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\"The WHO Handbook on Indoor Radon\" is a key product of the WHO International Radon Project, which was launched in 2005. The \"Handbook\" focuses on residential radon exposure from a public health point of view and provides detailed recommendations on reducing health risks from radon and sound policy options for preventing and mitigating radon exposure. The material in the \"Handbook\" reflects the epidemiological evidence that indoor radon exposure is responsible for a substantial number of lung cancers in the general population. The material is organized into six chapters, each introduced by key messages. Usually, technical terms are defined the first time they are used, and a glossary is also included. Information is provided on the selection of devices to measure radon levels and on procedures for the reliable measurement of these levels. Discussed also are control options for radon in new dwellings, radon reduction in existing dwellings as well as assessment of the costs and benefits of different radon prevention and remedial actions. Also covered are radon risk communication strategies and organization of national radon programs.This publication is intended for countries planning to develop their national radon programs or extend such activities, as well as for stakeholders involved in radon control such as the construction industry and building professionals.The overall goal of this \"Handbook\" is to provide an up-to-date overview of the major aspects of radon and health. It does not aim to replace existing radiation protection standards, rather it emphasizes issues relevant to the comprehensive planning, implementation and evaluation of national radon programs.

AbstractObjectiveTo assess risks and costs of hospital admission associated with short term exposure to fine particulate matter with diameter less than 2.5 µm (PM2.5) for 214 mutually exclusive disease groups.DesignTime stratified, case crossover analyses with conditional logistic regressions adjusted for non-linear confounding effects of meteorological variables.SettingMedicare inpatient hospital claims in the United States, 2000-12 (n=95 277 169).ParticipantsAll Medicare fee-for-service beneficiaries aged 65 or older admitted to hospital.Main outcome measuresRisk of hospital admission, number of admissions, days in hospital, inpatient and post-acute care costs, and value of statistical life (that is, the economic value used to measure the cost of avoiding a death) due to the lives lost at discharge for 214 disease groups.ResultsPositive associations between short term exposure to PM2.5 and risk of hospital admission were found for several prevalent but rarely studied diseases, such as septicemia, fluid and electrolyte disorders, and acute and unspecified renal failure. Positive associations were also found between risk of hospital admission and cardiovascular and respiratory diseases, Parkinson’s disease, diabetes, phlebitis, thrombophlebitis, and thromboembolism, confirming previously published results. These associations remained consistent when restricted to days with a daily PM2.5 concentration below the WHO air quality guideline for the 24 hour average exposure to PM2.5. For the rarely studied diseases, each 1 µg/m3 increase in short term PM2.5 was associated with an annual increase of 2050 hospital admissions (95% confidence interval 1914 to 2187 admissions), 12 216 days in hospital (11 358 to 13 075), US$31m (£24m, €28m; $29m to $34m) in inpatient and post-acute care costs, and $2.5bn ($2.0bn to $2.9bn) in value of statistical life. For diseases with a previously known association, each 1 µg/m3 increase in short term exposure to PM2.5 was associated with an annual increase of 3642 hospital admissions (3434 to 3851), 20 098 days in hospital (18 950 to 21 247), $69m ($65m to $73m) in inpatient and post-acute care costs, and $4.1bn ($3.5bn to $4.7bn) in value of statistical life.ConclusionsNew causes and previously identified causes of hospital admission associated with short term exposure to PM2.5 were found. These associations remained even at a daily PM2.5 concentration below the WHO 24 hour guideline. Substantial economic costs were linked to a small increase in short term PM2.5.

Researchers must find the particles that are most dangerous to health in each place so policies can reduce levels of those pollutants first, urge Xiangdong Li and colleagues. Researchers must find the particles that are most dangerous to health in each place so policies can reduce levels of those pollutants first, urge Xiangdong Li and colleagues. Photographers take photos on the roof of a building in heavy smog in Zhengzhou, China

ObjectiveThe association between exposure to ambient particles with a median aerodynamic diameter less than 10/2.5 µm (particulate matter, PM10/2.5) and COPD remains unclear. Our study objective was to examine the association between ambient PM10/2.5 concentrations and lung functions in adults.MethodsA cross-sectional study was conducted in southern China. Seven clusters were randomly selected from four cities across Guangdong province. Residents aged ≥20 years in the participating clusters were randomly recruited; all eligible participants were examined with a standardised questionnaire and spirometry. COPD was defined as a post-bronchodilator FEV1/FVC less than 70%. Atmosphere PM sampling was conducted across the clusters along with our survey.ResultsOf the subjects initially recruited, 84.4% (n=5993) were included for analysis. COPD prevalence and atmosphere PM concentration varied significantly among the seven clusters. COPD prevalence was significantly associated with elevated PM concentration levels: adjusted OR 2.416 (95% CI 1.417 to 4.118) for >35 and ≤75 µg/m3 and 2.530 (1.280 to 5.001) for >75 µg/m3 compared with the level of ≤35 µg/m3 for PM2.5; adjusted OR 2.442 (95% CI 1.449 to 4.117) for >50 and ≤150 µg/m3 compared with the level of ≤50 µg/m3 for PM1. A 10 µg/m3 increase in PM2.5 concentrations was associated with a 26 mL (95% CI −43 to −9) decrease in FEV1, a 28 mL (−49 to −8) decrease in FVC and a 0.09% decrease (−0.170 to −0.010) in FEV1/FVC ratio. The associations of COPD with PM10 were consistent with PM2.5 but slightly weaker.ConclusionsExposure to higher PM concentrations was strongly associated with increased COPD prevalence and declined respiratory function.Trial registration number ChiCTR-OO-14004264; Post-results.

Commercial chemicals are used extensively across urban centres worldwide 1 , posing a potential exposure risk to 4.2 billion people 2 . Harmful chemicals are often assessed on the basis of their environmental persistence, accumulation in biological organisms and toxic properties, under international and national initiatives such as the Stockholm Convention 3 . However, existing regulatory frameworks rely largely upon knowledge of the properties of the parent chemicals, with minimal consideration given to the products of their transformation in the atmosphere. This is mainly due to a dearth of experimental data, as identifying transformation products in complex mixtures of airborne chemicals is an immense analytical challenge 4 . Here we develop a new framework—combining laboratory and field experiments, advanced techniques for screening suspect chemicals, and in silico modelling—to assess the risks of airborne chemicals, while accounting for atmospheric chemical reactions. By applying this framework to organophosphate flame retardants, as representative chemicals of emerging concern 5 , we find that their transformation products are globally distributed across 18 megacities, representing a previously unrecognized exposure risk for the world’s urban populations. More importantly, individual transformation products can be more toxic and up to an order-of-magnitude more persistent than the parent chemicals, such that the overall risks associated with the mixture of transformation products are also higher than those of the parent flame retardants. Together our results highlight the need to consider atmospheric transformations when assessing the risks of commercial chemicals. A new framework is proposed for assessing the risks of the atmospheric transformation products of commercial chemicals, combining laboratory and field experiments, advanced techniques for screening suspect chemicals, and in silico modelling.

Regulatory oversight of toxic emissions from industrial plants and understanding about these emissions ' impacts are in their infancy. Applying a research design based on the openings and closings of 1,600 industrial plants to rich data on housing markets and infant health, we find that: toxic air emissions affect air quality only within 1 mile of the plant; plant openings lead to 11 percent declines in housing values within 0.5 mile or a loss of about $ 4.25 million for these households; and a plant's operation is associated with a roughly 3 percent increase in the probability of low birthweight within 1 mile.

IntroductionElevated particulate matter (PM) concentrations of anthropogenic and/or desert dust origin are associated with increased morbidity among children with asthma.ObjectiveThe Mitigating the Health Effects of Desert Dust Storms Using Exposure-Reduction Approaches randomised controlled trial assessed the impact of exposure reduction recommendations, including indoor air filtration, on childhood asthma control during high desert dust storms (DDS) season in Cyprus and Greece.Design, participants, interventions and settingPrimary school children with asthma were randomised into three parallel groups: (a) no intervention (controls); (b) outdoor intervention (early alerts notifications, recommendations to stay indoors and limit outdoor physical activity during DDS) and (c) combined intervention (same as (b) combined with indoor air purification with high efficiency particulate air filters in children’s homes and school classrooms. Asthma symptom control was assessed using the childhood Asthma Control Test (c-ACT), spirometry (forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC)) and fractional exhaled nitric oxide (FeNO).ResultsIn total, 182 children with asthma (age; mean=9.5, SD=1.63) were evaluated during 2019 and 2021. After three follow-up months, the combined intervention group demonstrated a significant improvement in c-ACT in comparison to controls (β=2.63, 95% CI 0.72 to 4.54, p=0.007), which was more profound among atopic children (β=3.56, 95% CI 0.04 to 7.07, p=0.047). Similarly, FEV1% predicted (β=4.26, 95% CI 0.54 to 7.99, p=0.025), the need for any asthma medication and unscheduled clinician visits, but not FVC% and FeNO, were significantly improved in the combined intervention compared with controls.ConclusionRecommendations to reduce exposure and use of indoor air filtration in areas with high PM pollution may improve symptom control and lung function in children with asthma.Trial registration number NCT03503812.

If implemented properly, China's air-quality standard would have far-reaching benefits: as well as protecting human health, it would reduce air and mercury pollution in the Northern Hemisphere and slow global warming. To meet the ambitious air-quality limits, China will have to overcome two major hurdles: its relentless increase in fossil-fuel use, which quickly wipes out any efforts to reduce emissions, and its decentralized system of environmental enforcement, which gives undue influence to local officials who favour economic development.

Exposure to traffic-related air pollution (TRAP) has been associated with increased risks of respiratory diseases, but the biological mechanisms are not yet fully elucidated. Our aim was to evaluate the respiratory responses and explore potential biological mechanisms of TRAP exposure in a randomized crossover trial. We conducted a randomized crossover trial in 56 healthy adults. Each participant was exposed to high- and low-TRAP exposure sessions by walking in a park and down a road with high traffic volume for 4 h in random order. Respiratory symptoms and lung function, including forced expiratory volume in the first second ( ), forced vital capacity (FVC), the ratio of to FVC, and maximal mid-expiratory flow (MMEF), were measured before and after each exposure session. Markers of 8-isoprostane, tumor necrosis ( ), and ezrin in exhaled breath condensate (EBC), and surfactant proteins D (SP-D) in serum were also measured. We used linear mixed-effects models to estimate the associations, adjusted for age, sex, body mass index, meteorological condition, and batch (only for biomarkers). Liquid chromatography-mass spectrometry was used to profile the EBC metabolome. Untargeted metabolome-wide association study (MWAS) analysis and pathway enrichment analysis using mummichog were performed to identify critical metabolomic features and pathways associated with TRAP exposure. Participants had two to three times higher exposure to traffic-related air pollutants except for fine particulate matter while walking along the road compared with in the park. Compared with the low-TRAP exposure at the park, high-TRAP exposure at the road was associated with a higher score of respiratory symptoms [2.615 (95% CI: 0.605, 4.626), ] and relatively lower lung function indicators [ (95% CI: , ), ] for and (95% CI: , ; ) for MMEF]. Exposure to TRAP was significantly associated with changes in some, but not all, biomarkers, particularly with a (95% CI: 0.297, 0.691; ) increase for serum SP-D and a (95% CI: , ; ) decrease for EBC ezrin. Untargeted MWAS analysis revealed that elevated TRAP exposure was significantly associated with perturbations in 23 and 32 metabolic pathways under positive- and negative-ion modes, respectively. These pathways were most related to inflammatory response, oxidative stress, and energy use metabolism. This study suggests that TRAP exposure might lead to lung function impairment and respiratory symptoms. Possible underlying mechanisms include lung epithelial injury, inflammation, oxidative stress, and energy metabolism disorders. https://doi.org/10.1289/EHP11139.

AbstractObjectiveTo investigate potential interactive effects of fine particulate matter (PM2.5) and ozone (O3) on daily mortality at global level.DesignTwo stage time series analysis.Setting372 cities across 19 countries and regions.PopulationDaily counts of deaths from all causes, cardiovascular disease, and respiratory disease.Main outcome measureDaily mortality data during 1994-2020. Stratified analyses by co-pollutant exposures and synergy index (>1 denotes the combined effect of pollutants is greater than individual effects) were applied to explore the interaction between PM2.5 and O3 in association with mortality.ResultsDuring the study period across the 372 cities, 19.3 million deaths were attributable to all causes, 5.3 million to cardiovascular disease, and 1.9 million to respiratory disease. The risk of total mortality for a 10 μg/m3 increment in PM2.5 (lag 0-1 days) ranged from 0.47% (95% confidence interval 0.26% to 0.67%) to 1.25% (1.02% to 1.48%) from the lowest to highest fourths of O3 concentration; and for a 10 μg/m3 increase in O3 ranged from 0.04% (−0.09% to 0.16%) to 0.29% (0.18% to 0.39%) from the lowest to highest fourths of PM2.5 concentration, with significant differences between strata (P for interaction <0.001). A significant synergistic interaction was also identified between PM2.5 and O3 for total mortality, with a synergy index of 1.93 (95% confidence interval 1.47 to 3.34). Subgroup analyses showed that interactions between PM2.5 and O3 on all three mortality endpoints were more prominent in high latitude regions and during cold seasons.ConclusionThe findings of this study suggest a synergistic effect of PM2.5 and O3 on total, cardiovascular, and respiratory mortality, indicating the benefit of coordinated control strategies for both pollutants.