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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. 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. 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. 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. 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. [Display omitted] • Postnatal exposure to outdoor CO, O 3 , SO 2 , and PM 10 was related with children's food allergy (FA). • Renovation- and smoke-related indoor air pollution (IAP) elevated the risk of childhood FA. • Dampness- and plant- related indoor allergens exposure increased risk of childhood FA. • Life-time and early-life antibiotic use increased the risk of childhood FA. • Children without using antibiotic had higher FA risk of outdoor and indoor environment exposure. [ABSTRACT FROM AUTHOR]

Although mounting evidence has linked environmental factors with childhood allergies, some specific key issues still remain unclear: what is the main environmental factor? what is the critical timing window? And whether these contribute to the development of disease? This selective review summarizes recent epidemiological studies on the association between early-life exposure to indoor/outdoor air pollution and childhood allergic diseases. A literature search was conducted in the PubMed and Web of Science for peer-reviewed articles published until April 2020. Exposure to the traffic-related air pollutant, NO2, exposure during pregnancy and early postnatal periods is found to be associated with childhood allergies, and exposure during different trimesters causes different allergic diseases. However, exposure to classical air pollutants (PM10 and SO2) also contributes to childhood allergy in developing countries. In addition, early-life exposure to indoor renovation and mold/dampness significantly increases the risk of allergy in children. A synergistic effect between indoor and outdoor air pollution is found in the development of allergic diseases. Early-life exposure to outdoor air pollution and indoor environmental factors plays an important role in the development of childhood allergic diseases, and the synergy between indoor and outdoor exposures increases allergy risk. The available findings support the hypothesis of the 'fetal origins of childhood allergy,' with new implications for the effective control and early prevention of childhood allergies. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Background Pneumonia is a common early-childhood respiratory infection that leads to long-term health impacts, but its risk factors remain unclear. Objective To examine the association between early life exposure to both outdoor and indoor air pollution and childhood pneumonia. Methods We conducted a retrospective cohort study of 2598 children aged 3–6 years in Changsha, China (2011-2012). Children's life-time prevalence of pneumonia and exposure to indoor air pollution related to home renovation were surveyed by a questionnaire answered by the parents. Children's exposure to outdoor air pollution, including nitrogen dioxide (NO 2 ), sulfur dioxide (SO 2 ), and particulate matter with an aerodynamic diameter ≤ 10 μm (PM 10 ), was estimated using the measured concentrations at monitoring stations. Association between childhood pneumonia and exposure to indoor and outdoor air pollution during both prenatal and postnatal periods were examined by using logistic regression model in terms of odds ratio (OR) and 95% confidence interval (CI). Results Life-time prevalence of pneumonia in preschool children in Changsha is high, up to 38.6%.We found that childhood pneumonia was associated with postnatal exposure to outdoor particulate air pollutant PM 10 , adjusted OR (95% CI) = 1.26 (1.00–1.57) for per 6 μg/m 3 increase in the concentration. Pneumonia was also associated with postnatal exposure to indoor renovation, adjusted OR (95% CI) = 1.30 (1.02–1.64) for new furniture and 1.30 (1.00–1.69) for redecoration. Combined exposure to outdoor high PM 10 and indoor renovation significantly increased the pneumonia risk. Sensitivity analysis indicated that the association was heterogeneous in different subgroups, but stronger in male and younger children. Conclusion High prevalence of childhood pneumonia in China may be associated with postnatal exposure to ambient particulate air pollution and house renovation. [ABSTRACT FROM AUTHOR]

The urbanization and industrialization in China is accompanied by bad air quality, and the prevalence of asthma in Chinese children has been increasing in recent years. To investigate the associations between ambient PM 2.5 levels and asthmatic and allergic diseases or symptoms in preschool children in China, we assigned PM 2.5 exposure data from the Global Burden of Disease (GBD) project to 205 kindergartens at a spatial resolution of 0.1° × 0.1° in six cities in China (Shanghai, Nanjing, Chongqing, Changsha, Urumqi, and Taiyuan). A hierarchical multiple logistical regression model was applied to analyze the associations between kindergarten-level PM 2.5 exposure and individual-level outcomes of asthmatic and allergic symptoms. The individual-level variables, including gender, age, family history of asthma and allergic diseases, breastfeeding, parental smoking, indoor dampness, interior decoration pollution, household annual income, and city-level variable-annual temperature were adjusted. A total of 30,759 children (average age 4.6 years, 51.7% boys) were enrolled in this study. Apart from family history, indoor dampness, and decoration as predominant risk factors, we found that an increase of 10 μg/m 3 of the annual PM 2.5 was positively associated with the prevalence of allergic rhinitis by an odds ratio (OR) of 1.20 (95% confidence interval [CI] 1.11, 1.29) and diagnosed asthma by OR of 1.10 (95% CI 1.03, 1.18). Those who lived in non-urban (vs. urban) areas were exposed to more severe indoor air pollution arising from biomass combustion and had significantly higher ORs between PM 2.5 and allergic rhinitis and current rhinitis. Our study suggested that long-term exposure to PM 2.5 might increase the risks of asthmatic and allergic diseases or symptoms in preschool children in China. Compared to those living in urban areas, children living in suburban or rural areas had a higher risk of PM 2.5 exposure. [ABSTRACT FROM AUTHOR]

Background Otitis media (OM) is a common infection in early childhood with repeated attacks that lead to long-term complications and sequelae, but its etiology still remains unclear. Objective To examine the association between early life exposure to air pollution and childhood OM, with the purpose of identifying critical windows of exposure and key components of air pollution in the development of OM. Methods We conducted a prospective cohort study of 1617 children aged 3–4 years in Changsha, China (2011–2012). The prevalence of OM was assessed by a questionnaire administered by the parents. Individual exposures to nitrogen dioxide (NO 2 ), sulfur dioxide (SO 2 ) and particulate matter with an aerodynamic diameter ≤ 10 μm (PM 10 ) during prenatal, postnatal, and current windows were estimated using the measured concentrations at monitoring stations. We used logistic regression model to examine the OM risk in terms of odds ratio (OR) and 95% confidence interval (CI) for exposure to different air pollutants during different timing windows, adjusting for covariates, multi-pollutants, and multi-windows. Results Life-time prevalence of doctor-diagnosed OM in preschool children in Changsha was 7.3%. Childhood OM was associated only with prenatal exposure to the industrial air pollution with adjusted OR (95% CI) = 1.44 (1.09–1.88) for a 27 μg/m3 increase in SO 2 , particularly during the first trimester of pregnancy. We further found that prenatal SO 2 exposure was not associated with the repeated attacks but was associated with the onset of OM, adjusted OR (95% CI) = 1.47 (1.10–1.96). The association between prenatal SO 2 exposure and early childhood OM was robust after adjusting for other pollutants and windows. Sensitivity analysis indicated that the association was stronger in females, children with parental atopy, and children living in houses with cockroaches, new redecoration, and condensation on window pane during winter. Conclusion We provide new evidence that prenatal exposure to industrial air pollution is associated with early childhood OM in China and may contribute to the onset of childhood OM. Our findings are helpful in developing more effective preventative strategies for childhood OM. [ABSTRACT FROM AUTHOR]

Background Childhood pneumonia is one of the leading single causes of mortality and morbidity in children worldwide, but its etiology still remains unclear. Objective We investigate the association between childhood pneumonia and exposure to diurnal temperature variation (DTV) in different timing windows. Methods We conducted a prospective cohort study of 2,598 children aged 3–6 years in Changsha, China. The lifetime prevalence of pneumonia was assessed by a questionnaire administered by the parents. Individual exposure to DTV during both prenatal and postnatal periods was estimated. Logic regression models was used to examine the association between childhood pneumonia and DTV exposure in terms of odds ratios (OR) and 95% confidence interval (CI). Results Lifetime prevalence of childhood pneumonia in preschool children in Changsha was high up to 38.6%. We found that childhood pneumonia was significantly associated with prenatal DTV exposure, with adjusted OR (95%CI) =1.19 (1.02–1.38), particularly during the second trimester. However, childhood pneumonia not associated with postnatal DTV exposure. Sensitivity analysis indicated that boys are more susceptible to the pneumonia risk of diurnal temperature variation than girls. We further observed that the prevalence of childhood pneumonia was decreased in recent years as DTV shrinked. Conclusions Early childhood pneumonia was associated with prenatal exposure to the diurnal temperature variation (DTV) during pregnancy, particularly in the second trimester, which suggests fetal origin of childhood pneumonia. [ABSTRACT FROM AUTHOR]

Intestinal parasitic infections (IPIs) have been recognized as one of the most significant causes of illness among disadvantaged communities. Many studies have been conducted on the prevalence of IPIs in Malaysia. However, these studies mostly focused on the indigenous groups in Peninsular Malaysia. The present study was conducted to provide the current baseline data on prevalence of IPIs, anaemia, malnutrition and associated risk factors among the indigenous communities in Sarawak, situation at northwest Borneo island of Malaysia. A cross sectional study was conducted among the longhouses communities. Stool samples were obtained and examined for the presence of IPIs using microscopy technique. Haemoglobin measurement was done using a portable haemoglobin analyzer. Malnutrition (i.e., stunting, underweight and wasting) was assessed using the WHO Anthro software. Statistical analysis was carried out using SPSS software. A total of 341participants took part in this study. The overall prevalence of IPIs was 57.5%. Multivariate analysis indicated that the absence of toilets (OR = 1.6; 95% CI = 1.1–2.7; p = 0.002) and close contact with animals (OR = 1.8; 95% CI = 1.3–2.9; p = 0.027) as significant predictors for IPIs. The incidence of anaemia was 36.4%. The incidence of underweight, wasting and stunting were 22.2%, 5.6% and 35.4%, respectively. Multivariate analysis demonstrated that low level of parental education attainment (OR = 1.9; 95% CI = 1.2–3.0; p = 0.006) was identified as significant predictor for anaemia. The incidence of wasting was significantly associated with mild anaemia (OR = 1.2; 95% CI = 0.9–1.7; p = 0.024). Low household income was identified as significant predictor for stunting (OR = 2.1; 95% CI = 9.8–22.2; p = 0.001) and underweight (OR = 1.9; 95% CI = 5.6–18.7; p = 0.037), respectively. Essentially, the present study highlighted that intestinal parasitic infections, anaemia and malnutrition are still prevalent among rural indigenous community in Sarawak. Improvement of socioeconomic status, periodic mass deworming, iron supplementation and health education program should be included in the control and prevention of public health strategies. [ABSTRACT FROM AUTHOR]

Otitis media (OM) is a common pediatric infectious disease worldwide. Increasing evidence have associated indoor environment with OM, yet the role of home environmental factor(s) exposure during which critical window(s) on childhood OM are unclear. To examine the association between indoor environmental factors exposure and childhood OM, to identify main indoor factor(s) and key window(s). A retrospective cohort study involving 8689 preschoolers aged 3–6 was performed in Changsha, China. The data about each child's health outcome and home environments was obtained through a standard questionnaire. Exposure timing windows included 1 year before pregnancy, pregnancy, first year of life, and past year. Multiple logistic regression models were used to analyze the association between indoor environmental factors and childhood OM. We found that exposure to mold/damp stains and mold/damp clothes or bedding during preconceptional, prenatal, and postnatal periods was consistently associated with childhood OM, with ORs ranged from 1.25 (1.02–1.54) to 1.38 (1.13–1.68). Past year was identified as a critical time window for mold/damp stains exposure in relation to OM risk. We further found that exposures to new furniture during pregnancy and environmental tobacco smoke (ETS) and grandparental smoking during first year were significantly associated with an increase in childhood OM, with ORs (95% CI) = 1.28 (1.00–1.64), 1.20 (1.01–1.42), and 1.21 (1.00–1.48). Moreover, current exposure to total plants especially for non-flowering plants significantly increased OM risk, with ORs (95% CI) = 1.23 (1.05–1.44) and 1.25 (1.06–1.46). The association between early life exposure to indoor environmental factors and OM was stronger among children living near traffic roads. Outdoor air pollution and temperature could modify the effect of indoor environmental exposure on childhood OM. Our sensitivity analysis indicated that some subgroups were more susceptible to OM risk of indoor exposure. Our findings suggest that exposure to home environmental factors played an important role in childhood OM, and the association can be interacted by outdoor air pollution and temperature. [Display omitted] • Both pre- and post-birth exposure to home environmental factors increase risk of childhood OM. • Dampness related indoor allergen plays a key role in the development of otitis media. • Renovation exposure in pregnancy was associated with an increase in childhood otitis media. • Current period was identified as the critical time window for OM risk of home environment. • Our study supports a hypothesis of "Fetal origin of childhood OM" by indoor exposure. [ABSTRACT FROM AUTHOR]

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 (SO 2 ) as proxy of industrial air pollution, nitrogen dioxide (NO 2 ) as proxy of traffic pollution, and particulate matter≤10 µm in diameter (PM 10 ) 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. SO 2 and NO 2 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 SO 2 and NO 2 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. [ABSTRACT FROM AUTHOR]

Recent rapid increase of childhood asthma in China should be associated with exposure to the high air pollution, but it is unclear to which exposure window, to which kind of air pollution, and to what extent the effect. We investigated the effect of early life exposure to both outdoor and indoor air pollution on childhood asthma. Questionnaire survey was administered to 2490 children aged 3–6 years in Changsha. Early life exposure of each child in utero and during the first year of life was evaluated based on three outdoor air pollutants, i.e. particulate matters (PM 10 ), industry-related SO 2 and traffic-related NO 2 , and two kinds of indoor air pollution represented by new furniture and redecoration. Multivariate logistic regression method was used to estimate the effect of exposure on asthma. Results indicated that exposure to both industry- and traffic-related air pollutants (SO 2 and NO 2 ) significantly increased childhood asthma with odds ratio = 1.07 (95% CI: 1.03–1.12) and 1.16 (1.00–1.35) in utero and 1.09 (1.04–1.15) and 1.26 (1.06–1.50) during the first year for 10 μg/m 3 increase in concentration. Exposure to new furniture and home redecoration during pregnancy significantly increased childhood asthma with odds ratio 2.34 (1.16–4.74) and 2.21 (1.29–3.81) respectively. The effects of outdoor and indoor exposures were independent to each other. We conclude that early life exposures to both outdoor air pollution and indoor renovation contributes to the rapid development of childhood asthma in China, the former stronger after birth but the latter stronger before birth. [ABSTRACT FROM AUTHOR]

Pneumonia is the most important cause of child death in the world today. Recent findings suggest that exposure to outdoor air pollutants may increase the pneumonia occurrence, but so far the associations have not been clearly illustrated. Therefore, the effects of outdoor air pollutants and the episode day on childhood pneumonia were investigated by this study. A standardized questionnaire on health, home and environmental factors of 4988 children was conducted in the city of Changsha, China. Average exposure to ambient air pollutants during 2008–2011 was monitored by the air pollution monitoring stations of Changsha Environmental Protection Agency. A two-stage hierarchical regression approach was adopted to estimate the effects of PM10, SO2 and NO2 on pneumonia risk. The prevalence of pneumonia in children aged 3–6 years was 38.2%, which is greatly higher than the developed countries but lower than some developing countries. Furthermore, the increased risk of childhood pneumonia was significantly associated with elevated NO2 concentration (odds ratio (OR) = 1.157, 95% confidence interval (CI): 1.121–1.195) and the episode day (OR = 1.038, 95% CI: 1.024–1.051), but not significantly associated with PM10 and SO2. Exposure to traffic-related air pollution could play an important role in the development of pneumonia in preschool children. The revised National Ambient Air Quality Standards (2012) for NO2 has provided a better control strategy for ambient air quality to reduce the risk of adverse health effects such as pneumonia for children. [ABSTRACT FROM AUTHOR]

• We examined the deposition of particles in the airways of asthmatic children. • Particle deposition in the asthmatic children was significantly higher than that in healthy children. • Constricted airways increased the particle deposition in the upper airways by inertial impaction. • Asthmatic children were more susceptible to the acute effect of particulate air pollution. Mounting evidence has linked long- and short-term exposure to particulate air pollution with the incidence and exacerbation of asthma in children, but the biological pathogenesis is unclear. We examined the deposition of particles in the airways of asthmatic children. A planar and symmetric model of airways for 4-year-old asthmatic children was considered. Airflow and particle deposition in the upper (G3-G6) and lower (G9-G12) conducting airways were numerically investigated using computation fluid dynamics (CFD) method. We considered the manifestation of moderate (30% reduction in airway diameter) and severe (60% reduction) asthma. Micron particles (1–10 µm) were considered. We found that particle deposition in the asthmatic children was significantly higher than that in healthy children. The deposition efficiency increased slowly with particle size for healthy children, but increased rapidly for asthmatic children, such that smaller particles could be deposited in the conducting airways of asthmatics. For healthy children, particles were deposited by inertial impaction and gravitational sedimentation respectively in the upper and lower airways, but deposited by inertial impaction in asthmatic children. The severity of the asthma increased the particle deposition in the airways. Our study indicated that asthmatic children were more susceptible to the effect of particulate air pollution. The constricted airways increased the particle deposition by inertial impaction, which may be the biological pathogenesis that causes the hospitalization of asthma in children. Avoiding exposure during air pollution events will be an effective measure to reduce the asthma attack. [ABSTRACT FROM AUTHOR]

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. 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/m3 increase in exposure to particulate air pollution during in utero period and the first year of life. 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/m3 and 33.1 ± 6.9 μg/m3, 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/m3 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. 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. • The first study evaluated early-life exposure to ambient PM 1 and childhood AR. • Increased childhood AR risk associated with prenatal and postnatal exposures to ambient PM 1 and PM 2.5. • Later trimesters of gestation might be the sensitive window for early-life PM exposure and childhood AR. • Enhanced effect of early-life PM exposure on childhood AR was observed among younger and winter-born children. [ABSTRACT FROM AUTHOR]

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. [Display omitted] • Early life exposure to industry air pollution elevated risk of childhood pneumonia. • Exposure to an increase in temperature (T) decreased risk of childhood pneumonia. • DTV exposure in utero and first two trimesters was related with pneumonia risk. • Low T interacted with high PM10 and SO2 in preconception and utero on pneumonia. • There was an interaction of high DTV with high PM10 and SO2 exposure on pneumonia. [ABSTRACT FROM AUTHOR]