolic disease (FCMD), subsequently to CMM, and finally death. This study included 328,260 participants with a median follow-up of 12.5 years. The benefits of access to green space were observed for transitions from baseline to FCMD, from baseline to death, and from FCMD to death, with HRs of 0.975 (95 % CI: 0.959, 0.991), 0.956 (95 % CI: 0.931, 0.982) and 0.943 (95 % CI: 0.897, 0.990) per IQR increase in the percentage of green space, respectively. Although access to green space benefited early transitions related to FCMD, its protective role was not found in the progression from FCMD to CMM and finally death. Furthermore, access to green space was associated with a reduction in health inequalities influenced by sex and socioeconomic status in the earliest transition from healthy to FCMD. Future policies should prioritize green space investments to sustainably enhance cardiometabolic health and improve health inequalities.

Background:Tuberculosis (TB) is a major global health threat, with Ningbo reporting over 3,000 annual cases of pulmonary tuberculosis (PTB). This study analyzes the notification and mortality rates of PTB in Ningbo from 2004 to 2021. Methods:We calculated age-standardized annual notification and mortality rates for PTB per 100,000 population and employed interrupted time series regression to evaluate the impact of government policies on these rates. Results:From 2004 to 2021, Ningbo recorded 68,392 PTB cases and 236 deaths. The unstandardized notification and mortality rates were 51.31 and 0.18 per 100,000 population, respectively. Joinpoint trend analysis showed a significant decline in PTB notification from 2007 to 2016 (APC = -7.3%, P < 0.05). Although mortality decreased from 2017 to 2021, this reduction was not statistically significant (APC = -20.5%, P = 0.106). Interrupted time series analysis indicated that government policies led to an estimated reduction of three cases in age-standardized PTB notification and about 0.025 deaths per 100,000 population. Conclusion:Between 2004 and 2021, Ningbo saw a notable decrease in both the notification and mortality rates of PTB due to effective control measures. To achieve the End TB Strategy targets for 2035, it is crucial to enhance efforts in diagnosing and treating PTB-especially among males, adolescents, and older adults.

Satellite-based exposure of fine particulate matters has been seldom used as a predictor of mortality. PM2.5 was predicted using Aerosol Optical Depths (AOD) through a two-stage regression model. The predicted PM2.5 was corrected for the bias using two approaches. We estimated the impact by two different scenarios of PM2.5 in the model. We statistically found different distributions of the predicted PM2.5 over the region. Compared to the reference value (5 mu g/m(3)), 90th and 95th percentiles had significant adverse effect on total mortality (RR (90th percentile):1.45; CI 95%: 1.08-1.95 and RR (95th percentile):1.53; CI 95%: 1.11-2.1). Nearly 1050 deaths were attributed to any range of the air pollution (unhealthy range), of which more than half were attributed to high concentration range. Given the adverse effect of extreme values compared to the both scenarios, more efforts are suggested to define local-specific reference values and preventive strategies.

The risk of cardiovascular and respiratory diseases attributed to satellite-based PM2.5 has been less investigated. In this study, the attributable risk was estimated in an area of Iran. The predicted air PM2.5 using satellite data and a two-stage regression model was used as the predictor of the diseases. The dose-response linkage between the bias-corrected predictor employing a strong statistical approach and the outcomes was evaluated using the distributed lag nonlinear model. We considered two distinct scenarios of PM2.5 for the risk estimation. Alongside the risk, the attributable risk and number were estimated for different levels of PM2.5 by age and gender categories. The cumulative influence of PM2.5 particles on respiratory illnesses was statistically significant at 13–16 µg/m3 relative to the reference value (median), mostly apparent in the middle delays. The cumulative relative risk of 90th and 95th percentiles were 2.03 (CI 95

Background Stroke and dementia are the leading causes of neurological disease burden. Detrimental effects of air pollution on both conditions are increasingly recognised, while the impacts on the dynamic transitions have not yet been explored, and whether critical time intervals exist is unknown. Methods This prospective study was conducted based on the UK Biobank. Annual average air pollution concentrations at baseline year 2010 estimated by land-use regression models were used as a proxy for long-term air pollution exposure. Associations between multiple air pollutants (PM2.5, PM2.5-10, and NO2) indicated by air pollution score and the dynamic transitions of stroke and dementia were estimated, and the impacts during critical time intervals were explored. The date cutoff of this study was February 29, 2020. Findings During a median follow-up of 10.9 years in 413,372 participants, 6484, 3813, and 376 participants developed incident stroke, dementia, and comorbidity of stroke and dementia. For the overall transition from stroke to comorbid dementia, the hazard ratio (HR) for each interquartile range (IQR) increase in air pollution score was 1.38 (95% CI, 1.15, 1.65), and the risks were limited to two time intervals (within 1 year and over 5 years after stroke). As for the transition from dementia to comorbid stroke, increased risk was only observed during 2-3 years after dementia. Interpretation Our findings suggested that air pollution played an important role in the dynamic transition of stroke and dementia even at concentrations below the current criteria. The findings provided new evidence for alleviating the disease burden of neurological disorders related to air pollution during critical time intervals.Copyright (c) 2023 The Author(s). Published by Elsevier Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

Emerging evidence has indicated the linkage of traffic noise with cardiovascular diseases, However, there's a lack of extensive studies exploring the linkage of traffic noise with cardio-metabolic risk factors such as obesity. Additionally, the role of diet in the associations remains unknown. The aim is to prospectively examine the linkage of road traffic noise with obesity, especially by focusing on evaluating the impact of meat. Participants recruited in the UK Biobank with at least one repeated measurement of obesity indicators including body mass index (BMI), waist circumference (WC), waist-to-hip ratio (WhR), and waist-to-height ratio (WhtR) were included. The Common Noise Assessment Methods of the simplified version were used to estimate road traffic noise exposure. Participants were categorized into "less meat intake" and "more meat intake" based on the median of meat intake, assessed by the frequency of unprocessed red meat and processed meat consumption. Modified Poisson regression models were employed to evaluate the linkage of road traffic noise with obesity. Additionally, the modification effects of meat intake on this relationship were evaluated. The incidence risk ratios (IRRs) and 95% confidence interval (CI) of overall obesity, WC-based central obesity, WhR-based central obesity, and WhtR-based central obesity were 1.11 (1.02, 1.21), 1.09 (1.03, 1.14), 1.06 (1.02, 1.10), and 1.08 (1.02, 1.13), respectively, for every 10 dB(A) increase for noise. Compared with individuals with lower meat intake, those with higher meat intake exhibited a stronger linkage of road traffic noise with central obesity. The prospective study demonstrates a linkage of road traffic noise with obesity, emphasizing the significance of diet on traffic noise-related obesity risk.

OBJECTIVE:To assess the impact of exposure to particulate matter with aerodynamic diameter ≤2.5 μm (PM2.5) on non-accidental mortality under different apparent temperature levels and to further explore the modification effect of apparent temperature. METHODS:This study used time-series design. Tianjin and Ningbo from China, Bangkok and Chiang Mai from Thailand were selected as the research sites, and the apparent temperature was applied as the exposure index. Through the quantitative estimation of the threshold temperature, the corresponding pollutant concentration was divided into high and low levels, and the generalized Poisson additive model was used to evaluate the association between PM2.5 exposure and non-accidental death of residents at different temperature levels. RESULTS:The ave-rage concentrations of PM2.5 in Tianjin, Ningbo, Bangkok, and Chiang Mai during the study period were (73.6±35.6), (48.0±32.1), (33.5±28.4) and (32.6±28.6) μg/m3, respectively; the average daily non-accidental death counts were 148, 57, 28, and 8. The analysis of the generalized Poisson additive model showed that the daily non-accidental death counts increased by 0.43% (95%CI: 0.33%-0.54%) per 10 μg/m3 increase of PM2.5 in lag 0 day in Tianjin of China; 0.27% (95%CI: 0.08%-0.46%) per 10 μg/m3 increase of PM2.5 in lag 2 days in Ningbo of China. The effect was magnified in high temperature levels in Tianjin and in low temperatures in Ningbo and Bangkok. The mortality effect of PM2.5 in various temperature levels stayed still in co-pollutant regression models. CONCLUSION:Exposure to fine particulate matter had an adverse effect on non-accidental mortality, which reminded us to give further attention to the pollution control. The findings also indicated that apparent temperature might modify mortality effects of PM2.5 and the modification effect varied in different regions. Protective policies due to regional differences should be made and more scientific and social attention on mutual effect of air pollution and climate change needs to be appealed.

OBJECTIVE:To investigate personal exposures to nitrogen oxides (NOX) and nitrogen di-oxide (NO2) and the influence of baseline personal characteristics, living environment and daily activity patterns of the participants on the exposures among adults over 35 in Tianjin and Shanghai. METHODS:In this panel study, 91 healthy nonsmoking adults aged over 35 from Tianjin and Shanghai participated in our study. The study was conducted in summer and winter. The participants were followed for three times with an interval of at least two weeks. Only participants in Shanghai were followed once in winter because of the COVID-19 pandemic. Twenty-seven participants completed follow-up visits in both seasons. We measured their 24 h personal exposures to NOX and NO2and collected their baseline and time-activity information through questionnaire/diary. The linear mixed model was used to analyze the associations between potential influencing factors and personal NOX and NO2 exposure levels. RESULTS:There were 349 follow-up visits with valid 24 h personal NO2 and NOX exposure measurements in the two cities. The ave-rage 24 h personal exposures to NO2 and NOX (volume fraction) in Tianjin participants were 18.0×10-9 and 26.2×10-9 in summer, and 31.0×10-9 and 54.9×10-9 in winter, respectively; and the average 24 h personal exposures to NO2 and NOX in Shanghai participants were 38.7×10-9 and 100.0×10-9 in summer, and 45.5×10-9 and 139.2×10-9 in winter, respectively. The results of univariate regression analysis showed that their personal NOX exposure levels were significantly associated with city, season, gender, average daily cooking times, and ambient NO2 concentrations measured at fixed-site monitoring stations. In addition to the above factors, the personal NOX exposure levels were also significantly associated with educational level and the personal NO2 exposure levels were also significantly associated with passive smoking, average daily home time, cooking energy type, residential distance from main traffic road, and use of kitchen ventilators. Multivariate regression analysis showed that the personal exposure levels of NO2 and NOX were significantly lower in Tianjin than that in Shanghai, were significantly lower in summer than that in winter, and were significantly and positively associated with ambient NO2 concentrations measured at fixed-site monitoring stations. In addition, personal NOX exposure levels were significantly lower in females than in males, and personal NO2 exposure levels were significantly positively associated with average daily cooking times and significantly inversely associated with average daily home time. For every interquartile range (IQR) increase (12.7×10-9) in ambient NO2, the personal NO2 exposure levels increased by 27.5% (95%CI: 17.0%-38.9%), and personal NOX exposure levels increased by 16.1% (95%CI: 7.1%-25.8%). CONCLUSION:Season, city and ambient NO2 concentrations are significant influencing factors of personal exposure levels of NO2and NOX. At the same time, the personal exposures levels of NO2are also affected by lifestyle factors. Our study provides scientific evidence for making precise air pollution control decisions and reducing the exposure levels of NOX in the population.

BackgroundArterial stiffness (AS) is an important predicting factor for cardiovascular disease. However, no epidemiological studies have ever explored the mediating role of biomarkers in the association between ozone and AS, nor weather fish oil modified such association.MethodsStudy participants were drawn from the UK biobank, and a total of 95,699 middle-aged and older adults were included in this study. Ozone was obtained from Community Multiscale Air Quality (CMAQ) model matched to residential addresses, fish oil from self-reported intake, and arterial stiffness was based on device measurements. First, we applied a double robust approach to explore the association between ozone or fish oil intake and arterial stiffness, adjusting for potential confounders at the individual and regional levels. Then, how triglycerides, apolipoprotein B (Apo B)/apolipoprotein A (ApoA) and non-high-density lipoprotein cholesterol (Non-HDL-C) mediate the relationship between ozone and AS. Last, the modifying role of fish oil was further explored by stratified analysis.ResultsThe mean age of participants was 55 years; annual average ozone exposure was associated with ASI (beta:0.189 [95%CI: 0.146 to 0.233], P < 0.001), and compared to participants who did not consume fish oil, fish oil users had a lower ASI (beta: 0.061 [95%CI: -0.111 to -0.010], P = 0.016). The relationship between ozone exposure and AS was mediated by triglycerides, ApoB/ApoA, and Non-HDL-C with mediation proportions ranging from 10.90% to 18.30%. Stratified analysis showed lower estimates on the ozone-AS relationship in fish oil users (P = 0.011).ConclusionOzone exposure was associated with higher levels of arterial stiffness, in contrast to fish oil consumption, which showed a protective association. The association between ozone exposure and arterial stiffness was partially mediated by some biomarkers. In the general population, fish oil consumption might provide protection against ozone-related AS.

BACKGROUND:In the context of climate change and urbanization, the temporal variation of the adverse health effect of extreme temperature has attracted increasing attention. METHODS:The meteorological data and the daily death records of mortality from respiratory diseases of 136 Chinese cities were from 2006 to 2019. Heat wave and cold spell were selected as the indicator events of extreme high temperature and extreme low temperature, respectively. The generalized linear model and time-varying distributed lag model were used to perform a two-stage time-series analysis to evaluate the temporal variation of the mortality risk associated with extreme temperature in the total population, sub-populations (sex- and age- specific) and different regions (climatic zone and relative humidity level). RESULTS:During the study period, relative risk (RR) of respiratory mortality associated with heat wave decreased from 1.22 (95 %CI: 1.07-1.39) to 1.13 (95 %CI: 1.01-1.26) in the total population, and RR of respiratory mortality associated with cold spell decreased from 1.30 (95 %CI: 1.14-1.49) to 1.17 (95 %CI: 1.08-1.26). The impact of heat wave reduced in the males (P = 0.044) and in the females as with cold spell (P < 0.001). The respiratory mortality risk of people over 65 associated with cold spell decreased (P = 0.040 for people aged 65-74 and P < 0.001 for people over 75). The effect of cold spell reduced in cities from tropical or arid zone (P = 0.035). The effects of both heat wave and cold spell decreased in cities with the relative humidity in the first quartile (P = 0.046 and 0.010, respectively). CONCLUSION:The impact of heat wave on mortality of respiratory diseases decreased mainly in males and cities with the lowest relative humidity, while the impact of cold spell reduced in females, people over 65 and tropical and arid zone, suggesting adaptation to extreme temperature of Chinese residents to some extent.

Exposure to ambient particulate matter with an aerodynamic diameter ≤ 2.5 µm (PM2.5) has been associated with oxidative damage. This study investigated the PM2.5-bound polycyclic aromatic hydrocarbon (PAH) exposure levels during elevated PM2.5 levels and the oxidative damage among a preaging females in Chiang Mai, Thailand. The 64 female participants, aged between 50 and 65 years old, were followed for 5 weeks consecutively during the non-haze rainy season as the baseline and haze episodes. The morning void urine sample was collected weekly and analyzed for 8 species of hydroxylated-polycyclic aromatic hydrocarbons (OH-PAHs) and malondialdehyde (MDA). The results showed that the high increase in PM2.5 levels was positively associated with OH-PAH levels. In addition, for every 1 µg/gCre increase in individual urinary OH-PAH concentrations, the MDA concentration increased from 0.073 to 2.071 µg/gCre. Therefore, the present study suggested that detected urinary OH-PAHs were attributable to PM2.5-bound PAH exposure, particularly from inhalation. These study results provide useful information for policy makers and public health agencies to mitigate the chain effects of PM2.5 exposure from haze pollution. Keywords: Air pollution, Hydroxylated-PAHs, Oxidative stress, Urinary biomarkers