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.

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.

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.

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.

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 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.

Ambient air pollution, low-grade inflammation, and lung function: Evidences from the UK Biobank.

The associations of ambient air pollution exposure and low-grade inflammation with lung function remain uncertain. In this study, 276,289 subjects were enrolled in the UK Biobank. Individual exposure to ambient air pollution (including nitrogen dioxide [NO2], nitrogen oxides [NOx]), and particulate matter [PM2.5, PM10, PMcoarse]) were estimated by using the land-use regression model. Forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV1) were tested, and low-grade inflammation score (INFLA score) was calculated for each subject. In this cross-sectional study, the median concentrations of air pollution were 9.89 µg/m3 for PM2.5, 15.98 µg/m3 for PM10, 6.09 µg/m3 for PMcoarse, 25.60 µg/m3 for NO2, and 41.46 µg/m3 for NOx, respectively. We observed that PM2.5, PM10, PMcoarse, NO2, NOx was negatively associated with lung function. Besides, significant positive associations between PM exposure and low-grade inflammation were noted. Per interquartile range (IQR) increase in PM2.5, PM10, and PMcoarse was related to higher INFLA score, and the ß (95 % CI) was 0.06 (0.03, 0.08), 0.03 (0.02, 0.05), and 0.03 (0.01, 0.04), respectively. Additionally, we found significant negative associations between INFLA scores and lung function. One-unit increase in INFLA score was linked with 12.41- and 11.31-ml decreases in FVC and FEV1, respectively. Compared with individuals with low air pollution exposure and low INFLA scores, participants with high air pollution and high INFLA scores had the lowest FVC and FEV1. Additionally, we observed that INFLA scores could modify the relationships of PM2.5, NO2, and NOx with FVC and FEV1 (Pinteraction <0.05). The negative impact of air pollutants on lung function was more pronounced in subjects with high INFLA scores in comparison to those with low INFLA scores. In conclusion, we demonstrated negative associations between ambient air pollution and lung function, and the observed associations were strengthened and modified by low-grade inflammation.

Ambient air pollution and risk of allergic respiratory diseases in European and East Asian populations: A Mendelian randomization study.

BACKGROUND: Ambient air pollution has become a challenging global health issue since industrialization, especially affecting respiratory diseases. However, the causal link between air pollution and allergic respiratory diseases (ARDs) remains unclear due to confounding factors in conventional epidemiological studies across different populations. Thus, we aimed to clarify the causal associations between air pollution and ARDs in European and East Asian populations using Mendelian randomization (MR). METHODS: MR utilizes genetic variants and provides a satisfactory level of causal evidence. Genetic data for exposures (PM2.5, PM2.5 absorbance, PM10, PMcoarse, NO2 and NOx) and outcomes (allergic rhinitis, chronic rhinosinusitis, asthma, and obesity related asthma) were obtained from genome-wide association studies. Instrumental variables were strictly filtered based on core assumptions. Two-sample MR and sensitivity analyses were conducted separately for European and East Asian populations. RESULTS: PMcoarse was causally associated with an increased risk of chronic rhinosinusitis (OR = 1.588 [1.002-2.518]; p = 0.049) and obesity related asthma (OR = 1.956 [1.012-3.780]; p = 0.046) in European population, and PM10 was associated with a decreased risk of allergic rhinitis in East Asian population (OR = 0.882 [0.798-0.974]; p = 0.013). No heterogeneity or pleiotropy was detected in any significant causal association. CONCLUSION: Our findings indicate that ambient air pollution has opposite impacts on the etiology of ARDs in European and East Asian populations, which provides evidence for decisions on public policies and suggests that different responses to environmental factors such as air pollution may contribute to racial heterogeneity of ARDs.

Short-term exposure to sulfur dioxide and the occurrence of chronic obstructive pulmonary disease: An updated systematic review and meta-analysis based on risk of bias and certainty of evidence.

Several studies have documented a relationship between short-term exposure to atmospheric sulfur dioxide (SO2) and chronic obstructive pulmonary disease (COPD). However, findings vary across different regions. This meta-analysis employed a random-effects model to calculate the combined risk estimate for each 10-µg/m3 increase in ambient SO2 concentration. Subgroup analysis aimed to identify sources of heterogeneity. To assess potential bias, studies were evaluated using a domain-based assessment tool developed by the World Health Organization. Sensitivity analyses, based on bias risk, explored how model assumptions influenced associations. An evidence certainty framework was used to evaluate overall evidence quality. The study protocol was registered with PROSPERO (CRD42023446823). We thoroughly reviewed 191 full-text articles, ultimately including 15 in the meta-analysis. The pooled relative risk for COPD was 1.26 (95 % CI 0.94-1.70) per 10-µg/m3 increase in ambient SO2. Eleven studies were deemed high risk due to inadequate handling of missing data. Overall evidence certainty was rated as medium. Given SO2's significant public health implications, continuous monitoring is crucial. Future research should include countries in Africa and Oceania to enhance global understanding of atmospheric SO2-related health issues.

Causal relationships between genetically predicted particulate air pollutants and neurodegenerative diseases: A two-sample Mendelian randomization study.

Accumulating observational studies have linked particulate air pollutants to neurodegenerative diseases (NDDs). However, the causal links and the direction of their associations remain unclear. Therefore, we adopted a two-sample Mendelian randomization (TSMR) design using the GWAS-based genetic instruments of particulate air pollutants (PM2.5 and PM10) from the UK Biobank to explore their causal influence on four common neurodegenerative diseases. Estimates of causative relationships were generated by the Inverse variance weighted (IVW) method with multiple sensitive analyses. The heterogeneity and pleiotropy tests were additionally performed to verify whether our findings were robust. Genetically predicted PM2.5 and PM10 could elevate the occurrence of AD (odds ratio [OR] = 2.22, 95 % confidence interval [CI] 1.53-3.22, PIVW = 2.85×10-5, PFalsediscovery rate[FDR]= 2.85×10-4 and OR = 2.41, 95 % CI: 1.26-4.60, PIVW = 0.008, PFDR=0.039, respectively). The results were robust in sensitive analysis. However, no evidence of causality was found for other NDDs. Our present study suggests that PM2.5 and PM10 have a detrimental effect on AD, which indicates that improving air quality to prevent AD may have pivotal public health implications.

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.

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.

Exposure to air pollution as a risk factor for anaemia: a global scoping review.

Anaemia is an important global health issue with various factors responsible for its occurrence. Though nutritional deficiency is one of the main causes of the disease, evidence suggests a potential link between long-term exposure to ambient air pollution and an increased risk of developing anaemia. Our scoping review evaluates studies conducted across the world to examine possible associations between anaemia and ambient air pollution. Six databases were searched, 153 sources were identified, and 21 articles were included in the review. Apart from one article which showed no significant effect, studies reported positive associations between anaemia and air pollution. This was true for both indoor and outdoor air pollution, various types of particulate matter exposure, and across demographic groups. The review highlights the importance of recognizing exposure to air pollution as a potential risk factor for anaemia and emphasizes the imperative for focused interventions and policy measures to mitigate air pollution.

Ambient PM2.5 components and prevalence of chronic kidney disease: a nationwide cross-sectional survey in China.

OBJECTIVES: Chronic kidney disease (CKD) is a global public health concern, and accumulating evidence has indicated that air pollution increases the odds of CKD. However, a limited number of studies have examined the long-term effects of ambient fine particulate matter (PM2.5) components on the risk of CKD among general population; thus, major knowledge gaps remain. METHODS: Using data from a nationwide representative cross-sectional survey in China and a validated PM2.5 composition dataset, we established generalized linear models to quantify the association between five major components of PM2.5 and CKD prevalence. RESULTS: There were significant associations between long-term exposure to three PM2.5 components [including black carbon (BC), sulfate (SO42-), organic matter (OM)] and increased odds of CKD prevalence. Along with an interquartile range (IQR) increment in BC (3.3 µg/m3), SO42- (9.7 µg/m3), and OM (16.2 µg/m3) at a 4-year moving average, the odds ratios (ORs) for CKD prevalence were 1.28 (95% CI 1.07, 1.54), 1.23 (95% CI 1.03, 1.45), and 1.23 (95% CI 1.02, 1.47), respectively. We did not detect any significant association of the other two PM2.5 components [nitrate (NO3-) or ammonium (NH4+)] with CKD prevalence. Stratified analyses revealed no differences (P ≥ 0.05) in the effect estimates of subgroups based on administrative region, sex, age, and other demographic characteristics. For instance, along with an IQR increment in BC at a 4-year moving average, the ORs of CKD prevalence among males and females were 1.30 (95% CI 0.98, 1.73) and 1.29 (95% CI 1.01, 1.65), respectively. The odds of CKD were generally higher with increasing PM2.5 composition concentration. CONCLUSIONS: Our study demonstrated that long-term exposure to specific PM2.5 components including BC, SO42-, and OM increased CKD risk in the general population. This study could provide new insights into source-directed PM2.5 control and CKD prevention.

The association between ambient air pollution and migraine: a systematic review.

Some studies have shown the effect of air pollution on migraine. However, it needs to be confirmed in larger-scale studies, as scientific evidence is scarce regarding the association between air pollution and migraine. Therefore, this systematic review aims to determine whether there are associations between outdoor air pollution and migraine. A literature search was performed in Scopus, Medline (via PubMed), EMBASE, and Web of Science. A manual search for resources and related references was also conducted to complete the search. All observational studies investigating the association between ambient air pollution and migraine, with inclusion criteria, were entered into the review. Fourteen out of 1417 identified articles met the inclusion criteria and entered the study. Among the gaseous air pollutants, there was a correlation between exposure to nitrogen dioxide (NO2) (78.3% of detrimental relationships) and carbon monoxide (CO) (68.0% of detrimental relationships) and migraine, but no apparent correlation has been found for sulfur dioxide (SO2) (21.2% of detrimental relationships) and ozone (O3) (55.2% of detrimental relationships). In the case of particulate air pollutants, particulate matter with a diameter of 10 µm or less (PM10) (76.0% of detrimental relationships) and particulate matter with a diameter of 2.5 µm or less (PM2.5) (61.3% of detrimental relationships) had relationships with migraine. In conclusion, exposure to NO2, CO, PM10, and PM2.5 is associated with migraine headaches, while no conclusive evidence was found to confirm the correlation between O3 and SO2 with migraine. Further studies with precise methodology are recommended in different cities around the world for all pollutants with an emphasis on O3 and SO2.

Assessment of the health impacts of air pollution exposure in East African countries.

The health effects of air pollution remain a public concern worldwide. Using data from the Global Burden of Disease 2019 report, we statistically analyzed total mortality, disability-adjusted life years (DALY), and years of life lost (YLL) attributable to air pollution in eight East African countries between 1990 and 2019. We acquired ambient ozone (O3), PM2.5 concentrations and household air pollution (HAP) from the solid fuel from the State of Global Air report. The multilinear regression model was used to evaluate the predictability of YLLs by the air pollutants. We estimated the ratio rate for each health burden attributable to air pollution to compare the country's efforts in the reduction of air pollution health burden. This study found that the total number of deaths attributable to air pollution decreased by 14.26% for 30 years. The drop came from the reduction of 43.09% in mortality related to Lower Respiratory tract Infection (LRI). However, only five out of eight countries managed to decrease the total number of deaths attributable to air pollution with the highest decrease observed in Ethiopia (40.90%) and the highest increase in Somalia (67.49%). The linear regression model showed that HAP is the pollutant of the most concern in the region, with a 1% increase in HAP resulting in a 31.06% increase in regional YLL (R2 = 0.93; p < 0.05). With the increasing ground-level ozone, accompanied by the lack of adequate measures to reduce particulate pollutants, the health burdens attributable to air pollution are still a threat in the region.