Particulate air pollution is a continuing challenge in China, and its adverse effects on chronic obstructive pulmonary disease (COPD) have been widely reported. However, epidemiological evidence on the associations between size-fractionated particle number concentrations (PNCs) and COPD mortality is limited. In this study, we utilized a time-series approach to investigate the associations between PNCs of particles at 0.25–10 μm in diameter and COPD mortality in Shanghai, China. Quasi-Poisson regression generalized additive models were applied to evaluate these associations, with adjustment of time trend, day of week, holidays, temperature and relative humidity. Stratification analyses were performed by season and gender. There were a total of 3238 deaths due to COPD during the study period. We found that daily COPD deaths were significantly associated with PNCs of particles <0.5 μm, and the magnitude of associations increased with decreasing particle size. An interquartile range (IQR) increase in PNC₀.₂₅—₀.₂₈, PNC₀.₂₈—₀.₃, PNC₀.₃—₀.₃₅, PNC₀.₃₅—₀.₄, PNC₀.₄—₀.₄₅ and PNC₀.₄₅—₋₀.₅ was associated with increments of 7.51% (95%CI: 2.45%, 12.81%), 7.22% (95%CI: 2.16%, 12.53%), 6.95% (95%CI: 1.81%, 12.35%), 6.26% (95%CI: 1.25%, 11.52%), 5.24% (95%CI: 0.56%, 10.13%) and 4.15% (95%CI: 0.14%, 8.32%), respectively. The associations remained robustness after controlling for the mass concentrations of gaseous air pollutants. In stratification analyses, significant associations between PNCs and COPD mortality were observed in the cold seasons, and in males. Our results suggested that particles <0.5 μm in diameter might be most responsible for the adverse effects of particulate air pollution on COPD mortality, and COPD patients are more susceptible to PM air pollution in the cold seasons, especially for males.

Polychlorinated biphenyls (PCBs) are a class of widespread environmental pollutants, commonly found in human blood, that have been suggested to be linked to the occurrence of sporadic Parkinson's disease (PD). It has been reported that some non-coplanar PCBs accumulate in the brains of female PD patients. To improve our understanding of the association between PCB exposure and PD risk we have applied whole transcriptome gene expression analysis in blood cells from 594 PCB-exposed subjects (369 female, 225 male).Interestingly, we observe that in females, blood levels of non-coplanar PCBs appear to be associated with expression levels of PD-specific genes. However, no such association was detected in males. Among the 131 PD-specific genes affected, 39 have been shown to display similar changes in expression levels in the substantia nigra of deceased PD patients. Especially among the down-regulated genes, transcripts of genes involved in neurotransmitter vesicle-related functions were predominant.

The purpose of this study is to investigate the potential associations between air pollution and dry eye disease (DED). Data of outdoor air pollutants and meteorology as well as outpatient visits for DED were collected. A time-stratified case-crossover approach was used to analyze the associations between ambient air pollutants and outpatient visits for DED. Among the 5062 DED patients studied, 65.45% were female and 34.55% were male. In the single-pollutant model, significant associations were observed between an increase of 10 μg/m³ in the concentrations of fine-particulate matter with a median aerometric diameter of less than 10 μm (PM₁₀), fine-particulate matter with a median aerometric diameter of less than 2.5 μm (PM₂.₅), sulfur dioxide (SO₂), nitrogen dioxide (NO₂), and carbon monoxide (CO) and outpatient visits for DED. These results were consistent with those of the multipollutant model. The strongest associations between air pollutants and patient visits were observed during the cold season and in patients aged 21–40. The significant association between air pollutants (PM₁₀, PM₂.₅, SO₂, NO₂, and CO) and DED outpatient visits indicates the importance of increased environmental protection.

This study aimed to determine if there is a co-elevation of human blood arsenic and mercury levels in the Midwestern population of the United States (U.S.) and to determine any geographical patterns and variation of arsenic and mercury that may exist in Michigan. 58,800 blood specimens along with associated demographic/geographic data from the contiguous United States were reviewed. Univariate and multivariable logistic regression were used to analyze demographic/geographic variables associated with elevated arsenic concentrations. Furthermore, blood data from patients in Michigan were aggregated to the ZIP code tabulation area (ZCTA) in order to assess geographic variation using spatial regression models. SaTScan software was also used to analyze potential clustering of arsenic and mercury across Michigan ZCTAs. Within the contiguous United States, elevated mercury blood concentrations, older age, female sex, and coastal status were all associated with elevated arsenic blood concentrations (elevated mercury odds ratio (OR) 3.18 (3.04–3.33); female sex OR 1.06 (1.02–1.11); +10 yr age OR 1.12 (1.11–1.14); coastal state OR 1.33 (1.27–1.40). Within the state of Michigan, as with the continuous U.S., elevated mercury blood concentrations and older age were associated with elevated arsenic blood concentrations (elevated mercury OR 2.75 (2.38–3.18); female sex OR 1.06 (0.95–1.19); +10 yr age OR 1.10 (1.06–1.13). Using spatial regression, it was determined that within Michigan, economic inequality (measured via the Gini coefficient) was also associated with elevated concentrations of mercury in the blood. Clinical reference laboratory data, in conjunction with spatial analysis methods, may enhance our understanding of how elemental exposure affects human health and should be considered for studying how environmental contaminants, socioeconomics and geography affect the health of populations.

Analysis of persistent halogenated organic pollutants (HOPs) in human follicular fluid is important given previous reports of their adverse effects on the reproductivity of women. In the present work, HOPs, including polybrominated diphenyl ethers (PBDEs) and polychlorinated biphenyls (PCBs), were analyzed in 127 follicular fluid samples collected from patients who were undergoing in vitro fertilization in Central China. The concentrations of ∑₇BDEs (sum of BDE-28, -47, −99, −100, −153, −154, and −183) in follicular fluid ranged from not detected (n.d.) to 110 ng/g lipid weight (lw), with an average of 50 ± 24 ng/g lw. BDE-100 was suggested to be an indicator of BDE congeners in follicular fluid, with the highest concentrations and showing a significantly high correlation (p < 0.01) with ∑₇BDEs. Penta-BDE products were the principal source of PBDEs in follicular fluid samples. The concentrations of ∑₇CBs (CB-28, -52, −101, −118, −138, −153, and −180) in follicular fluids ranged from n.d. to 250 ng/g lw, with an average of 77 ± 69 ng/g lw. CB-28 and CB-52 were considered to be indicator CB congeners, with tri-CBs and tetra-CBs dominating in follicular fluid. No significant correlation was observed between patient age and PBDE or PCB concentrations in follicular fluid, indicating that age was not the controlling factor influencing the bioaccumulation of most HOPs in this study.

The effect of health status on the relationship between particulate matter (PM) and black carbon (BC) and cardiac autonomic function has not been examined sufficiently directly comparing patients with healthy participants.To evaluate the association patterns between size-fractioned indoor PM and BC and cardiac autonomic function in chronic obstructive pulmonary disease (COPD) patients and their healthy spouses.Twenty-four-hour heart rate variability (HRV) and heart rate (HR) was measured in eight pairs of stable COPD patients and their healthy spouses. Real-time size-fractioned indoor PM and BC levels were monitored on the same, and preceding, days. Mixed-effects models were used to estimate the changes in health indices and pollutants after controlling for potential confounding variables.Increases in size-fractioned PM and BC were associated with alterations in cardiac autonomic function in both COPD patients and their healthy spouses. However, the association patterns differed between the two groups. In COPD group, an IQR (13.65 μg/m3) increase in PM0.5 at 12-h moving average was associated with reductions of 14.62% (95% CI: -21.74%, -6.86%) in total power (TP) and 10.14% (95% CI: -16.11%, -3.76%) in high frequency (HF) power. In healthy volunteers, however, TP and HF declined immediately upon exposure to PM and then returned to normal levels gradually. In this group, an IQR increase in PM0.5 at 5 min moving average was associated a 20.30% (95% CI: -25.49%, -14.73%) reduction in TP and a 31.79% (95% CI: -36.48%, -26.72%) reduction in HF.Exposure to indoor PM and BC was associated with cardiac autonomic dysfunction in COPD patients and their healthy spouses. Exposure had a greater lagged effect on HRV in COPD patients than in healthy participants. These findings will aid the formulation of targeted measures to prevent the adverse effects of indoor air pollution for individuals with different health statuses.

Male fertility is progressively declining in many developed countries, but the relationship between male infertility and environmental factors is still unclear.To assess the influence of environmental temperature and air pollution on semen parameters, using a big-data approach.A big data analysis of parameters related to 5131 men, living in a province of Northern Italy and undergoing semen analyses between January 2010 and March 2016 was performed. Ambient temperature was recorded on the day of analysis and the 90 days prior to the analysis and the average value of particulate matter (PM) and NO2 in the year of the test. All data were acquired by geocoding patients residential address. A data warehouse containing 990,904,591 data was generated and analysed by multiple regressions.5573 semen analyses were collected. Both maximum and minimum temperatures registered on the day of collection were inversely related to total sperm number (p < .001), non-progressive motility (NPrM) (p < .005) and normal forms (p < .001). Results were confirmed considering temperature in the 30 and 60 days before collection, but not in the 90 days before collection. Total sperm number was lower in summer/autumn (p < .001) and was inversely related with daylight duration (p < .001). PM10 and PM2.5 were inversely related to PrM (p < .001 and p < .005) and abnormal forms (p < .001).This is the first evaluation of the relationship between male fertility-related parameters and environment using a big-data approach. A seasonal change in semen parameters was found, with a fluctuation related to both temperature and daylight duration. A negative correlation between air pollution and semen quality is suggested. Such seasonal and environmental associations should be considered when assessing changes of male fertility-related parameters over time.

The impact of chronic exposure to air pollution and outcomes in the acute respiratory distress syndrome (ARDS) is unknown. The Nationwide Inpatient Sample (NIS) from 2011 was utilized for this analysis. The NIS is a national database that captures 20% of all US in-patient hospitalizations from 47 states. Patients with ARDS who underwent mechanical ventilation from the highest 15 ozone pollution cities were compared with the rest of the country. Secondary analyses assessed outcomes of ARDS patients for ozone pollution and particulate matter pollution on a continuous scale by county of residence. A total of 8,023,590 hospital admissions from the 2011 NIS sample were analyzed. There were 93,950 patients who underwent mechanical ventilation for ARDS included in the study. Patients treated in high ozone regions had significantly higher unadjusted hospital mortality (34.9% versus 30.8%, p < 0.01) than patients in cities with control levels of ozone. After controlling for all variables in the model, treatment in a hospital located in a high ozone pollution area was associated with an increased odds of in-hospital mortality (OR 1.11, 95% CI 1.08–1.15, p < 0.01). After adjustment for all variables in the model, for each increase in ozone exposure by 0.01 ppm the OR for death was 1.07 (95% CI 1.06–1.08, p < 0.01). Similarly, for each increase in particulate matter exposure by 10 μg/m³, the OR for death was 1.08 (95% CI 1.02–1.16, p < 0.01).Chronic exposure to both ozone and particulate matter pollution is associated with higher rates of mortality in ARDS. These preliminary findings need to be confirmed by further detailed studies.

This study examined effects of short-term urban air pollution exposures on inflammation, thrombosis, and autonomic imbalance in subjects at risk for cardiovascular disease (CVD). We enrolled 61 patients with multiple CVD risk factors and measured high sensitive C-reactive protein (hs-CRP), fibrinogen, D-dimer, and heart rate variability (HRV) indices. Two health examinations for each participant were performed during December 2002 through September 2003. Changes in inflammation and thrombotic markers and HRV indices with exposures to PM2.5, organic carbon (OC), elemental carbon (EC), sulfur dioxide (SO2), nitrogen dioxide (NO2), and carbon monoxide (CO) at 1- to 3-day lags were analyzed using mixed models. The results showed inflammatory and thrombotic markers increased with 1- to 3-day lagged PM2.5 components and gaseous pollutants exposures. hs-CRP maximally increased 0.19 [95% confidence interval (CI): 0.07–0.31] and 0.15 (95% CI: 0.05–0.24) mg/L for an interquartile range (IQR) of 1-day lagged SO2 (2.3 ppb) and CO (0.5 ppm), respectively. D-dimer maximally increased 1.05 (95% CI: 0.13–1.75), 0.72 (95% CI: 0.09–1.21), 0.92 (95% CI: 0.13–1.50), and 0.90 (95% CI: 0.07–1.61) mg/dL for an IQR of 1-day lagged OC (3.9 μg/m3), EC (2.0 μg/m3), SO2, and NO2 (13.4 ppb), respectively. The HRV indices, including low frequency, very low frequency, and the ratio of low frequency to high frequency decreased 19.8 (95% CI: 4.4–32.7), 12.9 (95% CI: 0.8–23.4), and 17.6 (95% CI: 5.4–28.2)% for an IQR of 1-day lagged PM2.5 (20.2 μg/m3), respectively. Our findings demonstrated PM2.5 components and gaseous pollutants exert prolonged inflammatory and thrombotic reactions, while PM2.5 exert an immediate autonomic imbalance.

Environmental low-dose melamine exposure has been associated with urolithiasis risk in adults, but it is unclear if this exposure can cause early renal damage. This cross-sectional study investigated the association of this exposure and early renal damage in patients with calcium urolithiasis. We recruited patients diagnosed with upper urinary tract calcium urolithiasis from three hospitals in southwestern Taiwan between November 2010 and January 2015. All patients completed a structured questionnaire and provided one-spot urine samples for the measurement of melamine level and markers of early renal injury, including N-acetyl b-d-glucosaminidase (NAG), β2-microglobulin (β2-MG), and microalbumin. We used urinary melamine levels as an indicator of environmental melamine exposure. A total of 309 patients (mean age of 54.7 ± 12.8 years) were studied. Median urinary melamine level (μg/mmol Cr) was 1.26 (interquartile range 0.48–3.29). A significant and positive correlation was found between urinary melamine concentration and urinary NAG levels (Spearman correlation coefficient, r = 0.157, p = 0.006, n = 309). With urinary melamine levels categorized into quartiles, multivariate regression results showed the same relationship, particularly in those with first stone episode. In this group, patients with the highest quartile of urinary melamine concentration had a 3.95-fold risk (95% confidence interval = 1.43–10.94) of high NAG levels (dichotomized by median), compared to the lowest quartile after adjustment. No association was found between urinary melamine concentration and urinary microalbumin levels. In conclusion, urinary melamine is significantly associated with urinary marker of early renal tubular injury, NAG, in urolithiasis patients, especially ones with first stone episode.