In the face of emerging and re-emerging diseases, novel and innovative approaches to population scale surveillance are necessary for the early detection and quantification of pathogens. The last decade has seen the rapid development of wastewater and environmental surveillance (WES) to address public health challenges, which has led to establishment of wastewater-based epidemiology (WBE) approaches being deployed to monitor a range of health hazards. WBE exploits the fact that excretions and secretions from urine, and from the gut are discharged in wastewater, particularly sewage, such that sampling sewage systems provides an early warning system for disease outbreaks by providing an early indication of pathogen circulation. While WBE has been mainly used in locations with networked wastewater systems, here we consider its value for less connected populations typical of lower-income settings, and assess the opportunity afforded by pit latrines to sample communities and localities. We propose that where populations struggle to access health and diagnostic facilities, and despite several additional challenges, sampling unconnected wastewater systems remains an important means to monitor the health of large populations in a relatively cost-effective manner.

Severe surface ozone pollution has become widespread in China. To protect public health, Chinese scientific communities and government agencies have striven to mitigate ozone pollution. However, makers of pollution mitigation policies rarely consider epidemiological research, and communication between epidemiological researchers and the government is poor. Therefore, this article reviews the current mitigation policies and the National Ambient Air Quality Standard (NAAQS) for ozone from an epidemiological perspective and proposes recommendations for researchers and policy makers on the basis of epidemiological evidence. We review current nationwide ozone control measures for mitigating ozone pollution from four dimensions: the integration of ozone and particulate matter control, ozone precursors control, ozone control in different seasons, and regional cooperation on the prevention of ozone pollution. In addition, we present environmental and epidemiological evidence and propose recommendations and discuss relevant ozone metrics and the criteria values of the NAAQS. We finally conclude that the disease burden attributable to ozone exposure in China may be underestimated and that the epidemiological research regarding the health effects of integrating ozone and particulate matter control is insufficient. Furthermore, atmospheric volatile organic compounds are severely detrimental to health, and related control policies are urgently required in China. We recommend a greater focus on winter ozone pollution and conclude that the health benefits of regional cooperation on ozone control and prevention are salient. We argue that daily average ozone concentration may be a more biologically relevant ozone metric than those currently used by the NAAQS, and accumulating epidemiological evidence supports revision of the standards. This review provides new insight for ozone mitigation policies and related epidemiological studies in China.

Nitrogen dioxide (NO₂) is a well-established traffic emissions tracer and has been associated with multiple adverse health outcomes. Short- and long-term exposure to NO₂ has been studied and is well-documented in existing literature, but information on intermediate-term NO₂ effects and mortality is lacking, despite biological plausibility. We obtained daily NO₂ and mortality data from 42 counties in China from 2013 to 2015. Distributed-lag non-linear models were employed to investigate the relationship between non-accidental mortality and NO₂ up to 30 days before the event, including PM₂.₅, temperature, relative humidity, and holidays as covariates in a random effects meta-analysis pooling county-specific estimates. We repeated the analysis for cardiovascular- and respiratory-related mortality, and explored sex-stratified associations. Per 10 μg/m³ increase in NO₂, we estimated a 0.13% (95%CI: 0.03, 0.23%), 0.57% (95%CI: −0.04, 1.18%), and −0.14% (95%CI: −1.63, 1.37%) change in non-accidental mortality for same-day and previous-day NO₂ (lag0-1 cumulated), in the preceding 7 days (lag0-7 cumulated), and in the preceding 30 days (lag0-30 cumulated), respectively. The strongest estimate was observed for respiratory-related mortality in the lag0-30 cumulated effect for women (3.12%; 95%CI: −1.66, 8.13%). We observed a trend of higher effect estimates of intermediate-term NO₂ exposure on respiratory mortality compared to that of the short-term, although the differences were not statistically significant. Our results at longer lags for all-cause and cardiovascular mortality were sensitive to modeling choices. Future work should further investigate intermediate-term air pollution exposure given their potential biological relevance, but in larger scale settings.

The knowledge about the effects of environmental temperature on human epigenome is a potential key to understand the health impacts of temperature and to guide acclimation under climate change. We performed a systematic review on the epidemiological studies that have evaluated the association between environmental temperature and human epigenetic modifications. We identified seven original articles on this topic published between 2009 and 2019, including six cohort studies and one cross-sectional study. They focused on DNA methylation in elderly people (blood sample) or infants (placenta sample), with sample size ranging from 306 to 1798. These studies were conducted in relatively low temperature setting (median/mean temperature: 0.8–13 °C), and linear models were used to evaluate temperature-DNA methylation association over short period (≤28 days). It has been reported that short-term ambient temperature could affect global human DNA methylation. A total of 15 candidate genes (ICAM-1, CRAT, F3, TLR-2, iNOS, ZKSCAN4, ZNF227, ZNF595, ZNF597, ZNF668, CACNA1H, AIRE, MYEOV2, NKX1-2 and CCDC15) with methylation status associated with ambient temperature have been identified. DNA methylation on ZKSCAN4, ICAM-1 partly mediated the effect of short-term cold temperature on high blood pressure and ICAM-1 protein (related to cardiovascular events), respectively. In summary, epidemiological evidence about the impacts of environment temperature on human epigenetics remains scarce and limited to short-term linear effect of cold temperature on DNA methylation in elderly people and infants. More studies are needed to broaden our understanding of temperature related epigenetic changes, especially under a changing climate.

While exposure to ambient particulate matter (PM) and nitrogen dioxide (NO₂) is thought to be associated with diseases via inflammatory response, the association between exposure to ozone, an oxidative pollutant, and inflammation has been less investigated.We analyzed associations between short-term exposure to ozone and three inflammatory biomarkers among children and adolescents.These cross-sectional analyses were based on two follow-ups of the GINIplus and LISA German birth cohorts. We included 1330 10-year-old and 1591 15-year-old participants. Fractional exhaled nitric oxide (FeNO) and high-sensitivity C-reactive protein (hs-CRP) were available for both age groups while interleukin (IL)-6 was measured at 10 years only. Maximum 8-h averages of ozone and daily average concentrations of NO₂ and PM with an aerodynamic diameter <10 μm (PM₁₀) were adopted from two background monitoring stations 0 (same day), 1, 2, 3, 5, 7, 10 and 14 days prior to the FeNO measurement or blood sampling. To assess associations, we utilized linear regression models for FeNO, and logistic regressions for IL-6 and hs-CRP, adjusting for potential covariates and co-pollutants NO₂ and PM₁₀.We found that short-term ozone exposure was robustly associated with higher FeNO in adolescents at age 15, but not at age 10. No consistent associations were observed between ozone and IL-6 in children aged 10 years. The relationship between hs-CRP levels and ozone was J-shaped. Relatively low ozone concentrations (e.g., <120 μg/m³) were associated with reduced hs-CRP levels, while high concentrations (e.g., ≥120 μg/m³) tended to be associated with elevated levels for both 10- and 15-year-old participants.Our study demonstrates significant associations between short-term ozone exposure and FeNO at 15 years of age and a J-shaped relationship between ozone and hs-CRP. The finding indicates that high ozone exposure may favor inflammatory responses in adolescents, especially regarding airway inflammation.

Metal pollution is a severe environmental issue in China, which has been recently linked with the risk of hypertension. However, relevant epidemiological studies are limited. The present exploratory study was conducted to assess the associations of environmental exposure to metals with the odds of hypertension as well as blood pressure (BP) levels using urine samples in a Chinese general population. From May 2016 to April 2017, a total of 823 eligible participants were consecutively enrolled in our study in Wuhan, China. Hypertension was defined as systolic BP (SBP) of ≥140 mmHg or diastolic BP (DBP) of ≥90 mmHg, a self-reported physician diagnosis, or current use of antihypertensive medication. We used urine samples as biomarkers to reflect the levels of environmental exposure to 20 metals. Multivariable regression models were applied to assess the potential association. Multi-metal models were conducted to investigate the impacts of co-exposure to various metals. Based on the results from various models, positive trends for increased odds of hypertension with increasing quartiles of vanadium (V), iron (Fe), zinc (Zn) and selenium (Se) were suggested. Compared with those in the lowest quartiles, participants in the highest quartiles of V, Fe, Zn and Se had a 4.4-fold, 4.9-fold, 4.2-fold and 2.5-fold increased odds of having hypertension, respectively. High urinary Hg level was found to increase the levels of DBP. Individuals in the highest group of Hg were found to have a 4.3 mmHg higher level of DBP. Our findings suggest that environmental exposure to V, Fe, Zn, Se and Hg might increase the risk of hypertension or elevate the levels of BP. These findings warrant further prospective studies in a larger population.

Acrylonitrile is a colorless volatile liquid mostly present in tobacco smoke. Acrylonitrile exposure has shown to increase oxidative stress in animal studies; however, there was no previous research in human epidemiology. In this study, 853 subjects were recruited from a cohort of Taiwanese adolescents and young adults to investigate the association between urinary concentrations of the acrylonitrile metabolite N-acetyl-S-(2-cyanoethyl)-L-cysteine (CEMA), the oxidative stress product 8-hydroxydeoxyguanosine (8-OHdG) and cardiovascular disease (CVD) risk factors. The geometric mean (SD) of CEMA and 8-OHdG concentrations were 4.67 (8.61) μg/L and 2.97 (2.14) μg/L, respectively. 10% elevated in CEMA (μg/L) was positively correlated with the change of 8-OHdG levels (μg/L) (β = 0.325, SE = 0.105, P = 0.002) in multiple linear regression analyses. The urinary CEMA was not related to other CVD risk factors. In subpopulation analyses, the association between CEMA and 8-OHdG was evident in all genders, adolescents, homeostasis model assessment of insulin resistance score ≥0.89, and environmental tobacco smokers. In this study, we observed that higher levels of CEMA levels were correlated with increased levels of 8-OHdG in this cohort. Future research on exposure to acrylonitrile and oxidative stress was warranted.

Air pollution epidemiologic and health impact studies often rely on home addresses to estimate individual subject's pollution exposure. In this study, we used detailed cell phone location data, the call detail record (CDR), to account for the impact of spatiotemporal subject mobility on estimates of ambient air pollutant exposure. This approach was applied on a sample with 9886 unique simcard IDs in Shenzhen, China, on one mid-week day in October 2013. Hourly ambient concentrations of six chosen pollutants were simulated by the Community Multi-scale Air Quality model fused with observational data, and matched with detailed location data for these IDs. The results were compared with exposure estimates using home addresses to assess potential exposure misclassification errors. We found the misclassifications errors are likely to be substantial when home location alone is applied. The CDR based approach indicates that the home based approach tends to over-estimate exposures for subjects with higher exposure levels and under-estimate exposures for those with lower exposure levels. Our results show that the cell phone location based approach can be used to assess exposure misclassification error and has the potential for improving exposure estimates in air pollution epidemiology studies.

Reduced physical performance is an important feature of aging, and walking speed is a valid measure of physical performance and mobility in older adults. Previous epidemiological studies suggest that cadmium exposure, even at low environmental levels, may contribute to vascular, musculoskeletal, and cognitive dysfunction, which may all be associated with reductions in physical performance. To this end, we investigated the associations of blood and urine cadmium concentrations with walking speed in middle-aged and older adults in the U.S. general population. We studied U.S. adults from the National Health and Nutrition Examination Survey 1999 to 2002 who were ≥50 years of age, who had determinations of cadmium in blood or in urine, and who had measurements of the time taken to walk 20 feet. Walking speed (ft/sec) was computed as walked distance (20 ft) divided by measured time to walk (in seconds). The weighted geometric means of blood and urine cadmium were 0.49 [95% confidence interval (CI): 0.47, 0.52] μg/L and 0.37 (95% CI: 0.34, 0.42) ng/mL, respectively. After adjusting for sociodemographic, anthropometric, health-related behavioral, and clinical risk factors and inflammation markers, the highest (vs. lowest) quintile of blood cadmium was associated with a 0.18 (95% CI: 0.10, 0.25) ft/sec reduction in walking speed (p-Trend <0.001). No association was observed for urine cadmium levels with walking speed. Cadmium concentrations in blood, but not in urine, were associated with slower gait speed. Our findings add to the growing volume of evidence supporting cadmium's toxicity even at low levels of exposure.