Airborne Nanoparticle Concentrations Are Associated with Increased Mortality Risk in Canada's Two Largest Cities.

RATIONALE: Outdoor fine particulate air pollution (PM2.5) contributes to millions of deaths around the world each year, but much less is known about the long-term health impacts of other particulate air pollutants including ultrafine particles (a.k.a. nanoparticles) which are in the nanometer size range (<100 nm), widespread in urban environments, and not currently regulated. OBJECTIVES: Estimate the associations between long-term exposure to outdoor ultrafine particles and mortality. METHODS: Outdoor air pollution levels were linked to the residential addresses of a large, population-based cohort from 2001 - 2016. Associations between long-term exposure to outdoor ultrafine particles and nonaccidental and cause-specific mortality were estimated using Cox proportional hazards models. MEASUREMENTS: An increase in long-term exposure to outdoor ultrafine particles was associated with an increased risk of nonaccidental mortality (Hazard Ratio = 1. 073, 95% Confidence Interval = 1. 061, 1. 085) and cause-specific mortality, the strongest of which was respiratory mortality (Hazard Ratio = 1.174, 95% Confidence Interval = 1.130, 1.220). MAIN RESULTS: Long-term exposure to outdoor ultrafine particles was associated with increased risk of mortality. We estimated the mortality burden for outdoor ultrafine particles in Montreal and Toronto, Canada to be approximately 1100 additional nonaccidental deaths every year. Furthermore, we observed possible confounding by particle size which suggests that previous studies may have underestimated or missed important health risks associated with ultrafine particles. CONCLUSIONS: As outdoor ultrafine particles are not currently regulated, there is great potential for future regulatory interventions to improve population health by targeting these common outdoor air pollutants.

Long-Term Exposure to Fine Particulate Matter and Incidence of Esophageal Cancer: A Prospective Study of 0.5 Million Chinese Adults.

BACKGROUND & AIMS: Evidence is sparse and inconclusive on the association between long-term fine (≤2.5 µm) particulate matter (PM2.5) exposure and esophageal cancer. We aimed to assess the association of PM2.5 with esophageal cancer risk and compared the esophageal cancer risk attributable to PM2.5 exposure and other established risk factors. METHODS: This study included 510,125 participants without esophageal cancer at baseline from China Kadoorie Biobank. A high-resolution (1 × 1 km) satellite-based model was used to estimate PM2.5 exposure during the study period. Hazard ratios (HR) and 95% CIs of PM2.5 with esophageal cancer incidence were estimated using Cox proportional hazard model. Population attributable fractions for PM2.5 and other established risk factors were estimated. RESULTS: There was a linear concentration-response relationship between long-term PM2.5 exposure and esophageal cancer. For each 10-µg/m3 increase in PM2.5, the HR was 1.16 (95% CI, 1.04-1.30) for esophageal cancer incidence. Compared with the first quarter of PM2.5 exposure, participants in the highest quarter had a 1.32-fold higher risk for esophageal cancer, with an HR of 1.32 (95% CI, 1.01-1.72). The population attributable risk because of annual average PM2.5 concentration ≥35 µg/m3 was 23.3% (95% CI, 6.6%-40.0%), higher than the risks attributable to lifestyle risk factors. CONCLUSIONS: This large prospective cohort study of Chinese adults found that long-term exposure to PM2.5 was associated with an elevated risk of esophageal cancer. With stringent air pollution mitigation measures in China, a large reduction in the esophageal cancer disease burden can be expected.

The role of lifestyle in the association between long-term ambient air pollution exposure and cardiovascular disease: a national cohort study in China.

BACKGROUND: Cardiovascular disease (CVD) caused by air pollution poses a considerable burden on public health. We aim to examine whether lifestyle factors mediate the associations of air pollutant exposure with the risk of CVD and the extent of the interaction between lifestyles and air pollutant exposure regarding CVD outcomes. METHODS: We included 7000 participants in 2011-2012 and followed up until 2018. The lifestyle evaluation consists of six factors as proxies, including blood pressure, blood glucose, blood lipids, body mass index, tobacco exposure, and physical activity, and the participants were categorized into three lifestyle groups according to the number of ideal factors (unfavorable, 0-1; intermediate, 2-4; and favorable, 5-6). Satellite-based spatiotemporal models were used to estimate exposure to ambient air pollutants (including particles with diameters ≤ 1.0 µm [PM1], ≤ 2.5 µm [PM2.5], ≤ 10 µm [PM10], nitrogen dioxide [NO2], and ozone [O3]). Cox regression models were used to examine the associations between air pollutant exposure, lifestyles and the risk of CVD. The mediation and modification effects of lifestyle categories on the association between air pollutant exposure and CVD were analyzed. RESULTS: After adjusting for covariates, per 10 µg/m3 increase in exposure to PM1 (HR: 1.09, 95% CI: 1.05-1.14), PM2.5 (HR: 1.04, 95% CI: 1.00-1.08), PM10 (HR: 1.05, 95% CI: 1.03-1.08), and NO2 (HR: 1.11, 95% CI: 1.05-1.18) was associated with an increased risk of CVD. Adherence to a healthy lifestyle was associated with a reduced risk of CVD compared to an unfavorable lifestyle (HR: 0.65, 95% CI: 0.56-0.76 for intermediate lifestyle and HR: 0.41, 95% CI: 0.32-0.53 for favorable lifestyle). Lifestyle played a significant partial mediating role in the contribution of air pollutant exposure to CVD, with the mediation proportion ranging from 7.4% for PM10 to 14.3% for PM2.5. Compared to an unfavorable lifestyle, the relative excess risk due to interaction for a healthier lifestyle to reduce the effect on CVD risk was - 0.98 (- 1.52 to - 0.44) for PM1, - 0.60 (- 1.05 to - 0.14) for PM2.5, - 1.84 (- 2.59 to - 1.09) for PM10, - 1.44 (- 2.10 to - 0.79) for NO2, and - 0.60 (- 1.08, - 0.12) for O3. CONCLUSIONS: Lifestyle partially mediated the association of air pollution with CVD, and adherence to a healthy lifestyle could protect middle-aged and elderly people from the adverse effects of air pollution regarding CVD.

Impact of Legislation on Brominated Flame Retardant Concentrations in UK Indoor and Outdoor Environments: Evidence for Declining Indoor Emissions of Some Legacy BFRs.

Concentrations of polybrominated diphenyl ethers, hexabromocyclododecane (HBCDD), and novel brominated flame retardants (NBFRs) were measured in indoor dust, indoor air, and outdoor air in Birmingham, UK. Concentrations of ΣBFRs ranged from 490 to 89,000 ng/g, 46-14,000 pg/m3, and 22-11,000 pg/m3, respectively, in UK indoor dust, indoor air, and outdoor air. BDE-209 and decabromodiphenyl ethane (DBDPE) were the main contributors. The maximum concentration of DBDPE (10,000 pg/m3) in outdoor air is the highest reported anywhere to date. In contrast with previous studies of outdoor air in Birmingham, we observed significant correlations between concentrations of tri- to hepta-BDEs and HBCDD and temperature. This may suggest that primary emissions from ongoing use of these BFRs have diminished and that secondary emissions (e.g., evaporation from soil) are now a potentially major source of these BFRs in outdoor air. Conversely, the lack of significant correlations between temperature and concentrations of BDE-209 and DBDPE may indicate that ongoing primary emissions from indoor sources remain important for these BFRs. Further research to clarify the relative importance of primary and secondary sources of BFRs to outdoor air is required. Comparison with earlier studies in Birmingham reveals significant (p < 0.05) declines in concentrations of legacy BFRs, but significant increases for NBFRs over the past decade. While there appear minimal health burdens from BFR exposure for UK adults, dust ingestion of BDE-209 may pose a significant risk for UK toddlers.

Short-Term Increases in NO2 and O3 Concentrations during Pregnancy and Stillbirth Risk in the U.S.: A Time-Stratified Case-Crossover Study.

Associations between gaseous pollutant exposure and stillbirth have focused on exposures averaged over trimesters or gestation. We investigated the association between short-term increases in nitrogen dioxide (NO2) and ozone (O3) concentrations and stillbirth risk among a national sample of 116 788 Medicaid enrollees from 2000 to 2014. A time-stratified case-crossover design was used to estimate distributed (lag 0-lag 6) and cumulative lag effects, which were adjusted for PM2.5 concentration and temperature. Effect modification by race/ethnicity and proximity to hydraulic fracturing (fracking) wells was assessed. Short-term increases in the NO2 and O3 concentrations were not associated with stillbirth in the overall sample. Among American Indian individuals (n = 1694), a 10 ppb increase in NO2 concentrations was associated with increased stillbirth odds at lag 0 (5.66%, 95%CI: [0.57%, 11.01%], p = 0.03) and lag 1 (4.08%, 95%CI: [0.22%, 8.09%], p = 0.04) but not lag 0-6 (7.12%, 95%CI: [-9.83%, 27.27%], p = 0.43). Among participants living in zip codes within 15 km of active fracking wells (n = 9486), a 10 ppb increase in NO2 concentration was associated with increased stillbirth odds in single-day lags (2.42%, 95%CI: [0.37%, 4.52%], p = 0.02 for lag 0 and 1.83%, 95%CI: [0.25%, 3.43%], p = 0.03 for lag 1) but not the cumulative lag (lag 0-6) (4.62%, 95%CI: [-2.75%, 12.55%], p = 0.22). Odds ratios were close to the null in zip codes distant from fracking wells. Future studies should investigate the role of air pollutants emitted from fracking and potential racial disparities in the relationship between short-term increases in NO2 concentrations and stillbirth.

Ambient air pollution and adverse birth outcomes: A review of underlying mechanisms.

Epidemiological data provide varying degrees of evidence for associations between prenatal exposure to ambient air pollutants and adverse birth outcomes (suboptimal measures of fetal growth, preterm birth and stillbirth). To assess further certainty of effects, this review examines the experimental literature base to identify mechanisms by which air pollution (particulate matter, nitrogen dioxide and ozone) could cause adverse effects on the developing fetus. It likely that this environmental insult impacts multiple biological pathways important for sustaining a healthy pregnancy, depending upon the composition of the pollutant mixture and the exposure window owing to changes in physiologic maturity of the placenta, its circulations and the fetus as pregnancy ensues. The current body of evidence indicates that the placenta is a target tissue, impacted by a variety of critical processes including nitrosative/oxidative stress, inflammation, endocrine disruption, epigenetic changes, as well as vascular dysregulation of the maternal-fetal unit. All of the above can disturb placental function and, as a consequence, could contribute to compromised fetal growth as well increasing the risk of stillbirth. Furthermore, given that there is often an increased inflammatory response associated with preterm labour, inflammation is a plausible mechanism mediating the effects of air pollution on premature delivery. In the light of increased urbanisation and an ever-changing climate, both of which increase ambient air pollution and negatively affect vulnerable populations such as pregnant individuals, it is hoped that the collective evidence may contribute to decisions taken to strengthen air quality policies, reductions in exposure to air pollution and subsequent improvements in the health of those not yet born.

Development of an analytical method for the determination of more than 300 pesticides and metabolites in the particulate and gaseous phase of ambient air.

Pesticides can enter the atmosphere during spraying or after application, resulting in environmental or human exposure. The study describes the optimisation and validation of analytical methods for the determination of more than 300 pesticides in the particulate and gaseous phases of the air. Pesticides were sampled with high-volume air samplers on glass-fibre filters (GFFs) and glass columns filled with polyurethane foam (PUF) and XAD-2 resin. Comparing different extraction methods, a QuEChERS extraction with acetonitrile was selected for the GFFs. For the PUF/XAD-2 columns, a cold-column extraction with dichloromethane was used. Instrumental determination was performed using liquid chromatography/electrospray ionisation-time-of-flight mass spectrometry (LC/ESI-QTOF) and gas chromatography/electron impact ionisation-tandem mass spectrometry (GC/EI-MS/MS). Recovery experiments showed recovery rates between 70 and 120% for 263 compounds on the GFFs and 75 compounds on the PUF/XAD-2 columns. Semi-quantitative determination was performed for 39 compounds on the GFFs and 110 compounds on the PUF/XAD-2 columns. Finally, 27 compounds on the GFFs and 138 compounds on the PUF/XAD-2 columns could be determined only qualitatively. For the determination of the PUF/XAD-2 samples, signal suppression (LC) or signal enhancement (GC) due to matrix effects were determined. Method quantification limits of the optimised methods ranged from 30 to 240 pg/m3 for the target compounds on the GFFs, and from 8 to 60 pg/m3 on the PUF/XAD-2 columns. The applicability of the method was demonstrated by means of environmental air samples from an agricultural area in the Netherlands.

Exposure to ambient air toxicants and the risk of amyotrophic lateral sclerosis (ALS): A matched case control study.

BACKGROUND: Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder with few risk factors identified and no known cure. Gene-environment interaction is hypothesized especially for sporadic ALS cases (90-95%) which are of unknown etiology. We aimed to investigate risk factors for ALS including exposure to ambient air toxics. METHODS: This population-based case-control study included 267 ALS cases (from the United States [U.S.] Centers for Disease Control and Prevention/Agency for Toxic Substances and Disease Registry National ALS Registry and Biorepository) and 267 age, sex, and county-matched controls identified via a commercial database. Exposure assessment for 34 ambient air toxicants was performed by assigning census tract-level U.S. Environmental Protection Agency (EPA) 2011 National Air Toxics Assessment (NATA) data to participants' residential ZIP codes. Conditional logistic regression was used to compute adjusted odds ratios (aORs) and 95% confidence intervals (CIs) for individual compounds, chemical classes, and overall exposure. Sensitivity analyses using both conditional logistic regression and Bayesian grouped weighted quartile sum (GWQS) models were performed to assess the integrity of findings. RESULTS: Using the 2011 NATA, the highest exposure quartile (Q4) compared to the lowest (Q1) of vinyl chloride (aOR = 6.00, 95% CI: 1.87-19.25), 2,4-dinitrotoluene (aOR = 5.45, 95% CI: 1.53-19.36), cyanide (aOR = 4.34, 95% CI: 1.52-12.43), cadmium (aOR = 3.30, 95% CI: 1.11-9.77), and carbon disulfide (aOR = 2.98, 95% CI: 1.00-8.91) was associated with increased odds of ALS. Residential air selenium showed an inverse association with ALS (second quartile [Q2] vs. Q1: aOR = 0.38, 95% CI: 0.18-0.79). Additionally, residential exposure to organic/chlorinated solvents (Q4 vs Q1: aOR = 2.62, 95% CI: 1.003-6.85) was associated with ALS. CONCLUSIONS: Our findings using the 2011 NATA linked by census tract to residential area provide evidence of increased ALS risk in cases compared to controls for 2,4-dinitrotoluene, vinyl chloride, cyanide, and the organic/chlorinated solvents class. This underscores the importance of ongoing surveillance of potential exposures for at-risk populations.

Brick kiln pollution and its impact on health: A systematic review and meta-analysis.

Brick kiln emissions adversely affect air pollution and the health of workers and individuals living near the kilns; however, evidence of their impacts remains limited. We conducted a systematic review of brick kiln pollution (emissions, source contributions and personal exposures) and its effects on health. We extracted articles from electronic databases and through manual citation searching. We estimated pooled, sample-size-weighted means and standard deviations for personal exposures by job type; computed mean emission factors and pollutant concentrations by brick kiln design; and meta-analyzed differences in means or proportions for health outcomes between brick kiln workers and controls or for participants living near or far away from kilns. We identified 104 studies; 74 were conducted in South Asia. The most evaluated pollutants were particulate matter (PM; n = 48), sulfur dioxide (SO2; n = 24) and carbon monoxide (CO; n = 22), and the most evaluated health outcomes were respiratory health (n = 34) and musculoskeletal disorders (n = 9). PM and CO emissions were higher among traditional than improved brick kilns. Mean respirable silica exposures were only measured in 4 (4%) studies and were as high as 620 µg/m3, exceeding the NIOSH recommended exposure limit by a factor of over 12. Brick kiln workers had consistently worse lung function, more respiratory symptoms, more musculoskeletal complaints, and more inflammation when compared to unexposed participants across studies; however, most studies had a small sample size and did not fully describe methods used for sampling or data collection. On average, brick kiln workers had worse health outcomes when compared to unexposed controls but study quality supporting the evidence was low. Few studies reported silica concentrations or personal exposures, but the few that did suggest that exposures are high. Further research is needed to better understand the relationship between brick kiln pollution and health among workers, and to evaluate exposure mitigation strategies.

Study of secondary organic aerosol formation and aging using ambient air in an oxidation flow reactor during high pollution events over Delhi.

Secondary aerosols constitute a significant fraction of atmospheric aerosols, yet our understanding of their formation mechanism and fate is very limited. In this work, the secondary organic aerosol (SOA) formation and aging of ambient air of Delhi are studied using a potential aerosol mass (PAM) reactor, an oxidation flow reactor (OFR), coupled with aerosol chemical speciation monitor (ACSM), proton transfer reaction time of flight mass spectrometer (PTR-ToF-MS), and scanning mobility particle sizer with counter (SMPS + C). The setup mimics atmospheric aging of up to several days with the generation of OH radicals. Variations in primary volatile organic compounds (VOCs) and oxygenated volatile organic compounds (OVOCs) as a function of photochemical age were investigated. Primary VOCs such as benzene, toluene, xylene, trimethyl benzene, etc. decrease and OVOCs like formic acid, formaldehyde, acetone, ethanol, etc. increase substantially upon oxidation in OFR. The highest organic aerosol (OA) enhancement was observed for the 4.2 equivalent photochemical days of aging i.e., 1.84 times the ambient concentration, and net OA loss was observed at very high OH exposure, typically after 8.4 days of photochemical aging due to heterogeneous oxidation followed by fragmentation/evaporation. In ambient air, OA enhancement is highest during nighttime due to the high concentrations of precursor VOCs in the atmosphere. SMPS + C results demonstrated substantial new particle formation upon aging and decrement in preexisting aerosol mass. This is the first experimental study conducting an in-situ evaluation of potential SOA mass generated from the ambient aerosols in India.

Impact of Ambient Ultrafine Particles on Cause-Specific Mortality in Three German Cities.

Rationale: Exposure to ambient air pollution has been associated with adverse effects on morbidity and mortality. However, the evidence for ultrafine particles (UFPs; 10-100 nm) based on epidemiological studies remains scarce and inconsistent. Objectives: We examined associations between short-term exposures to UFPs and total particle number concentrations (PNCs; 10-800 nm) and cause-specific mortality in three German cities: Dresden, Leipzig, and Augsburg. Methods: We obtained daily counts of natural, cardiovascular, and respiratory mortality between 2010 and 2017. UFPs and PNCs were measured at six sites, and measurements of fine particulate matter (PM2.5; ⩽2.5 µm in aerodynamic diameter) and nitrogen dioxide were collected from routine monitoring. We applied station-specific confounder-adjusted Poisson regression models. We investigated air pollutant effects at aggregated lags (0-1, 2-4, 5-7, and 0-7 d after UFP exposure) and used a novel multilevel meta-analytical method to pool the results. Additionally, we assessed interdependencies between pollutants using two-pollutant models. Measurements and Main Results: For respiratory mortality, we found a delayed increase in relative risk of 4.46% (95% confidence interval, 1.52 to 7.48%) per 3,223-particles/cm3 increment 5-7 days after UFP exposure. Effects for PNCs showed smaller but comparable estimates consistent with the observation that the smallest UFP fractions showed the largest effects. No clear associations were found for cardiovascular or natural mortality. UFP effects were independent of PM2.5 in two-pollutant models. Conclusions: We found delayed effects for respiratory mortality within 1 week after exposure to UFPs and PNCs but no associations for natural or cardiovascular mortality. This finding adds to the evidence on the independent health effects of UFPs.

Association between ambient air pollution and age-related macular degeneration: a meta-analysis.

BACKGROUND: Several epidemiological studies have investigated the association between ambient air pollution and age-related macular degeneration (AMD). However, a consensus has not yet been reached. Our meta-analysis aimed to clarify this association. METHODS: Databases, including PubMed, EMBASE, and Web of Science, were searched for relevant studies from 01 January 2000 to 30 January 2024. English-language, peer-reviewed studies using cross-sectional, prospective, or retrospective cohorts and case-control studies exploring this relationship were included. Two authors independently extracted data and assessed study quality. A random-effects model was used to calculate pooled covariate-adjusted odds ratios. Heterogeneity across studies was also tested. RESULTS: We identified 358 relevant studies, of which eight were included in the meta-analysis. Four studies evaluated the association between particulate matter less than 2.5 µm in diameter (PM2.5) and AMD, and three studies explored the relationship between nitrogen dioxide (NO2) or ozone (O3) and AMD. The pooled odds ratios were 1.16 (95% confidence interval [CI]: 1.11-1.21), 1.17 (95% CI: 1.09-1.25), and 1.06 (95% CI: 1.05-1.07), respectively. CONCLUSION: Current evidence suggests a concomitant positive but not causal relationship between PM2.5, NO2, or O3 and AMD risk.

Association of ambient air pollution with hemoglobin levels and anemia in the general population of Korean adults.

BACKGROUND: Emerging evidence has suggested significant associations between ambient air pollution and changes in hemoglobin levels or anemia in specific vulnerable groups, but few studies have assessed this relationship in the general population. This study aimed to evaluate the association between long-term exposure to air pollution and hemoglobin concentrations or anemia in general adults in South Korea. METHODS: A total of 69,830 Korean adults from a large-scale nationwide survey were selected for our final analysis. Air pollutants included particulate matter with an aerodynamic diameter less than or equal to 10 micrometers (PM10), particulate matter with an aerodynamic diameter less than or equal to 2.5 micrometers, nitrogen dioxide, sulfur dioxide (SO2), and carbon monoxide (CO). We measured the serum hemoglobin concentration to assess anemia for each participant. RESULTS: In the fully adjusted model, exposure levels to PM10, SO2, and CO for one and two years were significantly associated with decreased hemoglobin concentrations (all p < 0.05), with effects ranging from 0.15 to 0.62% per increase in interquartile range (IQR) for each air pollutant. We also showed a significant association of annual exposure to PM10 with anemia (p = 0.0426); the odds ratio (OR) [95% confidence interval (CI)] for anemia per each increase in IQR in PM10 was estimated to be 1.039 (1.001-1.079). This association was also found in the 2-year duration of exposure (OR = 1.046; 95% CI = 1.009-1.083; adjusted Model 2). In addition, CO exposure during two years was closely related to anemia (OR = 1.046; 95% CI = 1.004-1.091; adjusted Model 2). CONCLUSIONS: This study provides the first evidence that long-term exposure to air pollution, especially PM10, is significantly associated with reduced hemoglobin levels and anemia in the general adult population.

Smoke exposure, hemoglobin levels and the prevalence of anemia: a cross-sectional study in urban informal settlement in Southern Ghana.

BACKGROUND: In sub-Saharan African cities, more than half of the population lives in informal settlements. These settlements are close to smoky dumpsites, industrial plants, and polluted roads. Furthermore, polluting fuels remain their primary sources of energy for cooking and heating. Despite evidence linking smoke and its components to anaemia, none of these studies were conducted on populations living in urban informal settlements. This study investigated the risks of anemia/mean Haemoglobin (HB) levels in an informal settlement in Accra, Ghana. Exposure to smoke was examined across various sources, encompassing residences, neighborhoods, and workplaces. METHODS: The study was a facility-based cross-sectional design among residents at Chorkor, an informal settlement in the Greater Accra region of Ghana. A questionnaire was administered at a community hospital during an interview to gather data on sources of smoke exposure in the household, in the neighbourhood, and in the workplace. A phlebotomist collected blood samples from the participants after the interview to assess their anaemia status. RESULTS: The population (n = 320) had a high prevalence of anemia, with 49.1% of people fitting the WHO's definition of anemia, while the average HB level was 12.6 ± 2.1 g/dL. Anemia was associated with the number of different types of waste burnt simultaneously [(1 or 2: prevalence ratio (PR): 95% confidence interval (CI), 1.14, 0.99-1.28: 3+: 1.16, 1.01-1.63, p-for-trend = 0.0082)], fuel stacking [(mixed stacking: 1.27, 1.07-1.20: dirty stacking:1.65, 1.19-2.25, p-for-trend = 0.0062)], and involvement in fish smoking (1.22, 0.99-1.06). However, the lower limit of the CIs for number of different forms of garbage burned simultaneously and engagement in fish smoking included unity. Reduced mean HB levels were associated with the number of different types of waste burnt simultaneously [(1 or 2: regression coefficient (ß): 95% confidence interval (CI), -0.01, -0.97- -0.99: 3+: -0.14, -0.77- -0.05)], current smoker [(yes, almost daily: -1.40, -2.01- -0.79: yes, at least once a month: -1.14, -1.79- -0.48)], Second-Hand-Smoking (SHS) (yes, almost daily: -0.77, -1.30- -0.21), fuel stacking [(mixed stacking-0.93, -1.33-0.21: dirty stacking-1.04, -1.60- -0.48)], any smoke exposure indicator in the neighbourhood (-0.84, -1.43- -0.25), living close to a major road (-0.62, -1.09- -0.49), and fish smoking (-0.41,-0.93- -0.12). CONCLUSION: Although the cross-sectional design precludes causality, smoke exposure was associated with mean HB levels and anaemia among populations living in informal settlements.

Association between short-term exposure to ambient air pollutants and the risk of hospital visits for acute upper respiratory tract infections among adults: a time-series study in Ningbo, China.

OBJECTIVES: Acute upper respiratory tract infections (AURTIs) are prevalent in the general population. However, studies on the association of short-term exposure to air pollution with the risk of hospital visits for AURTIs in adults are limited. This study aimed to explore the short-term exposure to air pollutants among Chinese adults living in Ningbo. METHODS: Quasi-Poisson time serious regressions with distributed lag non-linear models (DLNM) were applied to explore the association between ambient air pollution and AURTIs cases. Patients ≥ 18 years who visit three hospitals, being representative for urban, urban-rural junction and rural were included in this retrospective study. RESULTS: In total, 104,441 cases with AURTIs were enrolled in hospital during 2015-2019. The main results showed that particulate matter with an aerodynamic diameter less than 2.5 µm (PM2.5), nitrogen dioxide (NO2) and nitrogen dioxide (SO2), were positively associated to hospital visits for AURTIs, except for nitrogen dioxide (O3), which was not statistically significant. The largest single-lag effect for PM2.5 at lag 8 days (RR = 1.02, 95%CI: 1.08-1.40), for NO2 at lag 13 days (RR = 1.03, 95%CI: 1.00-1.06) and for SO2 at lag 5 days (RR = 1.27, 95%CI: 1.08-1.48), respectively. In the stratified analysis, females, and young adults (18-60 years) were more vulnerable to PM2.5 and SO2 and the effect was greater in rural areas and urban-rural junction. CONCLUSIONS: Exposure to ambient air pollution was significantly associated with hospital visits for AURTIs. This study provides epidemiological evidence for policymakers to control better air quality and establish an enhanced system of air pollution alerts.

Associations between maternal exposure to air pollution during pregnancy and trajectories of infant growth: A birth cohort study.

OBJECTIVE: We examined the relationships between infants' growth trajectories and prenatal exposure to air pollution, which is still under-investigated. METHODS: A birth cohort study was constructed using medical records of pregnant women and infants born between 2015 and 2019 in Foshan, China. Using satellite-based spatial-temporal models, prenatal exposure to air pollutants including particulate matter with an aerodynamic dimension of < 2.5 µm (PM2.5), sulfur dioxide (SO2), nitrogen dioxide (NO2), and ozone (O3) was assessed at each woman's residence. Latent class growth modeling was used to identify trajectories of physical (body length and weight) growth and neurodevelopment, which were repeatedly measured within 1 year after birth. Logistic regression models were used to investigate the associations between prenatal exposure to air pollution and the risks of growth disorders, adjusting for an array of potential confounders. RESULTS: We identified two growth trajectories for body length [normal: 3829 (93%); retardation: 288 (7%)], three for weight [normal: 2475 (59.6%); retardation: 390 (9.4%); overgrowth: 1287 (31%)], and two for neurodevelopment [normal: 956 (66.1%); retardation: 491 (33.9%)]. For exposure over whole pregnancy, SO2 was associated with an increased risk of body length retardation (OR for per 1 µg/m3 increment: 1.09, 95%CI: 1.01-1.17); PM2.5 (OR: 1.05, 95%CI: 1.03-1.07), SO2 (OR: 1.15, 95%CI: 1.08-1.22), and NO2 (OR: 1.05, 95%CI: 1.03-1.07) were positively associated with neurodevelopmental retardation. Such associations appeared stronger for exposures over the first and second trimesters. No significant associations were detected for weight growth. CONCLUSIONS: Maternal exposure to air pollution during pregnancy was associated with higher risks of impairments in both physical growth, particularly body length, and neurodevelopment.

Association between short-term exposure to ambient air pollution and upper respiratory tract infection in Kunshan.

The health effects of air pollution have become a major public health problem. Studies on the relationship between short-term exposure to air pollutants and upper respiratory tract infection (URTI) related clinic visits and expenditures were scarce. From January 1, 2019, to December 31, 2021, we included all the URTI cases that turned to 11 public hospitals in Kunshan, and summarized individual medical cost. Daily meteorological factors and 24-h mean concentrations of four common air pollutants, including particulate matter with an aerodynamic diameter less than 2.5 µm (PM2.5) and 10 µm (PM10), sulfur dioxide (SO2), and nitrogen dioxide (NO2), were consecutively recorded. Generalized additive regression model was adopted to quantify the associations between each air pollutant and the daily clinic visits of URTI cases. We further calculated attributable number (AN) and attributable fraction, and performed sensitivity analysis by gender, age, and season. A total of 934,180 cases were retrieved during the study period. PM2.5, PM10, SO2, and NO2 showed significant associations with hospital visits and expenditures due to URTI. Relative risks for them were 1.065 (95% confidence interval [CI] 1.055, 1.076), 1.045 (95% CI 1.037, 1.052), 1.098 (95% CI 1.038, 1.163), and 1.098 (95% CI 1.085, 1.111) on lag 0-5 days, respectively. Thirty-one thousand four hundred fifty-five (95% CI 27,457, 35,436) cases could be ascribed to increased NO2 and accounted for 3.37% (95% CI 2.94%, 3.79%) of all clinic visits. Sensitivity analyses indicated that the effects of air pollution were generally consistent for male and female. PM2.5, PM10, and NO2 had stronger associations among people aged ≤ 18 years, followed by those aged 19-64 years and ≥ 65 years. The association strengths of air pollution varied seasonally. Short-term exposure to ambient air pollutants had significant associations with clinic visits and expenditures owing to URTI. Children and adolescents appeared to be more susceptible to adverse health effects of air pollution. NO2 may be a priority when formulating pollution control measures.

Assessment of phytodiversity and phytoremediation potential of plants in the vicinity of a thermal power plant.

A study was carried out to evaluate phytodiversity along with the metal accumulation potential of native plants growing in the vicinity of a thermal power plant (TPP). We documented 26 tree species, six shrubs, and 35 herbs. Importance value index (IVI), which measures the extent to which a species dominates in an area, was found highest for Senna siamea (95.7) followed by Tectona grandis (56.5), and Pithecellobium dulce (19.6). Soil was acidic (pH 5.4) in nature with higher concentrations of Al and Fe. The pH of ground water was found acidic while pH of nearby river was found slightly alkaline. Values of PM2.5 and PM10 were slightly higher than NAAQS standards for industrial areas. The concentration of metals was found higher in aquatic plants than in terrestrial plants. In general, herbs and shrubs showed more metal accumulation potential than trees. Our results suggest that Senna siamea could be used for revegetation purposes in FA landfills. Further, terrestrial and aquatic plants such as Ageratina adenophora and Stuckenia pectinata could be used for reclamation of Mn, Zn, Al, and Fe from contaminated soils. Hydrilla verticillata (Ni and Mn), Nelumbo nucifera, and Ipomoea aquatica (Cr) can be used for metal removal from contaminated water.

The study focuses on the assessment of phytodiversity, soil and water analysis, ambient air quality, and bioaccumulation of heavy metals in plants growing in and around a thermal power plant. The study assumes significance as more than 65% of India's electricity generation is still by coal-fired power plants, having major implications for air, soil, and water pollution. By selecting native plant species adapted to the region, we can enhance biodiversity, restore habitats, and contribute to the overall ecological health of the area surrounding the power plant.

Pathogen Detection via Impedance Spectroscopy-Based Biosensor.

This paper presents the development of a miniaturized sensor device for selective detection of pathogens, specifically Influenza A Influenza virus, as an enveloped virus is relatively vulnerable to damaging environmental impacts. In consideration of environmental factors such as humidity and temperature, this particular pathogen proves to be an ideal choice for our study. It falls into the category of pathogens that pose greater challenges due to their susceptibility. An impedance biosensor was integrated into an existing platform and effectively separated and detected high concentrations of airborne pathogens. Bio-functionalized hydrogel-based detectors were utilized to analyze virus-containing particles. The sensor device demonstrated high sensitivity and specificity when exposed to varying concentrations of Influenza A virus ranging from 0.5 to 50 µg/mL. The sensitivity of the device for a 0.5 µg/mL analyte concentration was measured to be 695 Ω· mL/µg. Integration of this pathogen detector into a compact-design air quality monitoring device could foster the advancement of personal exposure monitoring applications. The proposed sensor device offers a promising approach for real-time pathogen detection in complex environmental settings.

Lifetime losses due to cardiovascular and respiratory diseases attributable to air pollution in polluted and unpolluted areas.

The article assesses differences in lifetime losses caused by premature deaths from cardiopulmonary disease in populations living in areas with different environmental burdens. The results provide different perspectives on data on total years lost and lifetime losses attributable to air pollution. Such lifetime losses in the industrial area related to cardiovascular causes of death are 7.6 or 5.1 years per male or female deceased, representing an average lifetime loss of 0.01907 years (i.e. 7 days) per 1 male or 0.01273 years (i.e. 4.6 days) per 1 female in the entire population. Losses related to cerebrovascular or respiratory causes of death are about 5.4 or 5.9 years per 1 deceased male or 3.9 or 5 years per 1 deceased female, respectively, which represents a loss of 0.00481 (1.8 days), or 0.00148 years (0.5 days) per 1 male or 0.00466 (1.7 days), or 0.00058 years (0.2 days) per 1 female.