The link between zinc exposure and glucose metabolism or the development of type 2 diabetes (T2D) is controversial, and underlying mechanisms are unclear. This study aimed to explore the associations of zinc exposure with glucose-insulin homeostasis traits and the long-term effects of zinc on the development of T2D, and further to estimate the potential roles of inflammation and oxidative damage in such relationships. We investigated 3890 urban adults from the Wuhan-Zhuhai cohort, and followed up every three years. Mixed linear model was applied to estimate dose-response associations between urinary zinc and glycemia traits [fasting plasma insulin (FPI), fasting plasma glucose (FPG), insulin resistance (homeostasis model assessment of insulin resistance, HOMA-IR), and β-cell dysfunction (homeostasis model assessment of β-cell function, HOMA-B)], as well as zinc and biomarkers for systemic inflammation (C-reactive protein) and oxidative damage (8-isoprostane and 8-hydroxy-2′-deoxyguanosine). Logistic regression model and Cox regression model were conducted to evaluate the relationships between urinary zinc and prevalence and incidence of T2D, respectively. We further performed mediation analysis to assess the roles of inflammation and oxidative damage biomarkers in above associations. At baseline, we observed significant dose-response relationships of elevated urinary zinc with increased FPI, FPG, HOMA-IR, and T2D prevalence and decreased HOMA-B, and such associations could be strengthened by increased C-reactive protein, 8-isoprostane, and 8-hydroxy-2′-deoxyguanosine. Elevated C-reactive protein significantly mediated 9.09% and 17.67% of the zinc-related FPG and HOMA-IR increments, respectively. In longitudinal analysis, a significantly positive association between urinary zinc and T2D incidence was observed among subjects with persistent high urinary zinc levels when compared with those with persistent low zinc levels. Our results suggested that high levels of zinc exposure adversely affected on glucose-insulin homeostasis and further contributed to increased risk of T2D cross-sectionally and longitudinally. Moreover, inflammatory response might play an important role in zinc-related glucose metabolic disorder.

There is growing interest in understanding the contribution of environmental toxicant exposure in early life to development of cardiometabolic diseases (CMD) in adulthood. We aimed to assess associations of early life exposure to arsenic and cadmium with biomarkers of CMD in children in rural Bangladesh. From a longitudinal mother-child cohort in Matlab, Bangladesh, we followed up 540 pairs. Exposure to arsenic (U–As) and cadmium (U–Cd) was assessed by concentrations in urine from mothers at gestational week 8 (GW8) and children at ages 4.5 and 9 years. Blood pressure and anthropometric indices were measured at 4.5 and 9 years. Metabolic markers (lipids, glucose, hemoglobin A1c, adipokines, estimated glomerular filtration rate (eGFR) were determined in plasma/blood of 9 years old children. In linear regression models, adjusted for child sex, age, height-for-age z score (HAZ), BMI-for-age z score (BAZ), socioeconomic status (SES) and maternal education, each doubling of maternal and early childhood U–Cd was associated with 0.73 and 0.82 mmHg increase in systolic blood pressure (SBP) respectively. Both early and concurrent childhood U–Cd was associated with diastolic (D)BP (β = 0.80 at 4.5 years; β = 0.75 at 9 years). Each doubling of U–Cd at 9 years was associated with decrements of 4.98 mg/dL of total cholesterol (TC), 1.75 mg/dL high-density lipoprotein (HDL), 3.85 mg/dL low-density lipoprotein (LDL), 0.43 mg/dL glucose and 4.29 units eGFR. Each doubling of maternal U–Cd was associated with a decrement of 1.23 mg/dL HDL. Both maternal and childhood U–As were associated with decrement in TC and HDL. Multiple comparisons were checked with family-wise error rate Bonferroni-type-approach. The negative associations of arsenic and cadmium with biomarkers of CMD in preadolescent children indicated influence of both metal(loid)s on fat and carbohydrate metabolism, while cadmium additionally influenced kidney function and BP. Thus, fewer outcomes were associated with U–As compared to U–Cd at preadolescence.

Urban environments are characterized by multiple exposures that may influence body mass index (BMI) growth in early life. Previous studies are few, with inconsistent results and no evaluation of simultaneous exposures. Thus, this study aimed to assess the associations between exposure to air pollution, green spaces and built environment characteristics, and BMI growth trajectories from 0 to 5 years. This longitudinal study used data from an electronic primary care health record database in Catalonia (Spain), including 79,992 children born between January 01, 2011 and December 31, 2012 in urban areas and followed until 5 years of age. Height and weight were measured frequently during childhood and BMI (kg/m²) was calculated. Urban exposures were estimated at census tract level and included: air pollution (nitrogen dioxide (NO₂), particulate matter <10 μm (PM₁₀) and <2.5 μm (PM₂.₅₎), green spaces (Normalized Difference Vegetation Index (NDVI) and % green space) and built environment (population density, street connectivity, land use mix, walkability index). Individual BMI trajectories were estimated using linear spline multilevel models with several knot points. In single exposure models, NO₂, PM₁₀, PM₂.₅, and population density were associated with small increases in BMI growth (e.g. β per IQR PM₁₀ increase = 0.023 kg/m², 95%CI: 0.013, 0.033), and NDVI, % of green spaces and land use mix with small reductions in BMI growth (e.g. β per IQR % green spaces increase = −0.015 kg/m², 95%CI: −0.026, −0.005). These associations were strongest during the first two months of life. In multiple exposure models, most associations were attenuated, with only those for PM₁₀ and land use mix remaining statistically significant. This large longitudinal study suggests that early life exposure to air pollution, green space and built environment characteristics may be associated with small changes in BMI growth trajectories during the first years of life, and that it is important to account for multiple exposures in urban settings.

Evaluate the relationship between arthritis diagnosis in those over 50 and exposure to extreme air pollution in utero or infancy (<1 year of age).Compare rates of arthritis diagnosis between groups that experienced differential air pollution exposure in early-life due to quasi-random variation in birth location and date relative to the 1952 Great Smog in London. We use regression-estimated difference-in-differences analyses based on English Longitudinal Study of Aging (ELSA) data.In the 2816 respondent sample, aged 51–62, the arthritis diagnosis rate is 22.8%, with 16.4% reporting osteoarthritis and 4.6% reporting rheumatoid arthritis. We estimate that exposure to the Great Smog in infancy increases the arthritis diagnosis rate by 23.4 percentage points (95% CI: 1.97 to 44.8). Decomposing these results by type of arthritis reveals that the rheumatoid arthritis diagnosis rate increases due to infant exposure are larger and more significant than those for osteoarthritis: 14.9 percentage points (95% CI: 0.495 to 29.4) versus 9.5 percentage points (95% CI: −11.9 to 30.8). In utero exposure is not associated with significant increases in arthritis diagnosis rates.Our results are the first to link early-life air pollution exposure to later-life arthritis diagnoses, and suggest a particularly strong link for RA. These findings are consistent with those of shorter-term, correlational studies, and indicate that health effects of air pollution exposure can span decades and extend beyond cardiopulmonary systems.

Triclosan (TCS) is a suspected endocrine disrupting chemical which is widely used in consumer products as an antibacterial agent. But findings in human studies focusing on the fetal developmental effects of prenatal TCS exposure were rare and inconsistent. This study aimed to determine maternal urinary TCS and investigate its association with birth outcomes. Pregnant women (n = 1006) were randomly selected from the prospective Healthy Baby Cohort (HBC) enrolled in 2014. TCS levels were determined in maternal urine samples collected at delivery and recorded birth outcomes were obtained from the medical records. Multiple linear regressions were applied to evaluate associations of maternal urinary TCS levels with birth outcomes including birth weight, birth length, and gestational age. Logistic regressions were used to evaluate associations with preterm birth, late term birth, and low birth weight. The geometric mean concentrations for TCS and specific gravity (SG) adjusted TCS in maternal urines were 0.73, 0.78 ng/mL, respectively. In the crude model, one ln-unit increase of urinary SG-adjusted TCS concentration was associated with a 0.30-day [95% confidence interval (CI): 0.00, 0.60] increase in gestational age; however, the associations were not statistically significant after adjustment for covariates. No significant associations of SG-adjusted TCS concentrations with birth weight and birth length were observed. Maternal SG-adjusted TCS concentrations were not related to preterm birth, late term birth, and low birth weight (all p > 0.10). Our findings reported a relatively low level of TCS among Chinese pregnant women. With such exposure level, we did not find strong evidence for associations between maternal TCS exposure and birth outcomes. Longitudinal studies concerning about different potential effects of TCS on perinatal health are necessary.

Traffic noise stresses and disturbs sleep. It has been associated with various diseases, and has recently also been associated with lifestyle. Hence, the association between traffic noise and disease could partly operate via a pathway of lifestyle habits, including smoking and alcohol intake.We investigated associations between modelled residential traffic noise and smoking habits and alcohol consumption.In a cohort of 57,053 participants, we performed cross-sectional analyses using data from a baseline questionnaire (1993-97), and longitudinal analyses of change between baseline and follow-up (2000-02). Smoking status (never, former, current) and intensity (tobacco, g/day) and alcohol consumption (g/day) was self-reported at baseline and follow-up. Address history from 1987-2002 for all participants were found in national registries, and road traffic and railway noise was modelled 1 and 5 years before enrolment, and from baseline to follow-up. Analyses were performed using logistic and linear regression, and adjusted for demographics, socioeconomic variables, leisure-time sports, and noise from the opposite source (road/railway).Road traffic noise exposure 5 years before baseline was positively associated with alcohol consumption (adjusted difference per 10 dB: 1.38 g/day, 95% confidence interval (CI): 1.10–1.65), smoking intensity (adjusted difference per 10 dB: 0.40 g/day, 95% CI: 0.19–0.61), and odds for being a current vs. never/former smoker at baseline (odds ratio (OR): 1.14; 95% CI: 1.10–1.17). In longitudinal analyses, we found no association between road traffic noise and change in smoking and alcohol habits. Railway noise was not associated with smoking habits and alcohol consumption, neither in cross-sectional nor in longitudinal analyses.The study suggests that long-term exposure to residential road traffic is associated with smoking habits and alcohol consumption, albeit only in cross-sectional, but not in longitudinal analyses.

The negative health effects of water pollution remain a major source of morbidity and mortality in China. The Chinese government is making great efforts to strengthen water environment treatment; however, no studies have evaluated the effects of water treatment on human health by water pollution in China. This study evaluated the association between water pollution and health outcomes, and determined the extent to which environmental regulations on water pollution may lead to health benefits. Data were extracted from the 2011 and 2013 China Health and Retirement Longitudinal Study (CHARLS). Random effects model and random effects Logit model were applied to study the relationship between health and water pollution, while a Mediator model was used to estimate the effects of environmental water treatment on health outcomes by the intensity of water pollution. Unsurprisingly, water pollution was negatively associated with health outcomes, and the common pollutants in industrial wastewater had differential impacts on health outcomes. The effects were stronger for low-income respondents. Water environment treatment led to improved health outcomes among Chinese people. Reduced water pollution mediated the associations between water environment treatment and health outcomes. The results of this study offer compelling evidence to support treatment of water pollution in China.

Type 2 Diabetes (T2D) and particulate air pollution are associated with inflammatory dysregulation. We assessed the modifying effects of diabetes medications on the association of C-reactive protein (CRP), a marker of inflammation, and traffic exposure in adults with T2D (n = 379). CRP concentrations were significantly positively associated with residence ≤100 m of a roadway, >100 m and ≤200 m of a roadway and increased traffic density for individuals using insulin. For individuals using oral hypoglycemic medications (OHAs), CRP was significantly negatively associated with residence >100 m – ≤200 m of a roadway and multiple roadway exposure in an interaction model. Among people with diabetes, individuals on insulin appear to be most vulnerable to the effects of traffic exposure. Disease severity among insulin users may promote the pro-inflammatory response to traffic exposure, though diabetes medications may also modify the response. Possible anti-inflammatory effects of OHAs with traffic exposure merit further evaluation.

We used real-world exposure scenarios to evaluate the effect of six ambient air pollutant (PM₂.₅, PM₁₀, NO₂, SO₂, CO, and O₃) exposure on renal function among older adults without chronic kidney disease (CKD). We recruited 169 older adults without CKD in Beijing, China, for a longitudinal study from 2016 to 2018. The Modification of Diet in Renal Disease (MDRD) and the Chronic Kidney Disease Epidemiology Collaboration (EPI) equations were employed to derive the estimated glomerular filtration rate (eGFR). A linear mixed-effects model with random intercepts for participants was employed to determine the effects of air pollutants on renal function evaluated on the basis of eGFR and urinary albumin/creatinine ratio at different exposure windows (1-, 2-, 3-, 5-, 7-, 14-, 28-, 45-, and 60-days moving averages). An interquartile range (IQR) increase in NO₂ for was associated with significant decreases of in eGFR (MDRD equation) [percentage changes: −4.49 (95% confidence interval: −8.44, −0.37), −5.51 (−10.43, −0.33), −2.26 (−4.38, −0.08), −3.71 (−6.67, −0.65), −5.44 (−9.58, −1.11), −5.50 (−10.24, −0.51), −6.15 (−10.73, −1.33), and −6.34 (−11.17, −1.25) for 1-, 2-, 5-, 7-, 14-, 28-, 45-, and 60-days moving averages, respectively] and in eGFR (EPI equation) [percentage changes: −5.04 (−7.09, −2.94), −6.25 (−8.81, −3.62), −5.16 (−7.34, −2.92), −5.10 (−7.85, −2.28), −5.83 (−8.23, −3.36), −6.04 (−8.55, −3.47) for 1-, 2-, 14-, 28-, 45-, and 60-days moving averages, respectively]. In two-pollutant model, only the association of NO₂ exposure with eGFR remained robust after adjustment for any other pollutant. This association was stronger for individuals with hypertension for the EPI equation or BMI <25 kg/m² for the MDRD equation at lags 1 and 1–2. Our findings suggest that NO₂ exposure is associated with eGFR reduction among older adults without CKD for short (1-, 2-days) and medium (14-, 28-, 45-, 60-days) term exposure periods; thus, NO₂ exposure may contribute to renal impairment.

Evidence of the effects of long-term household air pollution (HAP) on human mental health is limited. This study aimed to explore the longitudinal relationship between long-term household air pollution exposure from solid fuel use and depression based on nationally representative follow-up dataset. A total of 7005 middle- and old-age adults from the latest four waves (2011, 2013, 2015, and 2018) of China Health and Retirement Longitudinal Study (CHARLS) were involved. The Center for Epidemiologic Studies Depression scale (CES-D 10) was used to measure depressive symptoms and individuals who got more than 12 points were considered to have depression symptoms. We conducted Cox proportional hazards regression models to examine the association between household air pollution and depression in overall population, and subgroup stratified by socio-demographic factors, lifestyle behaviors, chronic diseases, and residential environments. We found long-term household air pollution exposure from solid fuel use was significantly associated with higher depression risk among Chinese older adults (HR 1.27, 95% CI 1.14–1.42 in heating; 1.26, 1.13–1.40 in cooking). Longer duration of household air pollution exposure (1.47, 1.28–1.68 in heating; 1.36, 1.19–1.56 in cooking) and household air pollution from crop residue/wood burning (1.66, 1.41–1.94 in heating; 1.37, 1.23–1.53 in cooking) was correlated with higher depression risk. For subgroups analysis, the effect of household air pollution from solid fuel on depression varied. Compared with those who using clean fuel, older adults living in small size houses or houses with small number rooms had increasing depression risks if they used solid fuel for heating or cooking. Our findings indicate long-term household air pollution exposure from solid fuel use is associated with higher depression risk. Reducing household air pollution by restricting solid fuel use can be effective ways to prevent depression for Chinese older adults and decrease related public health burden.