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Background: Dementia is a major global health challenge and the impact of built and social environments’ characteristics on dementia risk have not yet been fully evaluated. Objective: To investigate associations between built and social environmental characteristics and diagnosed dementia cases and estimated dementia risk. Methods: We recruited 25,511 patients aged 65 and older from family physicians’ practices. We calculated a dementia risk score based on risk and protective factors for patients not diagnosed with dementia. Our exposure variables were estimated for each statistical area level 1: social fragmentation, nitrogen dioxide, public open spaces, walkability, socio-economic status, and the length of main roads. We performed a multilevel mixed effect linear regression analysis to allow for the hierarchical nature of the data. Results: We found that a one standard deviation (1-SD) increase in NO2 and walkability score was associated with 10% higher odds of any versus no dementia (95% CI: 1%, 21% for NO2 and 0%, 22% for walkability score). For estimated future risk of dementia, a 1-SD increase in social fragmentation and NO2 was associated with a 1% increase in dementia risk (95% CI: 0, 1%). 1-SD increases in public open space and socioeconomic status were associated with 3% (95% CI: 0.95, 0.98) and 1% decreases (95% CI: 0.98, 0.99) in dementia risk, respectively. There was spatial heterogeneity in the pattern of diagnosed dementia and the estimated future risk of dementia. Conclusion: Associations of neighborhood NO2 level, walkability, public open space, and social fragmentation with diagnosed dementia cases and estimated future risk of dementia were statistically significant, indicating the potential to reduce the risk through changes in built and social environments.

Background: There is limited information on risk factors for eczema in adults. Recent evidence suggests that air pollution may be associated with increased incidence of eczema in adults. We aimed to assess this possible association. Methods: Ambient air pollution exposures (distance from a major road, nitrogen dioxide [NO2 ], fine particulate matter with an aerodynamic diameter ≤2.5 µm [PM2.5 ]) were assessed for the residential address of Tasmanian Longitudinal Health Study participants at ages 43 and 53 years. Eczema incidence (onset after age 43 years), prevalence (at 53 years), and persistence were assessed from surveys, while IgE sensitization was assessed using skin prick tests. The presence or absence of eczema and sensitization was classified into four groups: no atopy or eczema, atopy alone, non-atopic eczema, and atopic eczema. Adjusted logistic and multinomial regression models were fitted to estimate associations between ambient air pollution and eczema, and interaction by sex was assessed. Results: Of 3153 participants in both follow-ups, 2369 had valid skin prick tests. For males, a 2.3 ppb increase in baselineNO2 was associated with increased odds of prevalent eczema (OR = 1.15 [95% CI 0.98-1.36]) and prevalent atopic eczema (OR = 1.26 [1.00-1.59]). These associations were not seen in females (p for interaction = 0.08, Conclusion: Increased exposure to residential ambient air pollutants was associated with an increased odds of eczema, only in males, and aeroallergen sensitization in both genders.

Objective: The main sources of nitrogen dioxide (NO2), road vehicles and electricity generation, are currently in a period of technological change. We assessed the number of cases of childhood asthma in New South Wales that could be avoided by lowering exposure to NO2 by 25% from current levels. Methods: Health impact assessment calculations for each of the 128 local government areas were based on the population of children aged 2 to 14, the prevalence of asthma derived from the 2017 NSW health survey, NO2 exposure from a land‐use regression model using satellite data, and risk estimates derived from two meta‐analyses and one Australian study. Results: A 25% reduction in NO2 below current exposure would lead to between 2,597 and 12,286 fewer children with asthma in NSW. The wide range in these estimates reflects the variation in concentration‐response functions used. Conclusions: Even the lowest of these estimates would be a worthwhile reduction in this common childhood illness. Implications for public health: A 25% reduction in NO2 is ambitious, but it is achievable through improved vehicle exhaust standards, increasing electric vehicle numbers, and reform of the electricity sector. Current Australian ambient air quality standards for annual NO2 should be revised downwards.

Purpose Endocrine-related diseases and disorders are on the rise globally. Synthetically produced environmental chemicals (endocrine-disrupting chemicals (EDCs)) mimic hormones like oestrogen and alter signalling pathways. Endometriosis is an oestrogen-dependent condition, affecting 10–15% of women of the reproductive age, and has substantial impacts on the quality of life. The aetiology of endometriosis is believed to be multifactorial, ranging from genetic causes to immunologic dysfunction due to environmental exposure to EDCs. Hence, we undertook a systematic review and investigated the epidemiological evidence for an association between EDCs and the development of endometriosis. We also aimed to assess studies on the relationship between body concentration of EDCs and the severity of endometriosis. Method Following PRISMA guidelines, a structured search of PubMed, Embase and Scopus was conducted (to July 2018). The included studies analysed the association between one or more EDCs and the prevalence of endometriosis. The types of EDCs, association and outcome, participant characteristics and confounding variables were extracted and analysed. Quality assessment was performed using standard criteria. Results In total, 29 studies were included. Phthalate esters were positively associated with the prevalence of endometriosis. The majority (71%) of studies revealed a significant association between bisphenol A, organochlorinated environmental pollutants (dioxins, dioxin-like compounds, organochlorinated pesticides, polychlorinated biphenyls) and the prevalence of endometriosis. A positive association between copper, chromium and prevalence of endometriosis was demonstrated in one study only. Cadmium, lead and mercury were not associated with the prevalence of endometriosis. There were conflicting results for the association between nickel and endometriosis. The relationship of EDCs and severity of endometriosis was not established in the studies. Conclusion We found some evidence to suggest an association between phthalate esters, bisphenol A, organochlorinated environmental pollutants and the prevalence of endometriosis. Disentangling these exposures from various other factors that affect endometriosis is complex, but an important topic for further research.

Q-VAX® is a vaccine used to prevent Q fever. Administration of the vaccine is complicated by the need to ensure, using intradermal and serological tests, that individuals have no prior immunity. Previous studies suggest that the vaccine is highly efficacious and long-lasting in adults. However, there has been no systematic follow-up of vaccine efficacy and the longevity of immunity using population-level data. We aimed to investigate the vaccine failure rate and duration of immunity in previously vaccinated individuals. We formulated a retrospective cohort study design within a linked data. We used a Q fever vaccination registry linked to Q fever notifications and hospital admissions (1991-2016) in the state of Queensland, which has Australia's highest incidence of Q fever. Q-VAX® failure was defined as occurrence of Q fever > 14 days' after vaccination. The incidence of Q fever in vaccinated and unvaccinated individuals was 5.40 (95% CI: 3.65, 7.72) and 89.50 (95% CI: 70.50, 112.00]) per 100,000 person-years of follow-up, respectively. The hazard ratio (HR) for Q fever was 0.07 (95% CI: 0.04, 0.10) in non-immune vaccinated compared with immune unvaccinated individuals. The overall vaccine effectiveness was found to be 94.37% suggesting that Q-VAX® is highly effective at preventing Q fever. However, the greater incidence observed in unvaccinated individuals considered immune during the pre-vaccination screening may suggest that pre-vaccination screening is sub-optimal among this study population.

Aims We investigated the effects of exposure to very low levels of particulate matter Methods and results This study included 606 asymptomatic adults (49% men, aged 56±7 years) recruited from communities in three states of Australia during 2017–2018. CCS was measured using coronary computed tomography scan at recruitment. Annual PM2.5 and NO2 concentrations were estimated on the year before recruitment using statistical exposure models and assigned to each participant’s residential address. Medical history, physical measurements, biochemistry, and sociodemographic and socioeconomic status were also recorded. Median concentrations of PM2.5 and NO2 were 6.9 µg/m3 [interquartile range (IQR) 6.0–7.7)] and 3.1 ppb [IQR 2.2–4.5], respectively. Of the 606 participants, 16% had high CCS (≥100) and 4% had very high CCS (≥400). Exposure to higher PM2.5 (per µg/m3) was significantly associated with greater odds of having high CCS (OR 1.20, 95% CI 1.02–1.43) and very high CCS (OR 1.55, 95% CI 1.05–2.29). Similar associations were observed for NO2 and high CCS (OR 1.14, 95% CI 1.02–1.27) and very high CCS (OR 1.23, 95% CI 1.07–1.51). These findings were robust to adjustment for sociodemographic factors, traditional cardiovascular risk factors, renal function, education, and socio-economic status. Conclusions Ambient air pollution even at low concentration was associated with degree of coronary artery calcification among asymptomatic low cardiovascular risk adults, independent of other risk factors. These findings suggest that air pollution is one of the residual risk factors of CAD.

Background Despite large reductions in under-5 lower respiratory infection (LRI) mortality in many locations, the pace of progress for LRIs has generally lagged behind that of other childhood infectious diseases. To better inform programmes and policies focused on preventing and treating LRIs, we assessed the contributions and patterns of risk factor attribution, intervention coverage, and sociodemographic development in 195 countries and territories by drawing from the Global Burden of Diseases, Injuries, and Risk Factors Study 2017 (GBD 2017) LRI estimates. Methods We used four strategies to model LRI burden: the mortality due to LRIs was modelled using vital registration data, demographic surveillance data, and verbal autopsy data in a predictive ensemble modelling tool; the incidence of LRIs was modelled using population representative surveys, health-care utilisation data, and scientific literature in a compartmental meta-regression tool; the attribution of risk factors for LRI mortality was modelled in a counterfactual framework; and trends in LRI mortality were analysed applying changes in exposure to risk factors over time. In GBD, infectious disease mortality, including that due to LRI, is among HIV-negative individuals. We categorised locations based on their burden in 1990 to make comparisons in the changing burden between 1990 and 2017 and evaluate the relative percent change in mortality rate, incidence, and risk factor exposure to explain differences in the health loss associated with LRIs among children younger than 5 years. Findings In 2017, LRIs caused 808 920 deaths (95% uncertainty interval 747 286–873 591) in children younger than 5 years. Since 1990, there has been a substantial decrease in the number of deaths (from 2 337 538 to 808 920 deaths; 65·4% decrease, 61·5–68·5) and in mortality rate (from 362·7 deaths [330·1–392·0] per 100 000 children to 118·9 deaths [109·8–128·3] per 100 000 children; 67·2% decrease, 63·5–70·1). LRI incidence declined globally (32·4% decrease, 27·2–37·5). The percent change in under-5 mortality rate and incidence has varied across locations. Among the risk factors assessed in this study, those responsible for the greatest decrease in under-5 LRI mortality between 1990 and 2017 were increased coverage of vaccination against Haemophilus influenza type b (11·4% decrease, 0·0–24·5), increased pneumococcal vaccine coverage (6·3% decrease, 6·1–6·3), and reductions in household air pollution (8·4%, 6·8–9·2). Interpretation Our findings show that there have been substantial but uneven declines in LRI mortality among countries between 1990 and 2017. Although improvements in indicators of sociodemographic development could explain some of these trends, changes in exposure to modifiable risk factors are related to the rates of decline in LRI mortality. No single intervention would universally accelerate reductions in health loss associated with LRIs in all settings, but emphasising the most dominant risk factors, particularly in countries with high case fatality, can contribute to the reduction of preventable deaths. Funding Bill & Melinda Gates Foundation.

Background: Accumulating evidence indicates early life exposure to air pollution, a suspected neurotoxicant, is negatively associated with children’s neurodevelopment. Objectives: To explore the role of multiple exposure periods to ambient particulate matter with diameter

The prevalence of allergic diseases has been increasing for several decades. This has been partly attributed to changing environmental factors such as exposure to traffic-related air pollution (TRAP) and nutrient deficiencies, including vitamin D. Furthermore, population-based studies have suggested that air pollution may contribute to vitamin D deficiency [1], while vitamin D levels may modify pollution-driven asthma symptoms in paediatric obesity [2]. Vitamin D supplementation has also been shown to reduce the effects of pollution on asthma and other chronic respiratory diseases [3]. To date, few mechanistic studies have aimed to identify the pathways that may explain these interactions., This study provides novel insights into mechanisms of traffic-related air pollution-induced allergy by down-regulation via complement regulators (CFI, PROS1 and PLG) and its interaction with vitamin D deficiency via the complement inhibitor PLG https://bit.ly/3x0jYOw

Environmental chemicals have been implicated in the etiology of impaired fetal growth. However, few studies have assessed the effects of chemical mixtures or considered the possibility of non-monotonic exposure-response relationships for chemicals that act through the endocrine system.We assessed exposure to polybrominated diphenyl ethers, organochlorine pesticides, metals, and perfluorinated alkyl substances in blood and urine samples collected approximately two weeks prior to delivery in 166 non-smoking pregnant women, and subsequent birth weight, length, and head circumference of neonates who were part of the Australian Maternal Exposures to Toxic Substances (AMETS) study. We used Bayesian structured additive regression models with spike-slab priors to estimate mixture effects, identify important exposures, and model non-linearity in exposure-response relationships.Mixtures of polybrominated diphenyl ethers, organochlorine pesticides, metals, and perfluorinated alkyl substances were not associated with fetal growth outcomes. Estimated change in fetal growth outcomes for an increase in exposure from the 25th to 75th percentile suggested no meaningful associations; the strongest evidence was for a small inverse association between birth weight and cesium exposure measured in whole blood (-124 g, 90% credible interval: -240 to -3 g). We identified several chemicals that may be associated with fetal growth non-linearly; however, 90% credible intervals contained small values consistent with no meaningful association.Using a Bayesian penalized regression method, we assessed the shapes of exposure-response relationships, controlled for confounding by co-exposure, and estimated the single and combined effects of a large mixture of correlated environmental chemicals on fetal growth. Our findings, based on a small sample of mother-neonate pairs, suggest that mixtures of persistent chemicals are not associated with birth weight, length, and head circumference. The potential for non-monotonic relationships between environmental chemicals and fetal growth outcomes warrants further study.

Background Although several studies have focused on the associations between particle size and constituents and blood pressure, results have been inconsistent. Methods and Results We conducted a panel study, between December 2017 and January 2018, in 88 healthy university students in Guangzhou, China. Weekly systolic blood pressure and diastolic blood pressure were measured for each participant for 5 consecutive weeks, resulting in a total of 440 visits. Mass concentrations of particles with an aerodynamic diameter of ≤2.5 µm (PM 2.5 ), ≤1.0 µm (PM 1.0 ), ≤0.5 µm (PM 0.5 ), ≤0.2 µm (PM 0.2 ), and number concentrations of airborne particulates of diameter ≤0.1 μm were measured. Linear mixed‐effect models were used to estimate the associations between blood pressure and particles and PM 2.5 constituents 0 to 48 hours before blood pressure measurement. PM of all the fractions in the 0.2‐ to 2.5‐μm range were positively associated with systolic blood pressure in the first 24 hours, with the percent changes of effect estimates ranging from 3.5% to 8.8% for an interquartile range increment of PM. PM 0.2 was also positively associated with diastolic blood pressure, with an increase of 5.9% (95% CI, 1.0%–11.0%) for an interquartile range increment (5.8 μg/m 3 ) at lag 0 to 24 hours. For PM 2.5 constituents, we found positive associations between chloride and diastolic blood pressure (1.7% [95% CI, 0.1%–3.3%]), and negative associations between vanadium and diastolic blood pressure (−1.6% [95% CI, −3.0% to −0.1%]). Conclusions Both particle size and constituent exposure are significantly associated with blood pressure in the first 24 hours following exposure in healthy Chinese adults.

BackgroundAmbient (outdoor) air pollution is a key risk factor for health, for which effective policy plays an important preventative role. Australian federal and related state air quality standards have historically relied on international evidence for guidance, which may not accurately reflect the Australian context. There has been, however, a large increase in Australian epidemiological studies over recent years.AimsTo provide an updated systematic literature review of peer-reviewed epidemiological studies that examined the health impacts of outdoor air pollution in Australia, including short- and long-term exposure.MethodsFollowing PRISMA guidelines, we conducted a systematic literature review. Broad search terms were applied to two databases (PubMed and Web of Science) and Google Scholar. Quality assessment and risk of bias were assessed using standard metrics. Included studies were summarised by tabulating key study characteristics, grouped by health outcomes.ResultsIn total, 72 studies were included in the review. Sixty-four studies (89%) used daily or hourly pollutant concentrations to examine short-term exposure impacts, of which 59 (92%) revealed significant associations with one or more health outcomes, including cardio-respiratory, all-cause mortality or morbidity, and birth outcomes. Eight studies (11%) used annual average pollutant concentrations to investigate long-term exposure finding significant associations with asthma, reduced lung function, atopy and cardio-respiratory mortality across five studies. The remaining three studies found no significant association with asthma, mortality and a range of self-reported diseases, respectively.ConclusionsAmbient air pollution has substantial health impacts in Australia. The body of domestic evidence has increased markedly since national air quality standards were first set in the 1990s, which could be drawn on by policy-makers when revising the existing standards, or considering new standards.

Healthcare-acquired infections (HAIs) continue to persist in hospitals, despite the use of increasingly strict infection-control precautions. Opportunistic airborne transmission of potentially pathogenic bioaerosols may be one possible reason for this persistence. Therefore, this study aimed to systematically review the concentrations and compositions of indoor bioaerosols in different areas within hospitals and the effects of different ventilation systems. Electronic databases (Medline and Web of Science) were searched to identify articles of interest. The search was restricted to articles published from 2000 to 2017 in English. Aggregate data was used to examine the differences in mean colony forming units per cubic metre (cfu/m3) between different hospital areas and ventilation types. A total of 36 journal articles met the eligibility criteria. The mean total bioaerosol concentrations in the different areas of the hospitals were highest in the inpatient facilities (77 cfu/m3, 95% confidence interval (CI): 55-108) compared with the restricted (13cfu/m3, 95% CI: 10-15) and public areas (14 cfu/m3, 95% CI: 10-19). Hospital areas with natural ventilation had the highest total bioaerosol concentrations (201 cfu/m3, 95% CI: 135-300) compared with areas using conventional mechanical ventilation systems (20 cfu/m3, 95% CI: 16-24). Hospital areas using sophisticated mechanical ventilation systems (such as increased air changes per hour, directional flow and filtration systems) had the lowest total bioaerosol concentrations (9 cfu/m3, 95% CI: 7-13). Operating sophisticated mechanical ventilation systems in hospitals contributes to improved indoor air quality within hospitals, which assists in reducing the risk of airborne transmission of HAIs.

This study aimed to assess if air pollutants and meteorological factors synergistically affect birth outcomes in Shenzhen, China.A total of 1,206,158 singleton live births between 2005 and 2012 were identified from a birth registry database. Daily average measurements of particulate matter ≤10 µm (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), ambient air temperature (T), and dew point temperature (Td), a marker of humidity, were collected. Multivariable logistic regression models were used to evaluate associations between air pollution and small for gestational age (SGA), and full-term low birth weight (TLBW). We classified births into those conceived in the warm (May-October) and cold seasons (November-April) and then estimated interactions between air pollutants and meteorological factors.An interquartile range (IQR) increase in PM10 exposure during the first trimester (23.1 µg/m) and NO2 during both the first and second trimesters (15.1 and 13.4 µg/m) was associated with SGA and TLBW risk; odds ratios ranged from 1.01 (95% confidence interval [CI] = 1.00, 1.02) to 1.09 (1.07, 1.12). We observed interactive effects of both air temperature and humidity on PM10 and SGA for newborns conceived in the warm season. Each IQR increase in PM10 (11.1 µg/m) increased SGA risk by 90% (95% CI = 19%, 205%), 29% (23, 34%), 61% (10, 38%), and 26% (21, 32%) when T5th percentile, 5thT95th percentile, Td5th percentile, and 5thTd95th percentile, respectively.Our study found evidence of an interactive effect of air temperature and humidity on the relationship between PM10 exposure and SGA among newborns conceived in the warm season (May-October). Relatively low air temperature or humidity exacerbated the effects of PM10.

Background Designing healthy, liveable cities is a global priority. Current liveability indices are aggregated at the city-level, do not reflect spatial variation within cities, and are often not aligned to policy or health. Objectives To combine policy-relevant liveability indicators associated with health into a spatial Urban Liveability Index (ULI) and examine its association with adult travel behaviours. Methods We developed methods to calculate spatial liveability indicators and the ULI for all residential addresses in Melbourne, Australia. Associations between the address-level ULI and adult travel behaviours from the 2012–2014 Victorian Integrated Survey of Travel and Activity (VISTA) (n = 12,323) were analysed using multilevel logistic regression. Sensitivity analyses to evaluate impact of methodological choices on distribution of liveability as assessed by the ULI and associations with travel mode choice were also conducted. Results Liveability estimates were calculated for 1,550,641 residential addresses. ULI scores were positively associated with active transport behaviour: for each unit increase in the ULI score the estimated adjusted odds ratio (OR) for: walking increased by 12% (95% Credible Interval: 9%, 15%); cycling increased by 10% (4%, 17%); public transport increased by 15% (11%, 19%); and private vehicle transport decreased by 12% (− 9%, − 15%). Conclusions The ULI provides an evidence-informed and policy-relevant measure of urban liveability, that is significantly and approximately linearly associated with adult travel behaviours in the Melbourne context. The ULI can be used to evaluate progress towards implementing policies designed to achieve more liveable cities, identify spatial inequities, and examine relationships with health and wellbeing. Electronic supplementary material The online version of this article (10.1186/s12942-019-0178-8) contains supplementary material, which is available to authorized users.

BACKGROUND AND OBJECTIVE: Aerosol transmission of Pseudomonas aeruginosa has been suggested as a possible mode of respiratory infection spread in patients with cystic fibrosis (CF); however, whether this occurs in other suppurative lung diseases is unknown. Therefore, we aimed to determine if (i) patients with bronchiectasis (unrelated to CF) or chronic obstructive pulmonary disease (COPD) can aerosolize P. aeruginosa during coughing and (ii) if genetically indistinguishable (shared) P. aeruginosa strains are present in these disease cohorts.METHODS: People with bronchiectasis or COPD and P. aeruginosa respiratory infection were recruited for two studies. Aerosol study: Participants (n = 20) underwent cough testing using validated cough rigs to determine the survival of P. aeruginosa aerosols in the air over distance and duration. Genotyping study: P. aeruginosa sputum isolates (n = 95) were genotyped using the iPLEX20SNP platform, with a subset subjected to the enterobacterial repetitive intergenic consensus polymerase chain reaction (ERIC-PCR) assay to ascertain their genetic relatedness.RESULTS: Aerosol study: Overall, 7 of 20 (35%) participants released P. aeruginosa cough aerosols during at least one of the cough aerosol tests. These cough aerosols remained viable for 4 m from the source and for 15 min after coughing. The mean total aerosol count of P. aeruginosa at 2 m was two colony-forming units. Typing study: No shared P. aeruginosa strains were identified.CONCLUSION: Low viable count of P. aeruginosa cough aerosols and a lack of shared P. aeruginosa strains observed suggest that aerosol transmission of P. aeruginosa is an unlikely mode of respiratory infection spread in patients with bronchiectasis and COPD.

Ambient air pollution is the leading environmental risk factor for disease globally. Air pollutants can increase the risk of some respiratory infections, but their effects on tuberculosis (TB) are unclear. In this systematic literature review, we aimed to assess epidemiological studies on the association between outdoor air pollutants and TB incidence, hospital admissions and death (collectively referred to here as ‘TB outcomes’). We sought to consolidate available evidence on this topic and propose recommendations for future studies. Following PRISMA guidelines, we searched PubMed, Web of Science, Google Scholar, and Scopus with no restrictions imposed on year of publication. A total of 11 epidemiological studies, performed in Asia, Europe and North America, met our inclusion criteria (combined sample size: 215,337 people). We extracted key study characteristics from each eligible publication, including design, exposure assessment, analytical approaches and effect estimates. The studies were assessed for overall quality and risk of bias using standard criteria. The pollutant most frequently associated with statistically significant effects on TB outcomes was fine particulate matter ( The existing epidemiological evidence is limited and shows mixed results. However, it is plausible that exposure to air pollutants, particularly PM2.5, may suppress important immune defence mechanisms, increasing an individual's susceptibility to development of active TB and TB-related mortality. Considering the small number of studies relative to the demonstrably large global health burdens of air pollution and TB, further research is required to corroborate the findings in the current literature. Based on a critical assessment of existing evidence, we conclude with methodological suggestions for future studies.

Maternal exposure to ambient air pollution has been associated with preterm birth (PTB), however, entire pregnancy or trimester-specific associations were generally reported, which may not sufficiently identify windows of susceptibility. Using birth registry data from Guangzhou, a megacity of southern China (population ~14.5 million), including 469,975 singleton live births between January 2015 and July 2017, we assessed the association between weekly air pollution exposure and PTB in a retrospective cohort study. Daily average concentrations of PM2.5, PM10, NO2, SO2, and O3 from 11 monitoring stations were used to estimate district-specific exposures for each participant based on their district residency during pregnancy. Distributed lag models (DLMs) incorporating Cox proportional hazard models were applied to estimate the association between weekly maternal exposure to air pollutant and PTB risk (as a time-to-event outcome), after controlling for temperature, seasonality, and individual-level covariates. We also considered moderate PTB (32–36 gestational weeks) and very PTB (28–31 gestational weeks) as outcomes of interest. Hazard ratios (HRs) and 95% confidential intervals (95% CIs) were calculated for an interquartile range (IQR) increase in air pollutants during the study period. An IQR increase in PM2.5 exposure during the 20th to 28th gestational weeks (27.0 μg/m3) was significantly associated with PTB risk, with the strongest effect in the 25th week (HR = 1.034, 95% CI:1.010–1.059). The significant exposure windows were the 19th–28th weeks for PM10, the 18th–31st weeks for NO2, and the 23rd–31st weeks for O3, respectively. The strongest associations were observed in the 25th week for PM10 (IQR = 37.0 μg/m3; HR = 1.048, 95% CI:1.034–1.062), the 26th week for NO2 (IQR = 29.0 μg/m3; HR = 1.060, 95% CI:1.028–1.094), and in the 28th week for O3 (IQR = 90.0 μg/m3; HR = 1.063, 95% CI:1.046–1.081). Similar patterns were observed for moderate PTB (32–36 gestational weeks) and very PTB (28–31 gestational weeks) for PM2.5, PM10, NO2 exposure, but the effects were greater for very PTB. We did not observe any association between pregnancy SO2 exposure and the risk of PTB. Our results suggest that middle to late pregnancy is the most susceptible air pollution exposure window for air pollution and PTB among women in Guangzhou, China. Keywords: Air pollution, Preterm birth, Distributed lag model, Susceptible exposure window

Most studies of long-term air pollution exposure and children's respiratory health have been performed in urban locations with moderate pollution levels. We assessed the effect of outdoor nitrogen dioxide (NO2), as a proxy for urban air pollution, on current asthma and lung function in Australia, a low-pollution setting.We undertook a national population-based cross-sectional study of children aged 7–11 years living in 12 Australian cities. We collected information on asthma symptoms from parents via questionnaire and measured children's lung function (forced expiratory volume in 1 s [FEV1], forced vital capacity [FVC]) and fractional exhaled nitric oxide [FeNO]). We estimated recent NO2 exposure (last 12 months) using monitors near each child's school, and used a satellite-based land-use regression (LUR) model to estimate NO2 at each child's school and home.Our analysis comprised 2630 children, among whom the prevalence of current asthma was 14.9%. Mean (±SD) NO2 exposure was 8.8 ppb (±3.2) and 8.8 ppb (±2.3) for monitor- and LUR-based estimates, respectively. Mean percent predicted post-bronchodilator FEV1 and FVC were 101.7% (±10.5) and 98.8% (±10.5), respectively. The geometric mean FeNO concentration was 9.4 ppb (±7.1).An IQR increase in NO2 (4.0 ppb) was significantly associated with increased odds of having current asthma; odds ratios (ORs) were 1.24 (95% CI: 1.08, 1.43) and 1.54 (95% CI: 1.26, 1.87) for monitor- and LUR-based estimates, respectively. Increased NO2 exposure was significantly associated with decreased percent predicted FEV1 (−1.35 percentage points [95% CI: −2.21, −0.49]) and FVC (−1.19 percentage points [95% CI: −2.04, −0.35], and an increase in FeNO of 71% (95% CI: 38%, 112%).Exposure to outdoor NO2 was associated with adverse respiratory health effects in this population-based sample of Australian children. The relatively low NO2 levels at which these effects were observed highlight the potential benefits of continuous exposure reduction. Keywords: Asthma, Air pollution, Australia, Children, Nitrogen dioxide, Exposure

Long-term exposure to air pollutants, especially particulates, in adulthood is related to cardiovascular diseases and vascular markers of atherosclerosis. However, whether vascular changes in children is related to exposure to air pollutants remains unknown. This study examined whether childhood exposure to air pollutants was related to a marker of cardiovascular risk, carotid intima–media thickness (CIMT) in children aged 11–12 years old. Longitudinal Study of Australian Children (LSAC) recruited parents and their children born in 2003–4. Among the participants, CheckPoint examination was conducted when the children were 11–12 years old. Ultrasound of the right carotid artery was performed using standardized protocols. Average and maximum far-wall CIMT, carotid artery distensibility, and elasticity were quantified using semiautomated software. Annual and life-time exposure to air pollutants was estimated using satellite-based land-use regression by residential postcodes. A total of 1063 children (50.4% girls) with CIMT data, serum cholesterol, and modeled estimates of NO2 and PM2.5 exposure for the period 2003 to 2015 were included. The average and maximum CIMT, carotid distensibility, and elasticity were 497 μm (standard deviation, SD 58), 580 μm (SD 44), 17.4% (SD 3.2), and 0.48%/mmHg (SD 0.09), respectively. The life-time average concentrations of PM2.5 and NO2 were 6.4 μg/m3 (SD 1.4) and 6.4 ppb (SD 2.4), respectively. Both average and maximum CIMT were significantly associated with average ambient PM2.5 concentration (average CIMT: +5.5 μm per μg/m3, 95% confidence interval, CI 2.4 to 8.5, and maximum CIMT: +4.9 μm per μg/m3, CI 2.3 to 7.6), estimated using linear regression, adjusting for potential confounders. CIMT was not significantly related to NO2 exposure. Carotid artery diameter, distensibility, and elasticity were not significantly associated with air pollutants. We conclude that life-time exposure to low levels of PM2.5 in children might have measurable adverse impacts on vascular structure by age 11–12 years.

Background Urban greenness may protect against obesity, but very few studies have assessed ‘street view’ (SV) greenness metrics, which may better capture people's actual exposure to greenness compared to commonly-used satellite-derived metrics. We aimed to investigate these associations further in a Chinese adult study. Methods Our analysis included 24,845 adults in the 33 Chinese Community Health Study in 2009. SV images from Tencent Map, segmented by machine learning algorithms, were used to determine the average proportion of green vegetation in SV images at community level in 800m road network buffer. Sensitivity analyses were performed with an alternative buffer size. Overall greenness was assessed as normalized difference vegetation index (NDVI) in 800 m buffer. We used predicted PM2.5 and monitored NO2 as proxies of air pollution. Body mass index (BMI), waist circumference (WC) and hip circumference (HC) were regressed on SV greenness by generalized linear mixed models, with adjustment for covariates. Mediation analyses were performed to assess the mediation effects of air pollution. Results Each interquartile range (IQR = 3.6%) increase in street view greenness was associated with a 0.15 kg/m2 (95% CI: −0.22, −0.09) decrease in BMI and 0.23 cm (95% CI: −0.35, −0.11) reduction in HC, and was associated with 7% lower odds of overweight (OR = 0.93, 95% CI:0.90, 0.96) and 18% lower odds of obesity (OR = 0.82, 95% CI:0.76, 0.89). Similar effect estimation was observed compared with commonly-used NDVI measures. PM2.5 and NO2 mediated 15.5% and 6.1% of the effects of SV greenness with BMI, respectively. Conclusions Our findings suggest beneficial associations between community-level SV greenness and lower body weight in Chinese adults. The effects were observed in women but not in men. Air pollution may partially mediate the association. These findings may have implications to support efforts to promote greening in urban areas.

Background Beneficial effects of greenness on birth outcomes have been reported, but few studies have investigated the associations in both urban and non-urban settings. We aimed to evaluate and compare linear and nonlinear associations between greenness and birth outcomes in urban and non-urban settings. Methods From October 2015 to December 2018, participants were recruited into the Maoming Birth Cohort Study. A total of 11 258 live birth records were obtained. Greenness exposure was assessed using the normalized difference vegetation index (NDVI) and enhanced vegetation index (EVI). Linear regression and nonlinear restricted cubic spline models were implemented to investigate the associations between greenness and birthweight, birth length, gestational age, preterm birth, low birthweight, small for gestational age and the potential for effect variation under urban or non-urban settings, after adjusting for covariates. Results A 0.1-unit increase in NDVI-500m was significantly associated with an increase of 35.4 g in birthweight [95% confidence interval (CI): 13.2, 57.7], 0.15 cm in birth length (95% CI: 0.03, 0.26), 0.88 days in gestational age (95% CI: 0.05, 1.71) and lower odds of low birthweight [odds ratio (OR) = 0.69, 95% CI: 0.56, 0.85] and preterm birth (OR = 0.70, 95% CI: 0.58, 0.85). No association with head circumference was observed. For all outcomes, no significant linear associations were observed among non-urban dwellers. Inversed ‘U-shaped’ associations between greenness exposure and birth outcomes were observed in the total study population. Conclusions Greenness exposure was associated with increased gestational age, birthweight and birth length in urban dwellers. Nonlinear associations assessed by restricted cubic splines suggested that health benefits could be larger when increasing greenness levels from low to medium compared with increasing greenness from medium to high levels. Further studies adopting nonlinear methods are warranted to verify our findings.

Multiple systematic reviews on greenspace and health outcomes exist, but the overall evidence base remains unclear. Therefore, we performed an umbrella review to collect and appraise all relevant systematic reviews of epidemiological studies on greenness exposure and health. We searched PubMed, Embase, and Web of Science from inception to June 28, 2021, and screened references of relevant articles. Systematic reviews with or without meta-analyses of epidemiological studies that examined the associations of greenness with any health outcome were included. Two independent investigators performed study selection and data extraction. We also evaluated the methodological quality of the included systematic reviews using the “Assessing the Methodological Quality of Systematic Reviews 2” checklist. A total of 40 systematic reviews and meta-analyses were included, of which most were cross-sectional studies conducted in high-income countries. Greenspace exposure was estimated with various objective and subjective parameters. Beneficial associations of greenspace with all-cause and stroke-specific mortality, CVD morbidity, cardiometabolic factors, mental health, low birth weight, physical activity, sleep quality, and urban crime were observed. No consistent associations between greenspace and other health outcomes (e.g., cancers) were observed. Most of the included systematic reviews and meta-analyses had one or more limitations in methodology. Our findings provide supportive evidence regarding the beneficial effects of greenspace exposure on some aspects of human health. However, the credibility of such evidence was compromised by methodological limitations. Better performed systematic reviews and meta-analyses as well as longitudinal designed primary studies are needed to validate this conclusion., Graphical abstract, Public summary • The evidence concerning greenspace and health outcomes remains unclear • We performed an umbrella review of 40 systematic reviews on greenspace and health • Greenspace exposure was estimated with various objective and subjective parameters • Greenspace was beneficially associated with several aspects of human health

Background The widely used Air Quality Index (AQI) has been criticized due to its inaccuracy, leading to the development of the air quality health index (AQHI), an improvement on the AQI. However, there is currently no consensus on the most appropriate construction strategy for the AQHI. Objectives In this study, we aimed to evaluate the utility of AQHIs constructed by different models and health outcomes, and determine a better strategy. Methods Based on the daily time-series outpatient visits and hospital admissions from 299 hospitals (January 2016–December 2018), and mortality (January 2017–December 2019) in Guangzhou, China, we utilized cumulative risk index (CRI) method, Bayesian multi-pollutant weighted (BMW) model and standard method to construct AQHIs for different health outcomes. The effectiveness of AQHIs constructed by different strategies was evaluated by a two-stage validation analysis and examined their exposure-response relationships with the cause-specific morbidity and mortality. Results Validation by different models showed that AQHI constructed with the BMW model (BMW-AQHI) had the strongest association with the health outcome either in the total population or subpopulation among air quality indexes, followed by AQHI constructed with the CRI method (CRI-AQHI), then common AQHI and AQI. Further validation by different health outcomes showed that AQHI constructed with the risk of outpatient visits generally exhibited the highest utility in presenting mortality and morbidity, followed by AQHI constructed with the risk of hospitalizations, then mortality-based AQHI and AQI. The contributions of NO2 and O3 to the final AQHI were prominent, while the contribution of SO2 and PM2.5 were relatively small. Conclusions The BMW model is likely to be more effective for AQHI construction than CRI and standard methods. Based on the BMW model, the AQHI constructed with the outpatient data may be more effective in presenting short-term health risks associated with the co-exposure to air pollutants than the mortality-based AQHI and existing AQIs.

Background Rigorous analysis of levels and trends in exposure to leading risk factors and quantification of their effect on human health are important to identify where public health is making progress and in which cases current efforts are inadequate. The Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019 provides a standardised and comprehensive assessment of the magnitude of risk factor exposure, relative risk, and attributable burden of disease. Methods GBD 2019 estimated attributable mortality, years of life lost (YLLs), years of life lived with disability (YLDs), and disability-adjusted life-years (DALYs) for 87 risk factors and combinations of risk factors, at the global level, regionally, and for 204 countries and territories. GBD uses a hierarchical list of risk factors so that specific risk factors (eg, sodium intake), and related aggregates (eg, diet quality), are both evaluated. This method has six analytical steps. (1) We included 560 risk-outcome pairs that met criteria for convincing or probable evidence on the basis of research studies. 12 risk-outcome pairs included in GBD 2017 no longer met inclusion criteria and 47 risk-outcome pairs for risks already included in GBD 2017 were added based on new evidence. (2) Relative risks were estimated as a function of exposure based on published systematic reviews, 81 systematic reviews done for GBD 2019, and meta-regression. (3) Levels of exposure in each age-sex-location-year included in the study were estimated based on all available data sources using spatiotemporal Gaussian process regression, DisMod-MR 2.1, a Bayesian meta-regression method, or alternative methods. (4) We determined, from published trials or cohort studies, the level of exposure associated with minimum risk, called the theoretical minimum risk exposure level. (5) Attributable deaths, YLLs, YLDs, and DALYs were computed by multiplying population attributable fractions (PAFs) by the relevant outcome quantity for each age-sex-location-year. (6) PAFs and attributable burden for combinations of risk factors were estimated taking into account mediation of different risk factors through other risk factors. Across all six analytical steps, 30 652 distinct data sources were used in the analysis. Uncertainty in each step of the analysis was propagated into the final estimates of attributable burden. Exposure levels for dichotomous, polytomous, and continuous risk factors were summarised with use of the summary exposure value to facilitate comparisons over time, across location, and across risks. Because the entire time series from 1990 to 2019 has been re-estimated with use of consistent data and methods, these results supersede previously published GBD estimates of attributable burden. Findings The largest declines in risk exposure from 2010 to 2019 were among a set of risks that are strongly linked to social and economic development, including household air pollution; unsafe water, sanitation, and handwashing; and child growth failure. Global declines also occurred for tobacco smoking and lead exposure. The largest increases in risk exposure were for ambient particulate matter pollution, drug use, high fasting plasma glucose, and high body-mass index. In 2019, the leading Level 2 risk factor globally for attributable deaths was high systolic blood pressure, which accounted for 10.8 million (95% uncertainty interval [UI] 9.51-12.1) deaths (19.2% [16.9-21.3] of all deaths in 2019), followed by tobacco (smoked, second-hand, and chewing), which accounted for 8.71 million (8.12-9.31) deaths (15.4% [14.6-16.2] of all deaths in 2019). The leading Level 2 risk factor for attributable DALYs globally in 2019 was child and maternal malnutrition, which largely affects health in the youngest age groups and accounted for 295 million (253-350) DALYs (11.6% [10.3-13.1] of all global DALYs that year). The risk factor burden varied considerably in 2019 between age groups and locations. Among children aged 0-9 years, the three leading detailed risk factors for attributable DALYs were all related to malnutrition. Iron deficiency was the leading risk factor for those aged 10-24 years, alcohol use for those aged 25-49 years, and high systolic blood pressure for those aged 50-74 years and 75 years and older. Interpretation Overall, the record for reducing exposure to harmful risks over the past three decades is poor. Success with reducing smoking and lead exposure through regulatory policy might point the way for a stronger role for public policy on other risks in addition to continued efforts to provide information on risk factor harm to the general public. Copyright (C) 2020 The Author(s). Published by Elsevier Ltd.

Key Points Question Is the general vegetation level of a residential area, referred to as residential greenness, associated with cardiovascular disease among adults, and does the presence of cardiometabolic disorders mediate or modify the association between residential greenness and cardiovascular disease? Findings In this cross-sectional study of 24 845 adults in China, residential areas with higher greenness levels were associated with a lower likelihood of cardiovascular disease. The presence of cardiometabolic disorders partially mediated the association between residential greenness and cardiovascular disease. Meaning The study’s findings may be helpful for health care professionals and policy makers in the development of strategies, such as planning for green spaces in residential areas, to mitigate the burden of cardiovascular disease., Importance Living in areas with more vegetation (referred to as residential greenness) may be associated with cardiovascular disease (CVD), but little data are available from low- and middle-income countries. In addition, it remains unclear whether the presence of cardiometabolic disorders modifies or mediates the association between residential greenness and CVD. Objective To evaluate the associations between residential greenness, cardiometabolic disorders, and CVD prevalence among adults in China. Design, Setting, and Participants This analysis was performed as part of the 33 Communities Chinese Health Study, a large population-based cross-sectional study that was conducted in 33 communities (ranging from 0.25-0.64 km2) in 3 cities within the Liaoning province of northeastern China between April 1 and December 31, 2009. Participants included adults aged 18 to 74 years who had resided in the study area for 5 years or more. Greenness levels surrounding each participant’s residential community were assessed using the normalized difference vegetation index and the soil-adjusted vegetation index from 2010. Lifetime CVD status (including myocardial infarction, heart failure, coronary heart disease, cerebral thrombosis, cerebral hemorrhage, cerebral embolism, and subarachnoid hemorrhage) was defined as a self-report of a physician diagnosis of CVD at the time of the survey. Cardiometabolic disorders, including hypertension, diabetes, dyslipidemia, and overweight or obese status, were measured and defined clinically. Generalized linear mixed models were used to evaluate the association between residential greenness levels and CVD prevalence. A 3-way decomposition method was used to explore whether the presence of cardiometabolic disorders mediated or modified the association between residential greenness and CVD. Data were analyzed from October 10 to May 30, 2020. Main Outcomes and Measures Lifetime CVD status, the presence of cardiometabolic disorders, and residential greenness level. Results Among 24 845 participants, the mean (SD) age was 45.6 (13.3) years, and 12 661 participants (51.0%) were men. A total of 1006 participants (4.1%) reported having a diagnosis of CVD. An interquartile range (1-IQR) increase in the normalized difference vegetation index within 500 m of a community was associated with a 27% lower likelihood (odds ratio [OR], 0.73; 95% CI, 0.65-0.83; P, This cross-sectional study uses the normalized difference vegetation index and the soil-adjusted vegetation index to examine the associations between the level of residential greenness, the presence of cardiometabolic disorders, and the prevalence of cardiovascular disease among adults in China.

Background: There is limited information on risk factors for eczema in adults. Recent evidence suggests that air pollution may be associated with increased incidence of eczema in adults. We aimed to assess this possible association. Methods: Ambient air pollution exposures (distance from a major road, nitrogen dioxide [NO2], fine particulate matter with an aerodynamic diameter ≤2.5 µm [PM2.5]) were assessed for the residential address of Tasmanian Longitudinal Health Study participants at ages 43 and 53 years. Eczema incidence (onset after age 43 years), prevalence (at 53 years) and persistence were assessed from surveys, while sensitisation was assessed using skin prick tests. The presence or absence of eczema and sensitisation was classified into four groups: no atopy or eczema, atopy alone, non-atopic eczema, and atopic eczema. Adjusted logistic and multinomial regression models were fitted to estimate associations between ambient air pollution and eczema, and interaction by sex was assessed. Results: Of 3153 participants in both follow ups, 2369 had valid skin prick tests. For males, a 2.3 ppb increase in baseline NO2 was associated with increased risk of prevalent eczema (OR=1.15 [95%CI 0.98-1.36]), both non-atopic (OR=1.39 [1.02-1.90]) and atopic eczema (OR=1.26 [1.00-1.59]). These associations were not seen in females (P for interaction=0.08

Artículo con numerosos autores. Sólo se hace referencia al primero que coincide con el de la UAM y al colectivo, Background Previous attempts to characterise the burden of chronic respiratory diseases have focused only on specific disease conditions, such as chronic obstructive pulmonary disease (COPD) or asthma. In this study, we aimed to characterise the burden of chronic respiratory diseases globally, providing a comprehensive and up-to-date analysis on geographical and time trends from 1990 to 2017. Methods Using data from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2017, we estimated the prevalence, morbidity, and mortality attributable to chronic respiratory diseases through an analysis of deaths, disability-adjusted life-years (DALYs), and years of life lost (YLL) by GBD super-region, from 1990 to 2017, stratified by age and sex. Specific diseases analysed included asthma, COPD, interstitial lung disease and pulmonary sarcoidosis, pneumoconiosis, and other chronic respiratory diseases. We also assessed the contribution of risk factors (smoking, second-hand smoke, ambient particulate matter and ozone pollution, household air pollution from solid fuels, and occupational risks) to chronic respiratory disease-attributable DALYs. Findings In 2017, 544·9 million people (95% uncertainty interval [UI] 506·9–584·8) worldwide had a chronic respiratory disease, representing an increase of 39·8% compared with 1990. Chronic respiratory disease prevalence showed wide variability across GBD super-regions, with the highest prevalence among both males and females in high-income regions, and the lowest prevalence in sub-Saharan Africa and south Asia. The age-sex-specific prevalence of each chronic respiratory disease in 2017 was also highly variable geographically. Chronic respiratory diseases were the third leading cause of death in 2017 (7·0% [95% UI 6·8–7·2] of all deaths), behind cardiovascular diseases and neoplasms. Deaths due to chronic respiratory diseases numbered 3 914 196 (95% UI 3 790 578–4 044 819) in 2017, an increase of 18·0% since 1990, while total DALYs increased by 13·3%. However, when accounting for ageing and population growth, declines were observed in age-standardised prevalence (14·3% decrease), agestandardised death rates (42·6%), and age-standardised DALY rates (38·2%). In males and females, most chronic respiratory disease-attributable deaths and DALYs were due to COPD. In regional analyses, mortality rates from chronic respiratory diseases were greatest in south Asia and lowest in sub-Saharan Africa, also across both sexes. Notably, although absolute prevalence was lower in south Asia than in most other super-regions, YLLs due to chronic respiratory diseases across the subcontinent were the highest in the world. Death rates due to interstitial lung disease and pulmonary sarcoidosis were greater than those due to pneumoconiosis in all super-regions. Smoking was the leading risk factor for chronic respiratory disease-related disability across all regions for men. Among women, household air pollution from solid fuels was the predominant risk factor for chronic respiratory diseases in south Asia and sub-Saharan Africa, while ambient particulate matter represented the leading risk factor in southeast Asia, east Asia, and Oceania, and in the Middle East and north Africa super-region. Interpretation Our study shows that chronic respiratory diseases remain a leading cause of death and disability worldwide, with growth in absolute numbers but sharp declines in several age-standardised estimators since 1990. Premature mortality from chronic respiratory diseases seems to be highest in regions with less-resourced health systems on a per-capita basis, Bill & Melinda Gates Foundation.

The relationship between maternal exposure to ambient air pollution and pregnancy complications is not well characterized. We aimed to explore the relationship between maternal exposure to ambient nitrogen dioxide (NO2) and fine particulate matter (PM2.5) and hypertensive disorders of pregnancy, gestational diabetes mellitus (GDM) and placental abruption. Using administrative data, we defined a state-wide cohort of singleton pregnancies born between 1 March 2012 and 31 December 2015 in Victoria, Australia. Annual average NO2 and PM2.5 was assigned to maternal residence at the time of birth. 285,594 singleton pregnancies were included. An IQR increase in NO2 (3.9 ppb) was associated with reduced likelihood of hypertensive disorders of pregnancy (RR 0.89, 95%CI 0.86, 0.91), GDM (RR 0.92, 95%CI 0.90, 0.94) and placental abruption (RR 0.81, 95%CI 0.69, 0.95). Mixed observations and smaller effect sizes were observed for IQR increases in PM2.5 (1.3 &micro, g/m3) and pregnancy complications, reduced likelihood of hypertensive disorders of pregnancy (RR 0.95, 95%CI 0.93, 0.97), increased likelihood of GDM (RR 1.02, 95%CI 1.00, 1.03) and no relationship for placental abruption. In this exploratory study using an annual metric of exposure, findings were largely inconsistent with a priori expectations and further research involving temporally resolved exposure estimates are required.

Background The relationship between maternal exposure to air pollution and birth outcomes is not well characterised where ambient air pollution is relatively low. Objectives We aimed to explore the association between maternal exposure to ambient nitrogen dioxide (NO2) and fine particulate matter (PM2.5) and a range of birth outcomes in Victoria, Australia. Secondary aims were to explore whether obstetric conditions, such as gestational diabetes mellitus (GDM) and hypertensive disorders of pregnancy, were effect modifiers in observed relationships. Methods We included all singleton births occurring in Victoria, Australia from 1st March 2012 to 31st December 2015 using routinely collected government data. Outcomes included birth weight, small for gestational age (SGA), term low birth weight (tLBW), large for gestational age (LGA), and spontaneous preterm birth (sPTB). We estimated exposure to annual ambient NO2 and PM2.5 concentrations, assigned to maternal residence at time of birth. Confounders included maternal, meteorological and temporal variables. Multivariable linear regression and log-binomial regression were used for continuous and dichotomous outcomes, respectively. Results There were 285,594 births during the study period. Average NO2 exposure was 6.0 parts per billion (ppb, median 5.6; interquartile range (IQR) 3.9) and PM2.5 was 6.9 μg/m3 (median 7.1, IQR 1.3). IQR increases in ambient NO2 and PM2.5 were associated with fetal growth restriction, including decrements in birth weight (NO2 β −22.8 g; 95%CI -26.0, −19.7; PM2.5 β −14.8 g; 95%CI -17.4, −12.2) and increased risk of SGA (NO2 RR 1.08; 95%CI 1.06, 1.10; PM2.5 RR 1.05; 95%CI 1.04, 1.07) and tLBW (NO2 RR 1.06; 95%CI 1.01, 1.10; PM2.5 RR 1.04; 95%CI 1.03, 1.08). Women with GDM and hypertensive disorders of pregnancy had greater decrements in birth weight in association with pollutant exposure. Discussion In this exploratory study using an annual metric of exposure, maternal exposure to low-level ambient air pollution was associated with fetal growth restriction, which carries substantial public health implications.

Smoke exposure from bushfires, such as those experienced in Australia during 2019-2020, can reach levels up to 10 times those deemed hazardous. Short-term and extended exposure to high levels of air pollution can be associated with adverse health effects, although the most recent fires have brought into sharp focus that several important knowledge gaps remain. In this article, we briefly identify and discuss the existing Australian evidence base and make suggestions for future research.

We aimed to describe the epidemiology, multi-drug resistance and seasonal distribution of bacteria cultured within 12 months following lower limb orthopaedic surgery in tropical and subtropical Australian hospitals between 2010 and 2017. We collected data from four tropical and two subtropical hospitals. Categorical variables were examined using the Pearson Chi-squared test or Fisher&rsquo, s Exact test, and continuous variables with the Student t-test or Mann&ndash, Whitney U test. A Poisson regression model was used to examine the relationship between season, weather and the incidence of Staphylococcus and nonfermentative species. We found that at tropical sites, nonfermenters (Pseudomonas aeruginosa and Acinetobacter baumannii) were more common (28.7% vs. 21.6%, p = 0.018), and patients were more likely to culture multi-drug-resistant (MDR) nonfermenters (11.4% vs. 1.3%, p = 0.009) and MDR Staphylococcus aureus (35.9% vs. 24.6%, p = 0.006). At tropical sites, patients were more likely to be younger (65.9 years vs. 72.0, p = &lt, 0.001), male (57.7% vs. 47.8%, p = 0.005), having knee surgery (45.3% vs. 34.5%, p = 0.002) and undergoing primary procedures (85.0% vs. 73.0%, p = &lt, 0.001). Species were similar between seasons in both tropical and subtropical hospitals. Overall, we found that following lower limb orthopaedic surgery in tropical compared with subtropical Australia, patients were more likely to culture nonfermenters and some MDR species.

BACKGROUND: Both extreme heat and air pollution exposure during pregnancy have been associated with preterm birth; however, their combined effects are unclear. OBJECTIVES: Our goal was to estimate the independent and joint effects of heatwaves and fine particulate matter [PM 0) for less extreme heatwaves (i.e., shorter or with relatively low temperature thresholds) but were less than additive (RERIs

Background Machine learning algorithms have very high predictive ability. However, no study has used machine learning to estimate historical concentrations of PM2.5 (particulate matter with aerodynamic diameter ≤ 2.5 μm) at daily time scale in China at a national level. Objectives To estimate daily concentrations of PM2.5 across China during 2005–2016. Methods Daily ground-level PM2.5 data were obtained from 1479 stations across China during 2014–2016. Data on aerosol optical depth (AOD), meteorological conditions and other predictors were downloaded. A random forests model (non-parametric machine learning algorithms) and two traditional regression models were developed to estimate ground-level PM2.5 concentrations. The best-fit model was then utilized to estimate the daily concentrations of PM2.5 across China with a resolution of 0.1° (≈10 km) during 2005–2016. Results The daily random forests model showed much higher predictive accuracy than the other two traditional regression models, explaining the majority of spatial variability in daily PM2.5 [10-fold cross-validation (CV) R2 = 83%, root mean squared prediction error (RMSE) = 28.1 μg/m3]. At the monthly and annual time-scale, the explained variability of average PM2.5 increased up to 86% (RMSE = 10.7 μg/m3 and 6.9 μg/m3, respectively). Conclusions Taking advantage of a novel application of modeling framework and the most recent ground-level PM2.5 observations, the machine learning method showed higher predictive ability than previous studies. Capsule Random forests approach can be used to estimate historical exposure to PM2.5 in China with high accuracy.

Evidence on the associations between airborne particulates of diameter ≤1 μm (PM 1 ) and airborne particulates of diameter ≤2.5 μm (PM 2.5 ) and childhood blood pressure (BP) is scarce. To help to address this literature gap, we conducted a study to explore the associations in Chinese children. Between 2012 and 2013, we recruited 9354 children, aged 5 to 17 years, from 62 schools in 7 northeastern Chinese cities. We measured their BP with a mercury sphygmomanometer. We used a spatiotemporal model to estimate daily ambient PM 1 and PM 2.5 exposures, which we assigned to participants’ home addresses. Associations between particulate matter exposure and BP were evaluated with generalized linear mixed regression models. The findings indicated that exposure to each 10 mg/m 3 greater PM 1 was significantly associated with 2.56 mm Hg (95% CI, 1.47–3.65) higher systolic BP and 61% greater odds for hypertension (odds ratio=1.61 [95% CI, 1.18–2.18]). PM 1 appears to play an important role in associations reported between PM 2.5 exposure and BP, and we found that the ambient PM 1 /PM 2.5 ratio (range, 0.80–0.96) was associated with BP and with hypertension. Age and body weight modified associations between air pollutants and BP ( P 1 is associated with hypertension in children, and that PM 1 might be a leading contributor to the hypertensive effect of PM 2.5 . Researchers and policy makers should pay closer attention to the potential health impacts of PM 1 .

Rationale: Interactions between early life and adult insults on lung function decline are not well understood, with most studies investigating prebronchodilator (pre-BD) FEV1 decline.Objectives: To investigate relationships between adult risk factors and pre- and post-BD lung function decline and their potential effect modification by early life and genetic factors.Methods: Multiple regression was used to examine associations between adult exposures (asthma, smoking, occupational exposures, traffic pollution, and obesity) and decline in both pre- and post-BD spirometry (forced expiratory volume in 1 s [FEV1], forced vital capacity [FVC], and FEV1/FVC) between ages 45 and 53 years in the Tasmanian Longitudinal Health Study (n = 857). Effect modification of these relationships by childhood respiratory risk factors, including low childhood lung function and GST (glutathione S-transferase) gene polymorphisms, was investigated.Results: Baseline asthma, smoking, occupational exposure to vapors/gases/dusts/fumes, and living close to traffic were associated with accelerated decline in both pre- and post-BD FEV1. These factors were also associated with FEV1/FVC decline. Occupational exposure to aromatic solvents was associated with pre-BD but not post-BD FEV1 decline. Maternal smoking accentuated the effect of personal smoking on pre- and post-BD FEV1 decline. Lower childhood lung function and having the GSTM1 null allele accentuated the effect of occupational exposure to vapors/gases/dusts/fumes and personal smoking on post-BD FEV1 decline. Incident obesity was associated with accelerated decline in FEV1 and more pronounced in FVC.Conclusions: This study provides new evidence for accentuation of individual susceptibility to adult risk factors by low childhood lung function, GSTM1 genotype, and maternal smoking.

To determine the proportion of the national childhood asthma burden associated with exposure to dampness and gas stoves in Australian homes. Comparative risk assessment modelling study. Setting, participants: Australian children aged 14 years or less, 2011. The population attributable fractions (PAFs) and number of disability-adjusted life years (DALYs) for childhood asthma associated with exposure to damp housing and gas stoves. 26.1% of Australian homes have dampness problems and 38.2% have natural gas as the main energy source for cooktop stoves. The PAF for childhood asthma attributable to damp housing was 7.9% (95% CI, 3.2-12.6%), causing 1760 disability-adjusted life years (DALYs; 95% CI, 416-3104 DALYs), or 42 DALYs/100 000 children. The PAF associated with gas stoves was 12.3% (95% CI, 8.9-15.8%), corresponding to 2756 DALYs (95% CI, 1271-4242), or 67 DALYs/100 000 children. If all homes with gas stoves were fitted with high efficiency range hoods to vent gas combustion products outdoors, the PAF and burden estimates were reduced to 3.4% (95% CI, 2.2-4.6%) and 761 DALYs (95% CI, 322-1199). Exposure to damp housing and gas stoves is common in Australia, and is associated with a considerable proportion of the childhood asthma burden. Strategies for reducing exposure to indoor dampness and gas combustion products should be communicated to parents of children with or at risk of asthma.

Rationale: People with cystic fibrosis (CF) generate Pseudomonas aeruginosa in droplet nuclei during coughing. The use of surgical masks has been recommended in healthcare settings to minimize pathogen transmission between patients with CF. Objectives: To determine if face masks and cough etiquette reduce viable P. aeruginosa aerosolized during coughing. Methods: Twenty-five adults with CF and chronic P. aeruginosa infection were recruited. Participants performed six talking and coughing maneuvers, with or without face masks (surgical and N95) and hand covering the mouth when coughing (cough etiquette) in an aerosol-sampling device. An Andersen Cascade Impactor was used to sample the aerosol at 2 meters from each participant. Quantitative sputum and aerosol bacterial cultures were performed, and participants rated the mask comfort levels during the cough maneuvers. Measurements and Main Results: During uncovered coughing (reference maneuver), 19 of 25 (76%) participants produced aerosols containing P. aeruginosa, with a positive correlation found between sputum P. aeruginosa concentration (measured as cfu/ml) and aerosol P. aeruginosa colony-forming units. There was a reduction in aerosol P. aeruginosa load during coughing with a surgical mask, coughing with an N95 mask, and cough etiquette compared with uncovered coughing (P

The toxicity of ultrafine particles (UFPs) on blood pressure (BP) has not been well studied. We aimed to evaluate the associations of long-term UFP exposure with different components of BP and the risk of prehypertension/hypertension. We included a total of 24 845 Chinese adults (18–74 years old) in a cross-sectional survey (Liaoning province, China). The 4 year (2006–2009) average concentrations of UFP was estimated using a chemical transport model. We measured systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP) and pulse pressure (PP), prehypertension and hypertension. We used a generalized linear mixed model to examine the associations while controlling for important individual covariates. One unit (1 μg m−3) increase in UFP was associated with an increase in SBP of 1.52 mm Hg [95% confidence interval (CI): 0.48–2.55], DBP of 0.55 mm Hg (95% CI: 0.01–1.08) in DBP, MAP of 0.92 mm Hg (95% CI: 0.23–1.61) and PP of 0.62 mm Hg (95% CI: 0.05–1.20). The UFP-BP associations were stronger in women than in men. One unit increase in UFP was associated with an increased risk of hypertension and prehypertension (OR = 1.23, 95% CI: 1.09–1.38; OR = 1.12, 95% CI: 1.04–1.21) compared to normotension group, and these associations were stronger in overweight/obese participants. Our study showed that long-term exposure to UFP was associated with elevated BP and higher odds of hypertension. These findings suggest that strategies to monitor and reduce UFPs, which are not a regulated pollutant, could have beneficial cardiovascular effects.

The paediatric intensive care unit (PICU) provides care to critically ill neonates, infants and children. These patients are vulnerable and susceptible to the environment surrounding them, yet there is little information available on indoor air quality and factors affecting it within a PICU. To address this gap in knowledge we conducted continuous indoor and outdoor airborne particle concentration measurements over a two-week period at the Royal Children's Hospital PICU in Brisbane, Australia, and we also collected 82 bioaerosol samples to test for the presence of bacterial and viral pathogens. Our results showed that both 24-hour average indoor particle mass (PM10) (0.6–2.2 μg m− 3, median: 0.9 μg m− 3) and submicrometer particle number (PN) (0.1–2.8 × 103 p cm− 3, median: 0.67 × 103 p cm− 3) concentrations were significantly lower (p, Highlights • Little is known about indoor air quality in Paediatric Intensive Care Unit (PICU). • Our study was conducted at the Royal Children's Hospital PICU in Brisbane, Australia. • Indoor, rather than outdoor sources were the main contributors to particles in the PICU. • Nebulization therapy, tracheal suction and cleaning activities were the main sources. • Particles generated at each location could be quickly transported to other locations.

Background The proportion of asthma patients with mild to moderate exacerbations is far greater than the number who experience episodes that are severe enough to require emergency room visits or hospital admission. However the routinely collected data from hospitals is absent in the past. Objective To evaluate associations between short-term exposures to air pollutants and hospital outpatient visits for asthma in China. Methods We obtained data for 143,057 asthma outpatient visits from the largest hospitals in 17 Chinese cities, between Jan 01 2013 and Dec 31 2015. We used daily concentrations of air pollutants measured by the China National Environmental Monitoring Centre. We used a time-stratified case-crossover design, and fitted conditional logistic regression models to determine the associations. Results Particulate matter ≤10μm in diameter (PM10) and nitrogen dioxide (NO2) were associated with increased risks of hospital outpatient visits for asthma on the same day, while the effects were delayed for particulate matter ≤2.5μm in diameter (PM2.5) and sulphur dioxide (SO2). For the cumulative effect model at lag05 days, 10 μg/m3 increase in air pollutants concentrations were correlated with hospital outpatient visits for asthma with odds ratios (ORs) and 95% confidence intervals 1.004 (1.000-1.008) for PM2.5, 1.005 (1.002-1.008) for PM10, 1.030 (1.021-1.040) for NO2, and 1.015 (1.008-1.021) for SO2. Almost one in nine (10.9%; 7.7, 13.9%) hospital outpatient visits for asthma were attributable to NO2. Conclusion Short-term exposures to PM2.5, PM10, NO2 and SO2 were associated with hospital outpatient visits for asthma in China.

Background Epidemiological studies have reported contradictory results regarding the effects of ambient air pollution on Parkinson's disease (PD). This study investigated the associations between long-term exposure to particulate matter Methods We conducted a cross-sectional analysis of long-term exposure to PM2.5 and NO2 concentrations and prevalence of PD using data from around 240,000 cohort members from the 45 and Up Study, NSW. Annual average concentrations of NO2 and PM2.5 were estimated at the participants’ residential address using satellite-based land use regression models. Logistic regression was used to quantify the associations between these pollutants and ever physician-diagnosed PD, after adjusting for a range of individual- and area-level covariates. Results Among the 236,390 participants with complete data, 1,428 (0.6%) reported physician-diagnosed PD. Annual mean PM2.5 and NO2 concentrations for the cohort were 5.8 and 11.9 μg m−3, respectively, and were positively, but not statistically significantly associated with PD. The odds ratio for a 1 μg m−3 increase in PM2.5 was 1.01 (95% confidence interval (CI): 0.98–1.04). The adjusted odds ratio for a 5 μg m−3 increase in NO2 was 1.03 (95% CI: 0.98–1.08). In subgroup analyses, larger associations for NO2 were observed among past smokers (OR 1.11 (95% CI: 1.02–1.20) per 5 μg m−3 increase). Conclusions Overall, we found limited evidence of associations between long-term exposure to NO2 or PM2.5 and PD. The associations observed among past smokers require further corroboration.

Background and Purpose— China bears a heavy burden of stroke because of its large population of elderly people and the propensity for stroke. Previous studies have examined the association between air pollution and stroke mortality or hospital admission. However, the global evidence for adverse effects of air pollution on survival after stroke is scarce. Methods— We used the first national hospital-based prospective registry cohort of stroke in China, which included 12 291 ischemic stroke patients who visited hospitals during 2007 to 2008. All patients were followed for 1-year poststroke. Deaths during the follow-up period were recorded. Participants’ 3-year prestroke exposures to ambient PM 1 , PM 2.5 , PM 10 (particulate matter with aerodynamic diameters ≤1, ≤2.5, and ≤10 μm, respectively) and NO 2 (nitrogen dioxide) were estimated by machine learning algorithms with satellite remote sensing, land use information, and meteorological data. Cox proportional hazards models were used to examine the association between air pollution and survival after ischemic stroke. Results— In total, 1649 deaths were identified during the 1-year follow-up period. After controlling for potential confounders, significant associations were observed between exposure to PM 1 and PM 2.5 and incident fatal ischemic stroke. The corresponding hazard ratios and 95% CIs associated with 10 µg/m 3 increase in PM 1 and PM 2.5 were 1.05 (1.02–1.09) and 1.03 (1.00–1.06), respectively. No significant association was observed for PM 10 or NO 2 (hazard ratios and 95% CIs, 1.01 [1.00–1.03] and 1.03 [0.99–1.06], respectively). Higher hazard ratios (and 95% CIs) were observed for male, elderly and obese individuals. Conclusions— Prestroke exposure to PM 1 and PM 2.5 was associated with increased incident fatal ischemic stroke in the year following an ischemic stroke in China. Improved air quality may be beneficial for people to recover from stroke.

Background: Prenatal exposures to endocrine-disrupting chemicals (EDCs) during critical developmental windows have been implicated in the etiologies of a wide array of adverse perinatal and pediatric outcomes. Epidemiological studies have concentrated on the health effects of individual chemicals, despite the understanding that EDCs act together via common mechanisms, that pregnant women are exposed to multiple EDCs simultaneously, and that substantial toxicological evidence of adverse developmental effects has been documented. There is a move toward multipollutant models in environmental epidemiology; however, there is no current consensus on appropriate statistical methods. Objectives: We aimed to review the statistical methods used in these studies, to identify additional applicable methods, and to determine the strengths and weaknesses of each method for addressing the salient statistical and epidemiological challenges. Methods: We searched Embase, MEDLINE, and Web of Science for epidemiological studies of endocrine-sensitive outcomes in the children of mothers exposed to EDC mixtures during pregnancy and identified alternative statistical methods from the wider literature. Discussion: We identified 74 studies and analyzed the methods used to estimate mixture health effects, identify important mixture components, account for nonmonotonicity in exposure–response relationships, assess interactions, and identify windows of exposure susceptibility. We identified both frequentist and Bayesian methods that are robust to multicollinearity, performing shrinkage, variable selection, dimension reduction, statistical learning, or smoothing, including methods that were not used by the studies included in our review. Conclusions: Compelling motivation exists for analyzing EDCs as mixtures, yet many studies make simplifying assumptions about EDC additivity, relative potency, and linearity, or overlook the potential for bias due to asymmetries in chemical persistence. We discuss the potential impacts of these choices and suggest alternative methods to improve analyses of prenatal exposure to EDC mixtures. https://doi.org/10.1289/EHP2207

Background: It is unknown whether giving birth via caesarean section (c-section) is a modifier for the association between air pollution and asthma. Methods: From 2012 to 2013, 59,754 children between the ages of 2 and 17 were randomly selected from 94 middle schools, elementary schools and kindergartens in seven Chinese cities for a cross-sectional study. The children's parents or guardians completed questionnaires, from which data on asthma as well as asthma-related symptoms were obtained. Participants' exposure to particles with an aerodynamic diameter ≤1·0μm (PM1), ≤2·5μm (PM2·5), and ≤10μm (PM10) and exposure to nitrogen dioxide (NO2) were estimated using random forest models. We used two-level logistic regressions and added an interaction term between mode of delivery and ambient air pollution into the model to estimate effect modification from c-sections after appropriate adjustments for potential confounding variables. Findings: Among children delivered by c-section, the adjusted ORs for asthma and its symptoms per 10 μg/m3 air pollutant increase (1·14 95% CI: 1·09-1·19 to 2·10 95% CI: 1·88-2·34) were significantly higher than those of children delivered vaginally (1·04 95% CI: 0·97-1·13 to 1·38 95%CI: 1·23-1·55). The interactions between c-sections and ambient air pollution were statistically significant for all studied respiratory disorders, except current wheeze. Interpretation: Delivery via c-section appears to increase the risks of air pollution on asthma and its symptoms in our study population of Chinese children. Funding Statement:This work was supported by the National Natural Science Foundation of China (81872582, 91543208, 81872583, 81673128, and 81703179), the National Key Research and Development Program of China (2018YFE0106900), the Guangdong Provincial Natural Science Foundation Team Project (2018B030312005), the Guangdong Province Natural Science Foundation (2017A050501062, and 2018B05052007), and the Fundamental Research Funds for the Central Universities (19ykjc01). Declaration of Interests: The authors declare no competing interest. Ethics Approval Statement: The study was designed and conducted in accordance with the World Medical Association’s Declaration of Helsinki Ethical Principles for Medical Research Involving Human Subjects. The Human Studies Committee of Sun Yat-sen University, Guangzhou, China approved this study. After approval was obtained from each school’s principal, parents or guardians of children were invited to take part in information sessions where consent form was signed and questionnaires were completed

The domestic combustion of polluting fuels is associated with an estimated 3 million premature deaths each year and contributes to climate change. In many low- and middle-income countries (LMICs), valid and representative estimates of people exposed to household air pollution (HAP) are scarce. The Demographic and Health Survey (DHS) is an important and consistent source of data on household fuel use for cooking and has facilitated studies of health effects. However, the body of research based on DHS data has not been systematically identified, nor its strengths and limitations critically assessed as a whole. We aimed to systematically review epidemiological studies using DHS data that considered cooking fuel type as the main exposure, including the assessment of the extent and key drivers of bias. Following PRISMA guidelines, we searched PubMed, Web of Science, Scopus and the DHS publication portal. We assessed the quality and risk of bias (RoB) of studies using a novel tool. Of 2748 records remaining after removing duplicates, 63 were read in full. A total of 45 out of 63 studies were included in our review, spanning 11 different health outcomes and representing 50 unique analyses. In total, 41 of 45 (91%) studies analysed health outcomes in children n = 17), death (all-cause) (n = 14), low birthweight (n = 5), stunting and anaemia (n = 5). Inconsistencies were observed between studies in how cooking fuels were classified into relatively high- and low-polluting. Overall, 36/50 (80%) studies reported statistically significant adverse associations between polluting fuels and health outcomes. In total, 18/50 (36%) of the analyses were scored as having moderate RoB, while 16/50 (32%) analyses were scored as having serious or critical RoB. Although HAP exposure assessment is not the main focus of the DHS, it is the main, often only, source of information in many LMICs. An appreciable proportion of studies using it to analyse the association between cooking fuel use and health have potential for high RoB, mostly related to confounder control, exposure assessment and misclassification, and outcome ascertainment. Based on our findings, we provide some suggestions for ways in which revising the information collected by the DHS could make it even more amenable to studies of household fuel use and health, and reduce the RoB, without being onerous to collect and analyse.

The prevalence of allergic diseases in Australian children is high, but few studies have assessed the potential role of outdoor air pollution in allergic sensitization. We investigated the association between outdoor air pollution and the prevalence of aeroallergen sensitization in a national cross-sectional study of Australian children aged 7–11 years. Children were recruited from 55 participating schools in 12 Australian cities during 2007–2008. Parents completed a detailed (70-item) questionnaire. Outdoor nitrogen dioxide (NO2), as a proxy for exposure to traffic-related emissions, was estimated using measurements from regulatory monitors near each school and a national land-use regression (LUR) model. Three averaging periods were assessed, using information on duration of residence at the address, including lifetime, previous (lifetime, excluding the last year), and recent (the last year only). The LUR model was used as an additional source of recent exposure estimates at school and home addresses. Skin prick tests (SPTs) were performed to measure sensitization to eight common aeroallergens. Multilevel logistic regression estimated the association between NO2 and sensitization (by individual allergens, indoor and outdoor allergens, and all allergens combined), after adjustment for individual- and area-level covariates. In total, 2226 children had a completed questionnaire and SPT. The prevalence of sensitization to any allergen was 44.4%. Sensitization to house dust mites (HDMs) was the most common (36.1%), while sensitization to Aspergillus was the least common (3.4%). Measured mean (±s.d.) NO2 exposure was between 9 (±2.9) ppb and 9.5 (±3.2) ppb, depending on the averaging period. An IQR (4 ppb) increase in measured previous NO2 exposure was associated with greater odds of sensitization to HDMs (OR: 1.21, 95% CI: 1.01–1.43, P = 0.035). We found evidence of an association between relatively low outdoor NO2 concentrations and sensitization to HDMs, but not other aeroallergens, in Australian children aged 7–11 years.