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The impact of early life exposure to residential greenness on childhood rhinitis and its interaction with particulate matter (PM) of different size fractions remain inconsistent. Herein, we recruited 40,486 preschool children from randomly selected daycare centers in 7 cities in China from 2019 to 2020, and estimated exposure to residential greenness by the normalized difference vegetation index (NDVI) with a 500 m buffer. Exposure to ambient PM (PM 1 , PM 2.5, and PM 10 ) was evaluated using a satellite-based prediction model (daily, at a resolution of 1 km × 1 km). By mixed-effect logistic regression, NDVI values during pregnancy, in the first (0-1 year old) and the second (1-2 years old) year of life were negatively associated with lifetime rhinitis (LR) and current rhinitis (CR) (P < 0.001). PM in the same time windows was associated with increased risks of LR and CR in children, with smaller size fraction of PM showing greater associations. The negative associations between prenatal and postnatal NDVI and LR and CR in preschool children remained robust after adjusting for concomitant exposure to PM, whereas the associations of postnatal NDVI and rhinitis showed significant interactions with PM. At lower levels of PM, postnatal NDVI remained negatively associated with rhinitis and was partly mediated by PM (10.0-40.9 %), while at higher levels of PM, the negative associations disappeared or even turned positive. The cut-off levels of PM were identified for each size fraction of PM. In conclusion, prenatal exposure to greenness had robust impacts in lowering the risk of childhood rhinitis, while postnatal exposure to greenness depended on the co-exposure levels to PM. This study revealed the complex interplay of greenness and PM on rhinitis in children. The exposure time window in prenatal or postnatal period and postnatal concomitant PM levels played important roles in influencing the associations between greenness, PM and rhinitis., Competing Interests: Declaration of competing interest None of the authors declares any conflict of interest., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Background: Increasing studies linked outdoor air pollution (OAP), indoor environmental factors (IEFs), and antibiotics use (AU) with the first wave of allergies (i.e., asthma, allergic rhinitis, and eczema), yet the role of their exposures on children's second wave of allergy (i.e., food allergy) are unknown., Objectives: To investigate the association between exposure to OAP and IEFs and childhood doctor-diagnosed food allergy (DFA) during the pre-pregnancy, prenatal, early postnatal, and current periods, and to further explore the effect of OAP and IEFs on DFA in children co-exposed to antibiotics., Methods: A retrospective cohort study involving 8689 preschoolers was carried out in Changsha, China. Data on the health outcomes, antibiotic use, and home environment of each child were collected through a questionnaire. Temperature and air pollutants data were obtained from 8 and 10 monitoring stations in Changsha, respectively. Exposure levels to temperature and air pollutants at individual home addresses were calculated by the inverse distance weighted (IDW) method. Multiple logistic regression models were employed to assess the associations of childhood DFA with exposure to OAP, IEF, and AU., Results: Childhood ever doctor-diagnosed food allergy (DFA) was linked to postnatal PM 10 exposure with OR (95% CI) of 1.18 (1.03-1.36), especially for CO and O 3 exposure during the first year with ORs (95% CI) = 1.08 (1.00-1.16) and 1.07 (1.00-1.14), as well as SO 2 exposure during the previous year with OR (95% CI) of 1.13 (1.02-1.25). The role of postnatal air pollution is more important for the risk of egg, milk and other food allergies. Renovation-related IAP (new furniture) and dampness-related indoor allergens exposures throughout all time windows significantly increased the risk of childhood DFA, with ORs ranging from 1.23 (1.03-1.46) to 1.54 (1.29-1.83). Furthermore, smoke-related IAP (environmental tobacco smoke [ETS], parental and grandparental smoking) exposure during pregnancy, first year, and previous year was related to DFA. Additionally, exposure to pet-related indoor allergens (cats) during first year and total plant-related allergens (particularly nonflowering plants) during previous year were associated with DFA. Moreover, exposure to plant-related allergy during first and previous year was specifically associated with milk allergy, while keeping cats during first year increased the risk of fruits/vegetables allergy. Life-time and early-life AU was associated with the increased risk of childhood DFA with ORs (95% CI) = 1.57 (1.32-1.87) and 1.46 (1.27-1.67), including different types food allergies except fruit/vegetable allergy., Conclusions: Postnatal OAP, life-time and early-life IEFs and AU exposure played a vital role in the development of DFA, supporting the "fetal origin of childhood FA" hypothesis., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Background: Few studies focus on the associations of green space composition and configuration with children's allergic rhinitis (AR)., Methods: A multi-center population-based cross-sectional study was performed in 7 cities in mainland of China between 2019 and 2020, recruiting 36,867 preschool children. Information on the current AR symptoms and demographics were collected by questionnaire. Exposure to residential greenness was estimated by Normalized Difference Vegetation Index (NDVI, 1000 m buffer) around the residences. Greenness composition was estimated in 3 main categories: forest, grassland, shrubland. Configuration of each category and total greenness (a spatial resolution of 10 m × 10 m) was estimated by 6 landscape pattern metrics to quantify their area, shape complexity, aggregation, connectivity, and patch density. Exposure to daily ambient particulate matter (PM 1 , PM 2.5 and PM 10 , a spatial resolution of 1 km × 1 km) was estimated. Multilevel logistic regression models were applied to analyze the associations of greenness and its composition and configuration with AR, and mediation effects by PMs were examined by mediation analysis models., Results: The prevalence of self-reported current AR in preschool children was 33.1%. Two indicators of forest, Aggregation Index of forest patches (AIforest) (odds ratio (OR):0.92, 95% Confidential Interval (CI): 0.88-0.97), and Patch Cohesion of forest (COHESIONforest) (OR: 0.93, 95% CI:0.89-0.98) showed significantly negative associations with AR symptoms. Mediation analyses found the associations were partially mediated by PMs. Age, exclusive breastfeed duration and season were the potential effect modifiers. The associations varied across seven cities., Conclusion: Our findings suggest the inverse associations of the aggregation and connectivity of forest patches surrounding residence addresses with AR symptoms. Since the cross-sectional study only provides associations rather than causation, further studies are needed to confirm our results as well as the underlying mechanisms., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests:Zhuohui zhao reports financial support was provided by the Shanghai 3-year Public Health Action Plan [grant numbers GWVI-11.2-XD11]. Zhuohui zhao reports financial support was provided by Shanghai International Science and Technology Partnership Project (No. 21230780200). Zhuohui zhao reports financial support was provided by Shanghai B&R Joint Laboratory Project [grant numbers No.22230750300]., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Background: Airborne particulate matter pollution has been linked to occurrence of childhood allergic rhinitis (AR). However, the relationships between exposure to particulate matter with an aerodynamic diameter ≤1 μm (PM 1 ) during early life (in utero and first year of life) and the onset of childhood AR remain largely unknown. This study aims to investigate potential associations of in utero and first-year exposures to size-segregated PMs, including PM 1 , PM 1-2.5 , PM 2.5 , PM 2.5-10 , and PM 10 , with childhood AR., Methods: We investigated 29286 preschool children aged 3-6 years in 7 Chinese major cities during 2019-2020 as the Phase II of the China Children, Families, Health Study. Machine learning-based space-time models were utilized to estimate early-life residential exposure to PM 1 , PM 2.5 , and PM 10 at 1 × 1-km resolutions. The concentrations of PM 1-2.5 and PM 2.5-10 were calculated by subtracting PM 1 from PM 2.5 and PM 2.5 from PM 10 , respectively. Multiple mixed-effects logistic models were used to assess the odds ratios (ORs) and 95% confidence intervals (CIs) of childhood AR associated with per 10-μg/m 3 increase in exposure to particulate air pollution during in utero period and the first year of life., Results: Among the 29286 children surveyed (mean ± standard deviation, 4.9 ± 0.9 years), 3652 (12.5%) were reported to be diagnosed with AR. Average PM 1 concentrations during in utero period and the first year since birth were 36.3 ± 8.6 μg/m 3 and 33.1 ± 6.9 μg/m 3 , respectively. Exposure to PM 1 and PM 2.5 during pregnancy and the first year of life was associated with an increased risk of AR in children, and the OR estimates were higher for each 10-μg/m 3 increase in PM 1 than for PM 2.5 (e.g., 1.132 [95% CI: 1.022-1.254] vs. 1.079 [95% CI: 1.014-1.149] in pregnancy; 1.151 [95% CI: 1.014-1.306] vs. 1.095 [95% CI: 1.008-1.189] in the first year of life). No associations were observed between AR and both pre- and post-natal exposure to PM 1-2.5 , indicating that PM 1 rather than PM 1-2.5 contributed to the association between PM 2.5 and childhood AR. In trimester-stratified analysis, childhood AR was only found to be associated with exposure to PM 1 (OR = 1.077, 95% CI: 1.027-1.128), PM 2.5 (OR = 1.048, 95% CI: 1.018-1.078), and PM 10 (OR = 1.032, 95% CI: 1.007-1.058) during the third trimester of pregnancy. Subgroup analysis suggested stronger PM-AR associations among younger (<5 years old) and winter-born children., Conclusions: Prenatal and postnatal exposures to ambient PM 1 and PM 2.5 were associated with an increased risk of childhood AR, and PM 2.5 -related hazards could be predominantly attributed to PM 1 . These findings highlighted public health significance of formulating air quality guideline for ambient PM 1 in mitigating children's AR burden caused by particulate air pollution., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Background: Parasitic infections (PIs) are common and pose substantial health hazards in children globally, but the fundamental environmental variables exposure during crucial time window(s) are unclear., Objectives: To identify key indoor and outdoor environmental factors leading to childhood PIs throughout critical time window(s)., Methods: A combined cross-sectional and retrospective cohort study was performed on 8689 children residing in Changsha, China. Data was acquired pertaining to the health status and environmental exposure of the children in their homes. Personal exposure to outdoor air pollutants at the residential address during the preconceptional, perinatal, and postnatal periods was computed using data from ten air quality monitoring stations. An analysis of the relationships between childhood PIs and both indoor and outdoor factors was conducted using a multiple logistic regression model., Results: Childhood PIs were associated with outdoor CO and ozone (O 3 ) exposure during the 10th-12th months prior to pregnancy, with ORs (95 % CI) of 1.68 (1.24-2.27) and 1.60 (1.15-2.22), respectively; childhood PIs were also associated with CO exposure during one year prior to pregnancy and the first trimester in utero [ORs = 1.57 (1.14-2.15) and 1.52 (1.17-1.97)]. Childhood PIs were found to be associated with PM 2.5 exposure during pregnancy and the first year, with odds ratios of 1.51 (1.14-2.00) and 1.95 (1.22-3.12) per IQR increase in pollutant exposure, respectively. Exposures to smoke, renovation-related indoor air pollution (IAP), dampness and plant-related indoor allergens in the early life and past year were all associated with childhood PI, with odds ratios (95 % CI) ranging from 1.40 (1.01-1.95) for environmental tobacco smoke (ETS) during pregnancy to 1.63 (1.12-2.37) for mold/damp stains in the past year. In terms of PI risk, the early life and present periods were critical time windows for outdoor and indoor exposures, respectively. Certain individuals were more vulnerable to the PI risk associated with both indoor and outdoor exposures. Antibiotic use during child's lifetime and early years increased and decreased the PI risk of exposure to outdoor and indoor environments, respectively., Conclusions: Exposure to outdoor air pollution in early life and indoor environments in the past year were found to be associated with childhood PI., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Background: The potential role of dermal exposure diisononyl phthalate (DINP) as an adjuvant in allergic inflammation and asthma has been suggested. However, the current findings do not provide enough evidence to support this claim., Objectives: The purpose of this investigation was to examine the impact and mechanisms of allergic asthma exacerbation through the dermal exposure to DINP., Methods: The study was undertaken using OVA-sensitized mice. Lung histopathology and airway hyperreactivity (AHR) were assessed. Expression levels of immunoglobulins (t-IgE, OVA-IgE and OVA-IgG1), cytokines (IL-31, IL-4, IL-5, IL-6, IL-13 and INF-γ), and TRPV1 were measured. To investigate the mechanism by which allergic asthma worsens due to dermal exposure to DINP, the blockade analysis using the IL-31 antagonist SB-431542 and the TRPV1 antagonist capsazepine (CZP) were performed., Results: The findings of the study revealed that the simultaneous exposure to DINP and OVA resulted in an increase in inspiratory resistance (Ri) and expiratory resistance (Re), a decrease in the minimum value of lung dynamic compliance (Cldyn), and worsened airway remodeling. Additionally, it was found that this exposure led to an increase in the levels of IL-31 and TRPV1, which are biomarkers of Th2 cytokines (IL-4, IL-5, IL-6, and IL-13), as well as immunoglobulins (Total IgE, OVA-lgE, and OVA-IgG1), while decreasing the biomarker of Th1 cytokines (IFN-γ). However, these impairments showed improvement after the administration of SB-431542 or CZP., Conclusion: The findings of this research indicate that the IL-31/TRPV1 pathway plays a moderating function in OVA-induced allergic asthma worsened by dermal exposure to DINP., Competing Interests: Declaration of competing interest The authors declare no competing financial interest., (Copyright © 2023. Published by Elsevier B.V.)

Background: Despite mounting evidence linking outdoor air pollution with otitis media (OM), the role of air pollutant(s) exposure during which critical window(s) on childhood OM remains unknown., Objectives: We sought to identify the key air pollutant(s) and critical window(s) associated with the onset and recurrent attacks of OM in kindergarten children., Methods: A combined cross-sectional and retrospective cohort study involving 8689 preschoolers aged 3-6 years was performed in Changsha, China. From 2013-2020, data on air pollutants were collected from ambient air quality monitoring stations in Changsha, and the exposure concentration to each child at their home address was calculated using the inverse distance weighted (IDW) method. The relationship between air pollution and OM in kindergarten children was studied using multiple logistic regression models., Results: Childhood lifetime OM was associated with PM 2.5 , SO 2 and NO 2 , with ORs (95% CI) of 1.43 (1.19-1.71), 1.18 (1.01-1.37) and 1.18 (1.00-1.39) by per IQR increase in utero exposure and with PM 2.5 , PM 2.5-10 and PM 10 , with ORs = 1.15 (1.00-1.32), 1.25 (1.13-1.40) and 1.49 (1.28-1.74) for entire post-natal exposure, respectively. The 2nd trimester in utero and the post-natal period, especially the 1st year, were key exposure time windows to PM 2.5 and PM 10 associated with lifetime OM and the onset of OM. Similarly, the 4th gestational month was a critical window for all pollutants except CO exposure in relation to lifetime OM and OM onset, but not recurrent OM attacks. PM 2.5 exposure during the nine gestational months and PM 10 exposure during the first three years had cumulative effects on OM development. Our subgroup analysis revealed that certain children were more susceptible to the OM risk posed by air pollution., Conclusions: Early-life exposure to air pollution, particularly PM 2.5 during the middle of gestation and PM 10 during the early post-natal period, was associated with childhood OM., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Nitrogen dioxide (NO 2 ) is a widespread air pollutant. Epidemiological evidence indicates that NO 2 is associated with an increase of incidence rate and mortality of asthma, but its mechanism is still unclear. In this study, we exposed mice to NO 2 (5 ppm, 4 h per day for 30 days) intermittently to investigate the development and potential toxicological mechanisms of allergic asthma. We randomly assigned 60 male Balb/c mice to four groups: saline control, ovalbumin (OVA) sensitization, NO 2 alone, and OVA+NO 2 groups. The involved mechanisms were found from the perspective of airway inflammation and oxidative stress. The results showed that NO 2 exposure could aggravate lung inflammation in asthmatic mice, and airway remodeling was characterized by significant thickening of the airway wall and infiltration of inflammatory cells. Moreover, NO 2 would aggravate the airway hyperresponsiveness (AHR), which is characterized by significantly elevated inspiratory resistance (Ri) and expiratory resistance (Re), as well as decreased dynamic lung compliance (Cldyn). In addition, NO 2 exposure promoted pro-inflammatory cytokines (IL-6 and TNF-α) and serum immunoglobulin (IgE) production. The imbalance of Th1/Th2 cell differentiation (IL-4 increased, IFN-γ reduced, IL-4/IFN-γ significantly increased) played a key role in the inflammatory response of asthma under NO 2 exposure. In a nutshell, NO 2 exposure could promote allergic airway inflammation and increase asthma susceptibility. The levels of ROS and MDA among asthmatic mice exposed to NO 2 increased significantly, while GSH levels sharply decreased. These findings may provide better toxicological evidence for the mechanisms of allergic asthma risk due to NO 2 exposure., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Background: Despite mounting evidence linked pneumonia with air pollution, it is unclear what main pollutant(s) exposure in which critical window(s) play a key role in pneumonia., Objective: To examine effects of intrauterine and post-natal exposure to air pollution on children's doctor-diagnosed pneumonia (DDP)., Methods: A combination of cross-sectional and retrospective cohort study was conducted at Changsha, China during 2019-2020. Personal exposure to outdoor air pollutants at each child's home address was estimated using inverse distance weighted (IDW) method based on data from 10 air quality monitoring stations. Associations between personal air pollution exposure and DDP were evaluated., Results: Children's DDP was associated with intrauterine and post-natal exposure to PM 2.5 , PM 2.5-10 , and PM 10 , adjusted ORs (95% CI) of 1.17 (1.04-1.30), 1.09 (1.01-1.17), and 1.07 (1.00-1.14) for IQR increase in intrauterine exposure and 1.12 (1.02-1.22), 1.13 (1.06-1.21), and 1.28 (1.16-1.41) for post-natal exposure. Intrauterine PM 2.5 exposure and post-natal PM 10 exposure were associated with a higher risk of pneumonia. We identified the 2nd trimester, 3rd trimester, and first year as critical windows respectively for PM 2.5 , PM 2.5-10 , and PM 10 exposure. Daytime exposure to traffic-related air pollution especially during early life increased DDP., Conclusion: Intrauterine and post-natal exposure to particulate matters played a dominant role in children's DDP., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Allergic asthma is a complicated respiratory disease with many concerns. Mounting epidemiological evidence linked temperature (T) and NO 2 with allergic asthma, yet toxicological studies remain scarce. We conducted an in vivo study to explore toxicological evidence in T-NO 2 interaction on allergic asthma, to investigate underlying toxicological mechanisms. 90 male Balb/c mice were randomly and equally divided into 6 groups including saline control, ovalbumin (OVA)-sensitized, OVA + 35 °C, OVA + NO 2 , OVA + 35 °C + NO 2 , and OVA + 35 °C + NO 2 + capsazepine (CZP), adopting treatment for 38 days. We measured pulmonary functions of inspiratory resistance (Ri), expiratory resistance (Re) and airway compliance (Cldyn), serum protein biomarkers, indexes of pulmonary inflammation, histopathological changes and protective effects of CZP. Airway hyperresponsiveness (AHR) was aggravated by high T (35 °C) and NO 2 (5 ppm) co-exposure with a series of aggravating asthmatic symptoms including airway wall thickening, lumen stenosis, goblet cell proliferation, mucus hypersecretion, and subepithelial fibrotic hyperplasia, providing evidence in the toxicological impact of high T-NO 2 interaction. The biomarkers of serum immune functions (Total-IgE, OVA-sIgE and IL-4), pro-inflammation (IL-6 and TNF-α), oxidative stress cytokines (8-OHdG, ROS and MDA), airway resistance (Ri and Re), and TRPV1 expression significantly increased, while IFN-γ, GSH and airway compliance (Cldyn) significantly decreased with co-exposure to high T and NO 2 . We observed that CZP addition significantly ameliorated these toxicological effects and biomarker levels induced by heat-NO 2 interaction. Our results suggest a toxicity of heat-NO 2 interaction on asthma with clear mechanisms, which can be ameliorated by CZP, indicating that both oxidative stress and TRPV1 expression may be primarily responsible for asthma of heat-NO 2 -induced toxicity., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Mounting evidence have linked ambient air pollution and temperature with childhood pneumonia, but it is unclear whether there is an interaction between air pollution and temperature on childhood pneumonia. We aim to assess the combined effect of ambient air pollution and temperature exposure during preconception and pregnancy on pneumonia by a case-control study of 1510 children aged 0-14 years in Changsha, China. We obtained the data of childhood pneumonia from XiangYa Hospital electrical records. We estimated personal exposure to outdoor air pollution (PM 10 , SO 2 and NO 2 ) by inverse distance weighted (IDW) method and temperature indicators. Multiple logistic regression models were used to evaluate associations of childhood pneumonia with air pollution, temperature (T), and diurnal temperature variation (DTV). We found that exposure to industry-related air pollution (PM 10 and SO 2 ) during preconception and pregnancy were associated with childhood pneumonia, with ORs (95% CI) of 1.72 (1.48-1.98) and 2.96 (2.50-3.51) during 1 year before pregnancy and 1.83 (1.59-2.11) and 3.43 (2.83-4.17) in pregnancy. Childhood pneumonia was negatively associated with T exposure during 1 year before pregnancy and pregnancy, with ORs (95% CI) of 0.57 (0.41-0.80) and 0.85 (0.74-0.98). DTV exposure during pregnancy especially during the 1st and 2nd trimesters significantly increased pneumonia risk, with ORS (95% CI) of 1.77 (1.19-2.64), 1.47 (1.18-1.83), and 1.37 (1.07-1.76) respectively. We further observed interactions of PM 10 and SO 2 exposure with low T and high DTV during conception and pregnancy in relation to childhood pneumonia. This study suggests that there were interactions air pollution with temperature and DTV on pneumonia development., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Background: The rapid increase of food allergy (FA) has become the "second wave" of allergy epidemic and is now a major global public health concern. Mounting evidence indicates that early life exposure to air pollution is associated with the "first wave" of allergy epidemic (including asthma, allergic rhinitis and eczema) in children, but little is known about its association with FA., Objectives: We hypothesize FA has triple exposure pathways, gut-skin-airway, and investigate the effects of airway exposure to outdoor and indoor air pollution on childhood FA., Methods: A cohort study of 2598 preschool children aged 3-6 years old was conducted in Changsha, China. The prevalence of FA was surveyed using a standard questionnaire by International Study of Asthma and Allergies in Childhood (ISAAC). Exposure to indoor air pollution was assessed by four indicators: new furniture, redecoration, mold or dampness, and window condensation. Exposure to outdoor air pollution was evaluated by the concentrations of PM10, SO2 and NO2, which were obtained from the monitored stations. Both prenatal and postnatal exposure windows were considered. The association between exposure to outdoor/indoor air pollution and childhood FA was estimated by multiple logistic regression models using odds ratio (OR) and a 95% confidence interval (CI)., Results: A total of 14.9% children reported FA. The prevalence was significantly associated with exposure to indoor air pollution, OR (95% CI) = 1.93 (1.35-2.75) for prenatal exposure to mold/dampness and 1.49 (1.07-2.10) and 1.41 (1.04-1.89) respectively for postnatal exposure to new furniture and window condensation. The prevalence of FA was also associated with prenatal and postnatal exposure to outdoor air pollution, particularly the traffic-related air pollutant NO2, with adjusted ORs (95% Cls) respectively 1.24 (1.00-1.54) and 1.38 (1.03-1.85) per interquartile range (IQR) increase. Sensitivity analysis showed that the association between outdoor/indoor air pollution and childhood FA was significant only in young children aged 3-4 years., Conclusion: Early-life exposure to high levels of outdoor and indoor air pollution in China due to the rapid economic growth and fast urbanization in the past decades may contribute to the rapid increase of food allergy (FA) in children. Our study indicates that, in addition to gut and skin, airway may be a new route of food sensitization. Air pollution leads to the first and second waves of allergy epidemics, suggesting a concept of 'one allergy' disease., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper, (Copyright © 2022 Elsevier Inc. All rights reserved.)

Background: The prevalence of childhood allergies has increased during past decades leading to serious hospitalization and heavy burden worldwide, yet the key factors responsible for the onset of early symptoms and development of diagnosed diseases are unclear., Objective: To explore the role of early life exposure to ambient air pollution and indoor environmental factors on early allergic symptoms and doctor diagnosed allergic diseases., Methods: A retrospective cohort study of 2598 preschool children was conducted at 36 kindergartens in Changsha, China from September of 2011 to February of 2012. A questionnaire was developed to survey each child's early onset of allergic symptoms (wheeze and rhinitis-like symptoms) and doctor diagnosis of allergic diseases (asthma and rhinitis) as well as home environments. Each mother's and child's exposures to ambient air pollutants (PM 10 , SO 2 , and NO 2 ) and temperature were estimated for in utero and postnatal periods. The associations of early symptoms and diagnosed diseases with outdoor air pollution and indoor environmental variables were examined by logistic regression models., Results: Childhood early allergic symptoms (33.9%) including wheeze (14.7%) and rhinitis-like symptoms (25.4%) before 2 years old were not associated with outdoor air pollution exposure but was significantly associated with maternal exposure of window condensation at home in pregnancy with ORs (95% CI) of 1.33 (1.11-1.59), 1.30 (1.01-1.67) and 1.27 (1.04-1.55) respectively, and was associated with new furniture during first year after birth with OR (95% CI) of 1.43 (1.02-2.02) for early wheeze. Childhood diagnosed allergic diseases (28.4%) containing asthma (6.7%) and allergic rhinitis (AR) (7.2%) were significantly associated with both outdoor air pollutants (mainly for SO 2 and NO 2 ) during first 3 years and indoor new furniture, redecoration, and window condensation. We found that sex, age, parental atopy, maternal productive age, environmental tobacco smoke (ETS), antibiotics use, economic stress, early and late introduction of complementary foods, and outdoor air pollution modified the effects of home environmental exposure in early life on early allergic symptoms and diagnosed allergic diseases., Conclusion: Our study indicates that early life exposure to indoor environmental factors plays a key role in early onset of allergic symptoms in children, and further exposure to ambient air pollution and indoor environmental factors contribute to the later development of asthma and allergic rhinitis., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Background: The novel coronavirus disease 2019 (COVID-19) has spread rapidly around the world since December 8, 2019. However, the key factors affecting the duration of recovery from COVID-19 remain unclear., Objective: To investigate the associations of long recovery duration of COVID-19 patients with ambient air pollution, temperature, and diurnal temperature range (DTR) exposure., Methods: A total of 427 confirmed cases in Changsha during the first wave of the epidemic in January 2020 were selected. We used inverse distance weighting (IDW) method to estimate personal exposure to seven ambient air pollutants (PM 2.5 , PM 2.5-10 , PM 10 , SO 2 , NO 2 , CO, and O 3 ) at each subject's home address. Meteorological conditions included temperature and DTR. Multiple logistic regression model was used to investigate the relationship of air pollution exposure during short-term (past week and past month) and long-term (past three months) with recovery duration among COVID-19 patients., Results: We found that long recovery duration among COVID-19 patients was positively associated with short-term exposure to CO during past week with OR (95% CI) = 1.42 (1.01-2.00) and PM 2.5 , NO 2 , and CO during past month with ORs (95% CI) = 2.00 (1.30-3.07) and 1.95 (1.30-2.93), and was negatively related with short-term exposure to O 3 during past week and past month with ORs (95% CI) = 0.68 (0.46-0.99) and 0.41 (0.27-0.62), respectively. No association was observed for long-term exposure to air pollution during past three months. Furthermore, increased temperature during past three months elevated risk of long recovery duration in VOCID-19 patients, while DTR exposure during past week and past month decreased the risk. Male and younger patients were more susceptible to the effect of air pollution on long recovery duration, while female and older patients were more affected by exposure to temperature and DTR., Conclusion: Our findings suggest that both TRAP exposure and temperature indicators play important roles in prolonged recovery among COVID-19 patients, especially for the sensitive populations, which provide potential strategies for effective reduction and early prevention of long recovery duration of COVID-19., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Background: Increasing evidence have associated pneumonia with early exposure to ambient air pollution. However, the role of indoor environmental factors exposure in early life on childhood pneumonia remains unclear., Objective: To examine the association between indoor environmental factors exposure during different timing windows and childhood pneumonia, and to identify the key indoor factor(s) in different critical window(s)., Methods: A retrospective cohort study of 8689 pre-schoolers was performed in Changsha, China during 2019-2020. Our questionnaire survey was designed to collect information on pre-schooler's outcome and residential environmental exposure containing indoor pollution and allergens during 1 year before pregnancy, pregnancy, first year, and past year. The associations were further estimated stratified by personal exposure level of outdoor NO 2 , CO, temperature (T) and different covariates. Associations were assessed by multiple logistic regression model in terms of odds ratio (OR) of 95% confidence interval (CI)., Results: Pre-schooler's pneumonia was significantly related with exposure of new furniture, redecoration, mold/damp stains, and mold or damp clothing or bedding exposure during the four periods, with the strongest associations observed during 1 year before pregnancy based on multi-window model, with ORs (95% CI) of 1.27 (1.12-1.44), 1.26 (1.09-1.46), 1.34 (1.14-1.57), and 1.28 (1.05-1.56) respectively. Environmental tobacco smoke (ETS) including both parental and grandparental smoking were significantly related with increased risk of pre-schooler's pneumonia, and ETS played a more important role in early life, with ORs (95% CI) of 1.17 (1.01-1.36) and 1.19 (1.02-1.39) in pregnancy and first year. Indoor plants particularly nonflowering plants significantly elevated pneumonia risk but only in past year, with ORs (95% CI) of 1.17 (1.05-1.30) and 1.14 (1.03-1.26). Higher pneumonia risk was observed for renovation exposure in pre-birth compared to post-birth, while mold/dampness exerted an accumulative effect with the highest risk for exposure during both pre- and post-birth. Living near traffic road and exposure to high level of traffic-related air pollution and high temperature significantly increased pneumonia risk. Sensitivity analysis found that some sub-groups were more susceptible to pneumonia risk of home environment exposure., Conclusion: Early life exposure to indoor environmental factors plays an important role in pneumonia development, supporting the hypothesis of "Preconceptional and Fetal Origin of Childhood Pneumonia" and "Developmental Origins of Health and Pneumonia"., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Background: There is growing evidence that allergic rhinitis (AR) is associated with indoor environmental factors, but their role in childhood AR during early life remains unclear., Objective: To investigate the association of preconceptional, prenatal, early postnatal, and current exposure to home environmental factors with childhood AR, and to further explore whether this association can be interacted by outdoor air pollution and temperature., Methods: A retrospective cohort study of 8689 preschool children was conducted during 2019-2020 in Changsha, China. A standard questionnaire was used to collect data on each family's health outcomes and home environments. We considered home environmental exposures during one year before conception, pregnancy, first year of life, and past year. Associations of indoor air pollution and allergens with AR were assessed by multiple logistic regression models., Results: Pre-birth exposure to indoor air pollution emitted by new furniture or redecoration and dampness related allergen derived from mold/damp stains and mold/damp clothes or bedding during 1 year before conception and pregnancy was significantly associated with increased AR, with adjusted ORs (95% CI) ranging from 1.35 (1.05-1.75) to 1.87 (1.55-2.27). Childhood AR was also significantly related with post-birth exposure to dampness related indoor allergen including mold/damp stains and mold/damp clothes or bedding in first year and past year and pollen allergen including total and nonflowing plants in past year, with a range of ORs (95% CI) from 1.20 (1.01-1.42) to 1.79 (1.42-2.27). We identified that pre-birth, particularly in utero exposure to both indoor air pollution from renovation and dampness related allergens, played a key role in AR development compared to post-birth exposures, and accumulative effect was observed with the highest risk of AR. High exposure to traffic-related air pollution (TRAP) including outdoor PM 2.5 , NO 2 , CO, and O 3 , as well as living near traffic road not only significantly increased adverse effect of home environmental factors but also decreased protective effect of household dogs on childhood AR. Early life exposure to low temperature in pregnancy and high temperature in first year significantly increased AR risk of home environmental exposure. Sensitivity analysis indicated that some sub-groups were more susceptible to AR risk of home environmental exposure., Conclusion: Our study suggests that pre-birth exposure to home environmental factors played an important role in AR development and this effect can be interacted by TRAP and temperature, which supports a hypothesis of "(pre)fetal origin of childhood AR"., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)

Early life environment can affect asthma and allergies but few cohort studies on this issue are available from China. Our aim was to investigate reported onset of childhood wheeze, rhinitis and eczema symptoms in relation to prenatal, perinatal and postnatal home environment. Data on home environment and symptoms (ISAAC based questions) in first two years of life and in the past 12 months were reported by parents of the children (3-6 y) in a cross-sectional questionnaire survey in ten day care centers in Taiyuan, northern China (N = 3606). Changes of symptoms from the first 2 years of life to the past 12 months (recall period) were calculated retrospectively. Multilevel logistic regression analysis was applied. Reported onset of wheeze, rhinitis and eczema were 11.8%, 22.2% and 3.3%, respectively. Redecorating during pregnancy increased reported onset of rhinitis (OR = 2.29) and eczema (OR = 4.91). New furniture during pregnancy increased reported onset of rhinitis (OR = 1.47). Perinatal indoor mould increased reported onset of wheeze (OR = 1.51), rhinitis (OR = 1.65) and eczema (OR = 1.91). Perinatal mould odour increased reported onset of wheeze (OR = 1.85). Perinatal window pane condensation increased reported onset of wheeze (OR = 1.54) and rhinitis (OR = 1.24). Perinatal stuffy air and dry air in the home increased reported onset of all three symptoms (ORs 1.46-2.24). Dog keeping increased reported onset of wheeze (OR = 1.69) and eczema (OR = 2.13). Based on principal component analysis, four exposure scores were calculated (renovation, new furniture, mould and indoor air quality scores). Dose-response relationships were observed between these exposure scores and reported onset of symptoms. In conclusion, prenatal and postnatal exposure to emissions from renovation and new furniture can increase reported onset of childhood wheeze, rhinitis and eczema. Perinatal indoor mould, mould odour, condensation on window panes and impaired indoor air quality at home can be associated with reported development of wheeze, rhinitis and eczema in preschoolers in northern China., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2021 The Authors. Published by Elsevier B.V. All rights reserved.)

Background: Increasing evidence has linked childhood pneumonia with early exposure to ambient air pollution. However, the impact of exposure to air pollutants before birth is unclear., Objective: To further clarify whether exposure to a particular pollutant during preconceptional and prenatal periods, may pose a higher risk of developing childhood pneumonia., Methods: This case-control cohort study consisted of 1510 children aged 0-14 years in Changsha, China between 2017 and 2019. Data of children's history of pneumonia and blood biomarkers were obtained from the XiangYa Hospital records. Each child's exposure to air pollutants, including nitrogen dioxide (NO 2 ), sulfur dioxide (SO 2 ), and particulate matter with an aerodynamic diameter ≤ 10 µm (PM 10 ), was calculated using data from ten air pollution monitoring stations. A multivariate logistic regression model was used to quantify the relationship between childhood pneumonia and exposure to ambient air pollution during the preconceptional and prenatal periods., Results: Childhood pneumonia was significantly associated with preconceptional and prenatal exposure to the industrial-related air pollutant, SO 2 , for 1 year before conception, for 3 months before conception and for the entire pregnancy, with ORs(95% CI)= 4.01(3.17-5.07), 4.06(3.29-5.00) and 6.51(4.82-8.79). Also, children who were sick with pneumonia had higher white blood cell and neutrophil counts, and children with low eosinophil count or hemoglobin are likely to get pneumonia. Sensitivity analysis showed that boys, and children in high temperature area were susceptible to the effect of both preconceptional and prenatal exposure to industrial SO 2 ., Conclusion: Preconceptional and prenatal exposure to industrial-related air pollution plays a significant role in the incidence and progression of childhood pneumonia, supporting the hypothesis of "(pre-)fetal origin of childhood pneumonia"., (Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.)

We investigated associations between prenatal and postnatal environmental factors and onset and remission of preschool childhood eczema across China. The study population was preschoolers in randomized day care centers in seven cities (N = 39,782). Data on eczema and prenatal and postnatal indoor and outdoor environment were obtained from a cross-sectional questionnaire sent to parents or other guardians. Reports on eczema in the first 2 years and in the past year was used to retrospectively calculate onset and remission (changes of reported eczema). Prenatal and postnatal outdoor temperature, NO 2 and PM 10 were modelled from official air pollution data. Associations were estimated by two-level logistic regression. Calculated onset rate was 3.2%/y and remission rate 29.2%/y. Exposure to NO 2 during pregnancy was associated with onset of eczema, similarly for all trimesters. Postnatal PM 10 and NO 2 were related to decreased remission. Postnatal outdoor temperature was associated with onset of eczema. Pre-natal and current redecoration or buying new furniture, and perinatal as well as current dampness and indoor mould, were associated with increased onset and decreased remission. Cockroaches in current home was another indoor risk factors. Prenatal exposure to farm environment and large family size were all negatively associated with eczema. In conclusion, a warmer climate and prenatal NO 2 can be associated with increased onset of eczema in Chinese preschoolers. Postnatal PM 10 and NO 2 can be associated with reduced remission. Perinatal and current dampness, indoor mould and cockroaches may increase onset and decrease remission. Exposure to chemical emissions from indoor materials after first year of life may increase onset. Prenatal exposure to farm environment and large family size could be protective., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 The Author(s). Published by Elsevier B.V. All rights reserved.)

We estimated associations between ambient air pollution, home environment and asthma as well as rhinitis among adults across China. A total of 40,279 young adults from eight Chinese cities participated in a questionnaire survey (participation rate 75%). There were questions on health and home environment. Information on city level gross domestic product (GDP) per capita, ambient temperature and PM 10 and NO 2 were collected from registers. Two-level logistic regression models were used to study health associations. Totally 1.6% reported asthma and 6.6% reported allergic rhinitis (AR). Higher temperature was associated with more asthma but less AR. Higher GDP was associated with less asthma but more AR. Higher degree of urbanization, higher level of NO 2 and living near heavily trafficked road were risk factors for asthma and AR. Participants in older buildings reported more asthma. Redecoration and buying new furniture were related to more asthma and AR (OR = 1.15-1.91). Using natural gas (OR = 1.34) and biomass (OR = 1.35) for cooking were risk factors for AR. Burning mosquito coils and incense increased the risk of asthma and AR. Cat keeping (OR = 2.88), dog keeping (OR = 2.04), cockroaches (OR = 1.54) and rats or mice (OR = 1.46) were associated with asthma. Cockroaches increased the risk of AR (OR = 1.22). Air humidifier and air cleaner were linked to asthma and AR. Frequent cleaning and exposing bedding to sunshine were protective. In conclusion, urbanization, NO 2 and traffic exhaust can increase the risk of adult asthma and AR. Higher ambient temperature was related to more asthma but less AR. Indoor animals such as cats, dogs, rats/mice and presence of cockroaches were associated with asthma or AR. Indoor chemical sources such as redecoration and new furniture were other risk factors. Cooking with natural gas or biomass and burning mosquito coils and incense were associated with asthma or AR. Frequent cleaning and exposing bedding to sunshine were protective., Competing Interests: Declaration of competing interest The authors declare that they have no known competing interest., (Copyright © 2020 The Authors. Published by Elsevier B.V. All rights reserved.)

This paper studied associations between reported common cold and home dampness and mould, cleaning habits and ventilation, climate and outdoor air pollution in China among young adults without asthma or allergic rhinitis. Parents of children attending day care in eight Chinese cities answered a questionnaire on their health and home environment (75% response rate). We restricted the population to subject without asthma or allergic rhinitis (N = 37,275). Temperature and air pollution data was obtained from monitoring stations. Associations were estimated by multilevel logistic regression. Totally 12.5% reported common cold (≥3 colds) and 1.6% frequent common cold (≥5 colds) in the past 12 months. Female gender (OR = 1.53; 95% CI 1.37-1.71), residents in southern China (OR = 1.89; 95% CI 1.16-3.07) and living in homes with water leakage (OR = 1.32; 95% CI 1.16-1.50), mould odour (OR = 1.48; 95% CI 1.28-1.72), indoor mould (OR = 1.47; 95% CI 1.28-1.70), condensation on window panes (OR = 1.42; 95% CI 1.32-1.52) and damp bed clothing (OR = 1.19; 95% CI 1.11-1.28) were associated with common cold. Having many signs of dampness increased ORs. Daily cleaning (OR = 0.91; 95% CI 0.85-0.97) and mechanical ventilation in kitchen or bathroom (OR = 0.75; 95% CI 0.64-0.89) were protective. Higher mean ambient temperature (OR = 1.11 per °C; 95% CI 1.02-1.21), PM 10 (OR = 1.17 per 10 μg/m 3 ; 95% CI 1.14-1.21) and PM 2.5 (OR = 1.28 per 10 μg/m 3 ; 95% CI 1.20-1.37) were associated with common cold. The association with particulate air pollution was stronger in southern China. Similar associations were found for frequent common cold. In conclusion, indoor dampness and mould, a warmer climate and PM 10 and PM 2.5 can be associated with reported common cold. Further intervention and prospective studies are needed to verify causality of observed association in this cross-sectional study., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 The Authors. Published by Elsevier B.V. All rights reserved.)

Hexavalent chromium [Cr(VI)] is seriously harmful to ecosystems and living organisms due to its strong toxicity. Role of dynamin-related protein 1 (Drp1) and Drp1-associated mitochondrial fragmentation in mitophagy and cytotoxicity after Cr(VI) exposure has not been clarified so far. We confirmed that Cr(VI) caused mitochondrial fission by up-regulating Drp1 expression and enhancing Drp1 mitochondrial translocation. By applying the intracellular Ca 2+ antagonist BAPTA-AM and mitochondrial Ca 2+ antagonist Ru360, we demonstrated that Cr(VI)-induced excessive mitochondrial fission was in a Ca 2+ -Drp1 dependent manner. The administration of Drp1 siRNA significantly suppressed the overactivation of mitophagy in Cr(VI)-induced hepatotoxicity. The specific Drp1 inhibitor mitochondrial division inhibitor-1 (Mdivi-1) blocked the overactive mitophagy and subsequently ameliorated hepatotoxicity caused by Cr(VI) in vivo. We reached the conclusion that Drp1-dependent mitochondrial fission contributes to Cr(VI)-induced mitophagy and hepatotoxicity, which may provide experimental basis for the study of chromium-associated toxicity, especially for the prevention of health damage in chromium-exposed population., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Although much has been determined about the molecular mechanisms of hexavalent chromium [Cr(VI)]-induced hepatotoxicity, more remains to be explored. In particular, explicit epigenetic alterations of microRNAs (miRNAs) which can negatively regulate mRNAs at post transcriptional level remain understudied. In the present study, cell apoptosis was determined using Annexin V/propidium iodide (PI) staining, while proliferative growth was analyzed by colony formation assay and proliferating cell nuclear antigen (PCNA) detection. miRNA microarray was performed to compare the global miRNAs expression patterns. miR-21-5p mimics (mi)/inhibitor (in), and PDCD4-siRNAs were transfected into L02 hepatocytes. Our results revealed that Cr(VI) induced apoptosis and inhibited proliferation in L02 hepatocytes via reactive oxygen species (ROS), the formation of which is closely related to mitochondrial damage, especially the inhibition of mitochondrial respiratory chain complex (MRCC). We also confirmed that ROS-mediated miR-21-5p inhibition participated in cell apoptosis and proliferative inhibition induced by Cr(VI). Furthermore, programmed cell death protein 4 (PDCD4), the up-regulation of which was related to ROS over-production, was predicted and verified as a target of miR-21-5p. Transcription factor PDCD4 silencing suppressed apoptosis and stimulated cell proliferation. In conclusion, from the perspective of epigenetics, the present study revealed that ROS-mediated miR-21-5p regulated the proliferation and apoptosis of Cr(VI)-exposed L02 hepatocytes via targeting PDCD4, which provided the new targets for molecular intervention and treatment of liver damage in Cr(VI)-exposed population., Competing Interests: Declaration of competing interest The authors have no conflicts of interest to declare., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Hexavalent chromium [Cr(VI)] is a common heavy metal pollutant widely used in various industrial fields. It is well known that mitochondria are the most vulnerable targets of heavy metals, but the key molecule/event that directly mediated mitochondrial dysfunction after Cr(VI) exposure is still unclear. The present study was aimed to explore whether Cr(VI) exposure could affect the mitochondrial fission/fusion process, and whether the related abnormal mitochondrial dynamics have been implicated in Cr(VI)-induced mitochondrial dysfunction. We found that the mitochondrial dysfunction caused by Cr(VI) exposure was characterized by decreased mitochondrial respiratory chain complex (MRCC) I/II activities and levels, collapsed mitochondrial membrane potential (MMP), depleted ATP, and increased reactive oxygen species (ROS) level. Cr(VI) induced abnormal mitochondrial fission/fusion events, the antioxidant Nacetyl-L-cysteine (NAC) restored the abnormal mitochondrial function as well as the fission/fusion dynamics. ROS was the up-stream regulator of extracellular regulated protein kinases (ERK) signaling, and the application of a specific ERK1/2 inhibitor PD98059 confirmed that activation of ERK1/2 signaling was associated with the abnormal mitochondrial fission/fusion and mitochondrial dysfunction. We also demonstrated that treatment with dynamic-like protein 1 (DLP1)-siRNA rescued mitochondrial dysfunction in Cr(VI)-exposed L02 hepatocytes. We reached the conclusion that blockage of ROS-ERK-DLP1 signaling and mitochondrial fission alleviates Cr(VI)-induced mitochondrial dysfunction in L02 hepatocytes, which may provide the new avenue for developing effective strategies to protect against Cr(VI)-induced hepatotoxicity., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Background: Although mounting evidence have linked traffic-related air pollution (TRAP) with increased risk of preterm birth (PTB), whether it can interact with indoor environmental factors remains unknown, and its window(s) susceptibility at the stage of gestation is unclear., Objective: To explore PTB risk for prenatal exposure to traffic-related air pollution and home environmental factors during pregnancy, so as to identify critical window(s) in the combined effect of traffic air pollution and main home environmental factor(s) on PTB development., Methods: A retrospective cohort study of 3,509 preschool children was performed in Changsha, China during 2011-2012. The PTB prevalence was reported by the parents based on a questionnaire. We estimated each mother's exposure to traffic-related air pollutant NO 2 in different windows of gestation, including conception month, three trimesters, birth month, and whole gestation. Maternal exposure to home environmental factors was considered by renovation (new furniture/redecoration) in pregnancy, and mold/damp stains and window condensation during perinatal period. Associations of PTB with both ambient NO 2 and home environmental factors, and their interactions on PTB were evaluated by logistic regression models using odds ratio (OR) with 95% confidence interval (CI)., Results: Traffic air pollutant NO 2 exposure in utero was significantly associated with PTB, with adjusted odds ratio (OR) (95% CI) of 1.41 (1.00-1.98) for an IQR increase in NO 2 exposure during whole pregnancy, particularly in the conception month and 1 st trimester. We further found a positive relationship between perinatal exposure to mold/damp stains in the homes and PTB, OR (95% CI) = 1.73 (1.04-2.90). Especially, we detected a significant interaction between outdoor NO 2 and indoor mold/damp stains on PTB risk. Male and female foetus were respectively more susceptible to perinatal mold/dampness at home and outdoor NO 2 exposure in early gestation., Conclusion: Our finding indicates that both outdoor traffic air pollutant and indoor mold/dampness play key roles in PTB development, and their interaction effect in early pregnancy significantly increases PTB risk., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Few studies exist from China on associations between home environment and adult health. We studied associations between home environment factors (other than dampness and mould) and rhinitis, throat and dermal symptoms and headache and fatigue among young parents in six cities across China (N = 36,541). They were recruited as parents from day care centers selected randomly and answered a questionnaire on medical symptoms and the home environment. Odds ratios (OR) were calculated by multilevel logistic regression adjusting for gender, atopy, smoking, home size and dampness/mould. Overall, 4.8% had skin symptoms 3.1% rhinitis, 2.8% eye, 4.1% throat symptoms, 3.0% headache and 13.9% had fatigue (all as weekly symptoms). Redecoration was associated with rhinitis, eye and skin symptoms, headache and fatigue. New furniture was associated with eye, throat and skin symptoms and fatigue. Gas cooking was associated with eye and throat symptoms, headache and fatigue. Biomass cooking was associated with eye and throat symptoms and headache. Burning incense was associated with eye, throat and skin symptoms, headache and fatigue. Presence of cockroaches and mosquitos or flies was associated with all six symptoms. Rats or mice were associated with eye and dermal symptoms. Cat keeping was associated with eye symptoms while dog keepers had less fatigue. Living near major roads was associated with rhinitis, eye, throat and skin symptoms and fatigue. Daily cleaning, a mechanical ventilation system in the kitchen or in the bathroom, living in older buildings and living in less urbanized areas were protective factors. In conclusion, urbanization, traffic exhaust, indoor emissions from redecoration and new furniture, gas cooking and air pollution from burning incense and biomass may cause dermal and mucosal symptoms, headache and fatigue among adults in China. Indoor animals (cats, mice/rats, cockroaches) were other risk factors. Daily cleaning, mechanical ventilation and living in older buildings can be protective., (Copyright © 2019. Published by Elsevier B.V.)

Background: Biomass burning is associated with childhood pneumonia but few studies exist on other indoor factors., Aim: To study pneumonia in relation to pre-natal and post-natal exposure among children across China., Methods: Children (3-6 y) (n = 39,782) from randomized day care centres in seven cities in China. Information on pneumonia and pre-natal and post-natal exposure to home environment factors were assessed by a parental questionnaire. Life-time outdoor temperature and GDP per capita were assessed on city level. Associations were calculated by multilevel logistic regression adjusting for fourteen co-variates., Results: Totally 32.0% had ever had pneumonia diagnosed by a physician. Children of farmer mothers (OR = 0.65), with breastfeeding (OR = 0.91) and living in rural (OR = 0.85) or suburban (OR = 0.90) areas had less pneumonia. Buying new furniture one year before conception (OR = 1.11) and after first year of life (OR = 1.10) increased the risk. Redecoration one year before conception (OR = 1.20), during pregnancy (OR = 1.18) and after first year of life (OR = 1.17) increased pneumonia risk. Children with mould (OR = 1.17), window pane condensation (WPC) (OR = 1.20) and mould odour (OR = 1.15) at home at birth only had a higher risk of pneumonia. Similar associations were seen for dampness and mould in the current home. Children in the oldest and newest homes had less pneumonia. Cockroaches (OR = 1.08), mosquitos or flies in the current home (OR = 1.18), an exhaust fan in the bathroom (OR = 1.10) and higher economic development level, measured as GDP per capita on city level (OR 1.11 per 10,000 RMB/year) were associated with childhood pneumonia., Conclusions: Perinatal and postnatal exposure to mould, mould odour and window pane condensation at home can be early life risk factors for childhood pneumonia in China. Moreover, pre-natal and post-natal exposure to chemical emissions from new furniture and renovation could increase the risk of childhood pneumonia. Breastfeeding, farm exposure, and living in rural or suburban areas could be protective., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Background: Although air pollution and social stress may independently increase childhood asthma, little is known on their synergistic effect on asthma, particularly in China with high levels of stress and air pollution., Objectives: To examine associations between exposure to a combination of parental stress and air pollution and asthma prevalence in children., Methods: We conducted a cohort study of 2406 preschool children in Changsha (2011-2012). A questionnaire was used to collect children's lifetime prevalence of asthma and their parental stress. Parental socioeconomic and psychosocial stresses were respectively defined in terms of housing size and difficulty concentrating. Children's exposure to ambient air pollutants was estimated using concentrations measured at monitoring stations. Associations between exposure to parental stress and air pollution and childhood asthma were estimated by multiple logistic regression models using odds ratio (OR) and 95% confidence interval (CI)., Results: Life time prevalence of asthma in preschool children (6.7%) was significantly associated with parental socioeconomic and psychosocial stresses with OR (95% CI) respectively 1.48 (1.02-2.16) and 1.64 (1.00-2.71). Asthma was also associated with exposure to air pollutants, with adjusted OR (95% CI) during prenatal and postnatal periods respectively 1.43 (1.10-1.86) and 1.35 (1.02-1.79) for SO 2 and 1.61 (1.19-2.18) and 1.76 (1.19-2.61) for NO 2 . The association with air pollution was significant only in children exposed to high parental stress, the association with parental stress was significant only in children exposed to high air pollution, and the association was the strongest in children exposed to a combination of parental stress and air pollution. Sensitivity analysis showed that the synergistic effects of parental stress and air pollution on childhood asthma were stronger in boys., Conclusions: Parental stress and air pollution were synergistically associated with increased childhood asthma, indicating a common biological effect of parental stress and air pollution during both prenatal and postnatal periods., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Background: Common cold is a frequent upper respiratory tract infection, but the role of ambient temperature in the infection is unclear., Objective: We investigated the role of prenatal exposure to diurnal temperature variation (DTV), the difference between the daily maximal and minimal temperatures, in the risk of common cold in children., Methods: We conducted a cohort study of 2598 preschool children in Changsha, China. Occurrence of common cold during the past year was surveyed using questionnaire. We then estimated each child's prenatal exposure to DTV during pregnancy. Multivariate logistic regression model was used to examine the association between occurrence of common cold and prenatal exposure to DTV in terms of odds ratios (OR) and 95% confidence interval (CI)., Results: About 45% children have common cold (≥3 times) during the past year. We found that common cold in children was associated with maternal DTV exposure during pregnancy, particularly during the first trimester with adjusted OR (95% CI) = 1.27 (1.10-1.46). Male and atopic children were more susceptible to the effect of DTV during pregnancy. The risk of common cold due to DTV is higher in children living in the suburban areas and the bigger houses and in those exposed to environmental tobacco smoke, mold/dampness, new furniture and redecoration. We observed that the risk of common cold in children has been increased in recent years due to increasing DTV., Conclusions: Common cold in children was associated with maternal exposure to temperature variation during pregnancy, suggesting that the risk of common cold may originate in pregnancy., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Background: Evidence linking prenatal exposure to outdoor air pollution with eczema in early childhood is scare, and the role of components of air pollution and exposure timing remains unclear., Objectives: We investigated the association between exposure to air pollution during preconceptional and perinatal period and the risk of eczema in preschool children., Methods: We conducted a prospective cohort study of 2598 children aged 3-6 years in Changsha, China. The prevalence of eczema was assessed by a standardized health questionnaire administered by the parents. Individual exposures to nitrogen dioxide (NO 2 ), sulfur dioxide (SO 2 ) and particulate matter with an aerodynamic diameter≤10μm (PM 10 ) during the 4th-6th and 1st-3rd month before pregnancy, entire pregnancy, and three trimesters were estimated by an inverse distance weighted (IDW) method based on concentrations measured at monitoring stations. Association between childhood eczema and exposure to air pollution was examined by logistic regression models in terms of odds ratio (OR) and 95% confidence interval (CI) for an interquartile range (IQR) increase in exposure., Results: Life-time prevalence of eczema in preschool children in Changsha was 28.6%. Childhood eczema was associated with traffic-related air pollutant NO 2 during 3 months before pregnancy and entire pregnancy with adjusted ORs=1.19 (95% CI: 1.04-1.37) and 1.21 (95% CI: 1.03-1.42) respectively. The highest risk of eczema was observed for the 1st trimester exposure to NO 2 [OR=1.26 (95% CI: 1.09-1.46)]. However, no association was detected for SO 2 and PM 10 exposure during any window. High-level exposure to NO 2 during the whole time period significantly increased the effect of NO 2 in all windows on eczema risk as compared with low-level exposure. Sensitivity analysis indicated that the association between both preconceptional and perinatal exposure to NO 2 and childhood eczema was consistent and robust, and this association was modified by some personal, parental hereditary and indoor environmental factors., Conclusion: Our findings support the hypothesis that early childhood eczema is associated with exposure to traffic-related air pollutant during both preconceptional and perinatal period, especially at a high level of exposure., (Copyright © 2016 Japanese Society for Investigative Dermatology. Published by Elsevier B.V. All rights reserved.)

Background: Evidence linking long-term exposure to outdoor air pollution with allergic rhinitis (AR) in children is scare, and the role of components of air pollution and timing of exposure remains unclear., Objective: To assess the association of pre- and post-natal exposure to air pollution with life-time prevalence of AR in preschool children., Methods: We conducted a cohort study of 2598 children aged 3-6 years in Changsha, China. The lifetime prevalence of AR was assessed by a questionnaire administered by parents. Children's exposures to dioxide nitrogen (NO 2 ), sulfur dioxide (SO 2 ) and particulate matter with an aerodynamic diameter ≤ 10 μm (PM 10 ) during different pre- and post-natal timing windows were estimated using the measured concentrations at monitoring stations. The odds ratio (OR) and 95% confidence interval (CI) of childhood AR for exposure to different air pollutants during different timing windows were assessed by logistic regression model in terms of an interquartile range (IQR) increase in exposure level., Results: Life-time prevalence of AR in preschool children (7.3%) was associated with both pre- and post-natal exposure to traffic-related air pollution (TRAP), but only significant during the third trimester of pregnancy with adjusted OR = 1.40 (95% CI: 1.08-1.82) for a 15 μg/m 3 increase in NO 2 and during the first-year of life with adjusted OR = 1.36 (95% CI: 1.03-1.78) and 1.54 (95% CI: 1.07-2.21) respectively for 11 and 12 μg/m 3 increase in NO 2 and PM 10 . The association of early life exposure to TRAP with childhood AR was robust by adjusting for other air pollutants and timing windows. Sensitivity analysis indicated that the association was higher in the children who are male, young, with genetic predisposition by parental atopy, and living in damp houses., Conclusion: Early life exposure to traffic-related air pollutant during pregnancy and first-year of life may contribute to childhood AR., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

Background: Mounting evidence suggests that exposure to ambient air pollution is associated with the development of childhood allergic diseases, but the effect of prenatal exposure to air pollution on the risk of childhood asthma and allergy is unclear., Objectives: We evaluated the association between maternal exposure to outdoor air pollution during different trimesters of pregnancy and incidence of asthma, allergic rhinitis, and eczema in 2598 preschool children aged 3-6 years in China., Methods: Children's lifetime incidence of allergic diseases was obtained using questionnaire. Individual exposure to outdoor air pollutants during trimesters of pregnancy was estimated by an inverse distance weighted (IDW) method based on the measured concentrations at monitoring stations. We used multiple logistic regression method to estimate the odds ratio (OR) of asthma, allergic rhinitis, and eczema for per interquartile range (IQR) increase in the exposure to air pollutant in each trimester, which was adjusted for the effect of other air pollutants and its effect in other trimesters by a multi-pollutant/trimester model., Results: Incidence of asthma (6.8%), allergic rhinitis (7.3%), and eczema (28.6%) in children was associated with maternal exposure to traffic-related pollutant NO2 during entire pregnancy with OR (95% confidence interval [CI]) respectively 1.63 (0.99-2.70), 1.69 (1.03-2.77), and 1.37 (1.04-1.80). After adjustment for other pollutants and trimesters, we found the association was significant only in specific trimester: the first trimester for eczema (1.54, 1.14-2.09), the second trimester for asthma (1.72, 1.02-2.97), and the third trimester for allergic rhinitis (1.77, 1.09-2.89). Sensitivity analysis indicated that the trimester sensitive to the development of allergic diseases was stable., Conclusion: Maternal exposure to traffic-related air pollutant NO2 during pregnancy, especially in specific trimesters, is associated with an increased risk of developing asthma, rhinitis, and eczema in children. Our results support the hypothesis that childhood allergic diseases originate in fetal life and are triggered by traffic-related air pollution in sensitive trimesters., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Indoor environment is associated with the sick building syndrome (SBS), but little is known about the contribution of outdoor air pollution and meteorological conditions to SBS. We studied associations between outdoor air pollution, meteorological parameters and selected indoor exposure and building characteristics at home and weekly SBS symptoms in a standardized questionnaire study among 3485 randomly selected adults in China. Outdoor factors included particulate matters with diameter <10μm (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), outdoor temperature (T), relative air humidity (RH), and wind speed (WS) during last three months. Multiple logistic regression was applied calculating odds ratios (OR) with 95% confidence interval (95% CI). Asthma or allergic rhinitis (atopy) was associated with all types of SBS symptoms except fatigue. Indoor factors played a major role in SBS symptoms. Mold/dampness on the floor/ceiling was associated with fatigue OR=1.60 (1.11-2.30) and headache OR=1.80 (1.07-3.04). Moldy odor was associated with fatigue OR=1.59 (1.07-2.37) and dermal symptoms OR=1.91 (1.21-3.02). Window pane condensation in winter was associated with fatigue OR=1.73 (1.30-2.31) and throat symptoms OR=1.53 (1.01-2.31). Damp bed clothing was related with throat symptom OR=1.62 (1.09-2.40). Home redecoration was associated with fatigue OR=1.49 (1.07-2.06). Frequent window opening was associated with less nose symptoms OR=0.54 (0.36-0.82) and mechanical ventilation in the bathroom reduced dermal symptoms OR=0.66 (0.44-0.99). Females were more susceptible to redecoration and window pane condensation than men. No associations with SBS were observed for outdoor air pollutants or meteorological parameters in the final models combining indoor and outdoor factors, although SO2, T, and RH were associated with some SBS symptoms (fatigue, eyes and nose symptoms) in the separate outdoor models. In conclusion, indoor mold/dampness, air pollution from redecoration and poorer ventilation conditions in dwellings can be risk factors for SBS symptoms in an adult Chinese population, especially among females., (Copyright © 2016 Elsevier B.V. All rights reserved.)

Background: Early life is suggested to be a critical time in determining subsequent asthma development, but the extent to which the effect of early-life exposure to ambient air pollution on childhood asthma is unclear., Objectives: We investigated doctor-diagnosed asthma in preschool children due to exposure to ambient air pollution in utero and during the first year of life., Methods: In total 2490 children aged 3-6 years participated in a questionnaire study regarding doctor-diagnosed asthma between September 2011 and January 2012 in China. Children's exposure to critical air pollutants, sulfur dioxide (SO2) as proxy of industrial air pollution, nitrogen dioxide (NO2) as proxy of traffic pollution, and particulate matter≤10µm in diameter (PM10) as a mixture, was estimated from the concentrations measured at the ambient air quality monitoring stations by using an inverse distance weighted (IDW) method. Logistic regression analysis was employed to determine the relationship between early-life exposure and childhood asthma in terms of odds ratio (OR) and 95% confidence interval (CI)., Results: Association between early-life exposure to air pollutants and childhood asthma was observed. SO2 and NO2 had significant associations with adjusted OR (95% CI) of 1.45 (1.02-2.07) and 1.74 (1.15-2.62) in utero and 1.62 (1.01-2.60) and 1.90 (1.20-3.00) during the first year for per 50 µg/m(3) and 15 µg/m(3) increase respectively. Exposure to the combined high level of SO2 and NO2 in China significantly elevated the asthmatic risk with adjusted OR (95% CI) of 1.76 (1.18-2.64) in utero and 1.85 (1.22-2.79) during the first year compared to the low level exposure. The associations were higher for males and the younger children aged 3-4 than females and the older children aged 5-6., Conclusions: Early-life exposure to ambient air pollution is associated with childhood asthma during which the level and source of air pollution play important roles. The high level and nature of combined industrial and traffic air pollution in China may contribute to the recent rapid increase of childhood asthma., (Copyright © 2015 Elsevier Inc. All rights reserved.)