The influences of weather and air pollutants on chronic obstructive pulmonary disease (COPD) have been well-studied. However, the heterogeneous effects of different influenza viral infections, air pollution and weather on COPD admissions and re-admissions have not been thoroughly examined. In this study, we aimed to elucidate the relationships between meteorological variables, air pollutants, seasonal influenza, and hospital admissions and re-admissions due to COPD in Hong Kong, a non-industrial influenza epicenter. A total number of 507703 hospital admissions (i.e., index admissions) and 301728 re-admission episodes (i.e., episodes within 30 days after the previous discharge) for COPD over 14 years (1998–2011) were obtained from all public hospitals. The aggregated weekly numbers were matched with meteorological records and outdoor air pollutant concentrations. Type-specific and all-type influenza-like illness positive (ILI+) rates were used as proxies for influenza activity. Generalized additive models were used in conjunction with distributed-lag non-linear models to estimate the associations of interest. According to the results, high concentrations of fine particulate matter, oxidant gases, and cold weather were strong independent risk factors of COPD outcomes. The cumulative adjusted relative risks exhibited a monotone increasing trend except for ILI+ B, and the numbers were statistically significant over the entire observed range of ILI+ total and ILI+ A/H3N2 when the reference rate was zero. COPD hospitalization risk from influenza infection was higher in the elderly than that in the general population. In conclusion, our results suggest that health administrators should impose clean air policies, such as strengthening emissions control on petrol vehicles, to reduce pollution from oxidant gases and particulates. An extension of the influenza vaccination program for patients with COPD may need to be encouraged: for example, vaccination may be included in hospital discharge planning, particularly before the winter epidemic.

Limited data were on the acute respiratory responses in the elderly in response to personal exposure of particulate matter (PM). In order to evaluate the changes of airway inflammation and pulmonary functions in the elderly in response to individual exposure of particles (PM₁.₀, PM₂.₅ and PM₁₀), we analyzed 43 elderly subjects with either asthma, chronic obstructive pulmonary disease (COPD) or Asthma COPD Overlap (ACO) and 40 age-matched subjects without asthma nor COPD in an urban community in Shanghai, China. Data were collected at the baseline and in 6 follow-ups from August 2016 to December 2018, once every 3 months except for the last twice with a 6-month interval. In each follow-up, pulmonary functions, fractional exhaled nitric oxide (FeNO), 7-day continuous personal exposure to airborne particles were measured. Multivariate linear mixed effect regression models were applied to investigate the quantitative changes of pulmonary functions and FeNO in two respective groups. The results showed that on average 4.7 follow-up visits were completed in each participant. In subjects with CRDs, an inter-quartile range (IQR) increase of personal exposure to PM₁.₀, PM₂.₅ and PM₁₀ was significantly associated with an average increase of FeNO(Lag1) of 6.7 ppb (95%CI 1.2, 9.9 ppb), 6.2 ppb (95%CI 1.5, 12.0 ppb) and 5.6 ppb (95%CI 1.5, 11.0 ppb), respectively, and an average decrease of FEV1(Lag2) of −3.6 L (95%CI -6.0, −1.1 L), −3.6 L (95%CI -6.4, −0.8 L) and −3.2 L (95%CI -5.8, −0.6 L), respectively, in the single-pollutant model. These associations remained consistent in the two-pollutant models adjusting for gaseous air pollutants. Stratified analysis showed that subjects with lower BMI, females and non-allergies were more sensitive to particle exposure. No robust significant effects were observed in the subjects without CRDs. Our study provided data on the susceptibility of the elderly with CRDs to particle exposure of PM₁.₀ and PM₂.₅, and the modification effects by BMI, gender and history of allergies.

Aging is a leading cause of mortality for the elderly and DNA methylation age is reported to be predictive of biological aging. However, few studies have investigated the associations between multiple metals exposure and accelerated aging in the elderly. We performed a pilot study of 288 elderly participants aged 50–115 years and measured genome-wide DNA methylation and 22 blood metals concentrations. Measures of DNA methylation age were estimated using CpGs from Illumina HumanMethylation EPIC BeadChip. Linear mixed regression and Bayesian kernel machine regression (BKMR) models were used to estimate the individual and overall associations between multiple metals and accelerated methylation aging. Single metal models revealed that each 1-standard deviance (SD) increase in log-transformed vanadium, cobalt, nickel, zinc, arsenic, and barium was associated with a −2.256, −1.318, 1.004, −1.926, 1.910 and −1.356 changes in ΔAge, respectively; meanwhile, for aging rate, the change was −0.019, −0.013, 0.010, −0.018, 0.023, and −0.012, respectively (all P < 0.05). The BKMR models showed reverse U-shaped associations of the overall metals mixture with ΔAge and aging rate. Downward trends of ΔAge and aging rate were observed for increasing quantiles of essential metals mixture, but upward trends were observed for non-essential metals mixture. Further individual analysis of the BKMR revealed that the 95% confidence interval of ΔAge and aging rate associated with vanadium, zinc, and arsenic did not cross 0, when other metals concentrations set at 25th, 50th, and 75th percentile. Our findings suggest reverse U-shaped associations of the overall metals mixture with accelerated methylation aging for the first time, and vanadium, zinc, and arsenic may be major contributors driving the associations.

People use a particulate respirator in order to reduce exposure to ambient fine particulate matter (PM₂.₅). Acute exposure to PM₂.₅ is known to increase blood pressure. However, systematic reviews or meta-analyses on blood pressure-related benefits of using a particulate respirator is lacking. Therefore, we reviewed randomized crossover intervention studies on blood pressure-related effects of particulate matter respirator use. We conducted a literature review of articles found on Embase, Medline, and Cochrane library on August 31, 2020. The study outcomes were systolic and diastolic blood pressure and mean arterial pressure. A random-effect model was used in the meta-analysis. Subgroup analyses, based on age (adult < 60 years, elderly ≥ 60 years), personal PM₂.₅ exposure levels (High: ≥ 25 μg/m³, Low: < 25 μg/m³), and types of monitoring methods (ambulatory and resting blood pressure) were conducted. We identified 297 references, and seven studies were included in our systematic review. None of the studies used a sham respirator as control and complete allocation concealment and blinding were impossible. The use of a particulate respirator was associated with a −1.23 mmHg (95% confidence interval (CI): −2.53, 0.07) change in systolic blood pressure and a −1.57 mmHg (95% CI: −3.85, 0.71) change in mean arterial pressure. There were significant heterogeneities and possibilities for publication bias. The subgroup analyses revealed that studies involving elderly individuals, those conducted in high PM₂.₅ personal exposure, and those in which resting blood pressure was monitored demonstrated a larger decrease in blood pressure resulting from respirator use. Further intervention studies with a large sample size and subjects with diverse characteristics and different personal PM₂.₅ levels may add the evidence to current literature.

An increasing number of epidemiological studies have examined air pollution as a possible contributor to adverse sleep health, but results are mixed. The aims of this systematic review are to investigate and summarize the associations between exposures to air pollutants and various sleep measures across the lifespan. PubMed, CINAHL, Cochrane, Scopus, Web of Science, and PsycInfo were searched through October 2019 to identify original data-based research examining direct epidemiological associations between ambient and indoor air pollution exposures and various sleep health measures, including sleep quality, sleep duration, sleep disturbances, and daytime sleepiness. Twenty-two articles from 2010 to 2019 were selected for inclusion in this review, including a wide range of study populations (from early childhood to elderly) and locations (10 Asian, 4 North American, 3 European, 5 other). Due to variation in both exposure and outcome assessments, conducting a meta-analysis was not plausible. Twenty-one studies reported a generally positive association between exposure and poor sleep quality. While most studies focused on ambient air pollutants, five assessed the specific effect of indoor exposure. In children and adolescents, increased exposure to both ambient and indoor pollutants is associated with increased respiratory sleep problems and a variety of additional adverse sleep outcomes. In adults, air pollution exposure was most notably related to sleep disordered breathing. Existing literature generally shows a negative relationship between exposures to air pollution and sleep health in populations across different age groups, countries, and measures. While many associations between air pollution and sleep outcomes have been investigated, the mixed study methods and use of subjective air pollution and sleep measures result in a wide range of specific associations. Plausible toxicological mechanisms remain inconclusive. Future studies utilizing objective sleep measures and controlling for all air pollution exposures and individual encounters may help ameliorate variability in the results reported by current published literature.

The influenza is a common viral infection that can be fatal, especially in high-risk groups such as children, pregnant women, elderly, and immune-deficient individuals. Vaccination is the most efficient approach to prevent the spreading of viral infection and promote individual and public health. In contrast, exposure to environmental pollutants such as cigarette smoke reduces the efficacy of vaccination. We investigated whether chronic exposure to hydroquinone (HQ), the most abundant compound of the tobacco particulate phase, could impair the adaptive immune responses elicited by influenza vaccination. For this, adult male C57BL/6 mice were daily exposed to either nebulized HQ or PBS for 1 h for a total of eight weeks. At weeks 6 and 8, the mice were primed and boosted with the trivalent influenza vaccine via IM respectively. Although the HQ exposure did not alter the body weight of the mice and the biochemical and hematological parameters, the pollutant increased the oxidative stress in splenocytes of immunized animals, modified the morphology of spleen follicles, and augmented the size of their lymph nodes. The lymphoid organs of HQ-exposed mice presented a similar number of vaccine-specific IgG-secreting cells, titers of vaccine-specific total IgG, and respective subclasses. Transcriptome studies with HQ, benzene, or cigarette smoke exposure were also analyzed. The genes up-regulated upon pollutant exposure were associated with neutrophil migration and were shown to be co-expressed with antibody-secreting cell genes. Therefore, these findings suggest that HQ exposure may trigger an immune-compensatory mechanism that enhances the humoral responses induced by influenza vaccination.

Current studies indicate that long-term exposure to ambient fine particulate matter (PM₂.₅) is related with global mortality, yet no studies have explored relationships of PM₂.₅ and its species with DNAm PhenoAge acceleration (DNAmPhenoAccel), a new epigenetic biomarker of phenotypic age. We identified which PM₂.₅ species had association with DNAmPhenoAccel in a one-year exposure window in a longitudinal cohort. We collected whole blood samples from 683 elderly men in the Normative Aging Study between 1999 and 2013 (n = 1254 visits). DNAm PhenoAge was calculated using 513 CpGs retrieved from the Illumina Infinium HumanMethylation450 BeadChip. Daily concentrations of PM₂.₅ species were measured at a fixed air-quality monitoring site and one-year moving averages were computed. Linear mixed-effect (LME) regression and Bayesian kernel machine (BKM) regression were used to estimate the associations. The covariates included chronological age, body mass index (BMI), cigarette pack years, smoking status, estimated cell types, batch effects etc. Benjamini-Hochberg false discovery rate at a 5% false positive threshold was used to adjust for multiple comparison. During the study period, the mean DNAm PhenoAge and chronological age in our subjects were 68 and 73 years old, respectively. Using LME model, only lead and calcium were significantly associated with DNAmPhenoAccel. For example, an interquartile range (IQR, 0.0011 μg/m³) increase in lead was associated with a 1.29-year [95% confidence interval (CI): 0.47, 2.11] increase in DNAmPhenoAccel. Using BKM model, we selected PM₂.₅, lead, and silicon to be predictors for DNAmPhenoAccel. A subsequent LME model showed that only lead had significant effect on DNAmPhenoAccel: 1.45-year (95% CI: 0.46, 2.46) increase in DNAmPhenoAccel following an IQR increase in one-year lead. This is the first study that investigates long-term effects of PM₂.₅ components on DNAmPhenoAccel. The results demonstrate that lead and calcium contained in PM₂.₅ was robustly associated with DNAmPhenoAccel.

Metabolic syndrome is an important risk factor for non-communicable diseases, particularly type 2 diabetes, coronary heart disease, and stroke. Long-term exposure to greenspace could be protective of metabolic syndrome, but evidence for such an association is lacking. Accordingly, we investigated the association between long-term exposure to greenspace and risk of metabolic syndrome.The present longitudinal study was based on data from four clinical examinations between 1997 and 2013 in 6076 participants of the Whitehall II study, UK (aged 45–69 years at baseline). Long-term exposure to greenspace was assessed by satellite-based indices of greenspace including Normalized Difference Vegetation Index (NDVI) and Vegetation Continuous Field (VCF) averaged across buffers of 500 and 1000 m surrounding the participants’ residential location at each follow-up. The ascertainment of metabolic syndrome was based on the World Health Organization (WHO) definition. Hazard ratios for metabolic syndrome were estimated using Cox proportional hazards regression models, controlling for age, sex, ethnicity, lifestyle factors, and socioeconomic status.Higher residential surrounding greenspace was associated with lower risk of metabolic syndrome. An interquartile range increase in NDVI and VCF in the 500 m buffer was associated with 13% (95% confidence interval (CI): 1%, 23%) and 14% (95% CI: 5%, 22%) lower risk of metabolic syndrome, respectively. Greater exposure to greenspace was also associated with each individual component of metabolic syndrome, including a lower risk of high levels of fasting glucose, large waist circumference, high triglyceride levels, low HDL cholesterol, and hypertension. The association between residential surrounding greenspace and metabolic syndrome may have been mediated by physical activity and exposure to air pollution.The findings of the present study suggest that middle-aged and older adults living in greener neighbourhoods are at lower risk of metabolic syndrome than those living in neighbourhoods with less greenspace.

Pyrethroids are a class of man-made insecticides associated with various adverse health outcomes including respiratory problems. However, there were limited evidences on the relation between 3-phenoxybenzoic acid (3-PBA) as a metabolite of pyrethroids and pulmonary function, particularly among elderly population who have declining pulmonary function. Therefore, we collected urine samples and performed pulmonary function test (PFT) repeatedly in a total of 559 Korean elderly living in Seoul as an urban area. After measurement of urinary 3-PBA levels, cross-sectional relations of visit-to-visit variation in 3-PBA level on visit-to-visit variation in PFT parameters were evaluated using linear mixed effect models and generalized additive mixed models after adjustment for age, sex, body mass index, smoking status, education, visit episode, and phthalate metabolite levels. The Korean elderly were highly exposed to pyrethroids with 30.2% of elderly people with 3-PBA level over reference value derived on the 95th percentile of representative samples (2 ng/mL). Forced expiratory volume in 1 second (FEV₁), forced vital capacity (FVC), and forced expiratory flow between 25% and 75% of FVC (FEF₂₅–₇₅) as PFT parameters showed significant reductions by an increase of 3-PBA level (FEV₁, β = −1.48, p-value < 0.01; FVC, β = −1.14, p-value < 0.01; and FEF₂₅₋₇₅, β = −1.11, p-value = 0.03). The negative associations of 3-PBA level with FEV₁, FVC, and FEF₂₅₋₇₅ were found only for females (FEV₁, β = −1.64, p-value < 0.01; FVC, β = −1.47, p-value < 0.01; and FEF₂₅₋₇₅, β = −1.06, p-value = 0.07), but not for males. However, the longitudinal effect of 3-PBA level on the trajectory of FEV₁, FVC, and FEF₂₅₋₇₅ declines in females was not found. Community-level exposure to pyrethroids was associated with pulmonary function reduction in elderly population, indicating that more stringent control of pyrethroids is necessary to protect the elderly who have declining pulmonary function.

Poor indoor air quality can have adverse effects on human health, especially in susceptible populations; however, few studies have measured multiple pollutants in facilities for susceptible populations at a national scale in South Korea. Therefore, we measured the concentrations of indoor pollutants (fine particulate matter (PM₁₀), CO₂, airborne bacteria (AB), total volatile organic compounds (TVOCs), and formaldehyde) to determine their possible relation to other indoor environmental factors and characteristics of facilities with susceptible populations, such as hospitals, geriatric hospitals, elderly care facilities, and postnatal care centers throughout South Korea. Indoor pollutants were sampled at 82 indoor facilities, including 62 facilities for susceptible populations. Spearman's correlation, Kruskal–Wallis, and Mann–Whitney analyses were used to examine the relationship among and differences between pollutants at indoor facilities and indoor/outdoor differences in PM₁₀ concentration. There were significant correlations between indoor temperature and AB concentration (r = 0.37, p < 0.01), TVOCs, and formaldehyde (r = 0.264, p < 0.01). Indoor PM₁₀ concentrations were higher than outdoor concentrations at all facilities for susceptible populations (p < 0.01). CO₂ might be a good indicator for predicting indoor pollutants when categorized into two levels (≤750 ppm and >750 ppm). The hazard quotient of formaldehyde was higher than the acceptable level of 1 for children under the age of eight in postnatal care centers, indicative of unsafe levels. Therefore, more depth study for exposure characteristics of formaldehyde and indoor air quality (IAQ) in postnatal care facilities as a national scale is needed for finding the children exposure levels.