Acrylamide exposure and pulmonary function reduction in general population: The mediating effect of systemic inflammation.

Acrylamide exposure along with resultant potential adverse health effects have attracted global concern, and the World Health Organization calls for more and urgent studies on the health risks from acrylamide. However, the association and mechanism between acrylamide exposure and pulmonary dysfunction remain unclear. Our goals were to investigate the relationship of internal acrylamide exposure with lung function reduction, and the potential mediating role of systematic inflammation in that relationship. Our study was conducted within the Wuhan-Zhuhai cohort. Urinary biomarkers of acrylamide exposure (N-acetyl-S-(2-carbamoylethyl)-l-cysteine, AAMA; N-acetyl-S-(2-carbamoyl-2-hydroxyethyl)-l-cysteine, GAMA) and lung function were determined among 3271 general adults, of whom 2595 had test results of systemic inflammatory marker plasma C-reactive protein (CRP). We employed linear mixed models to assess the relations among urinary acrylamide metabolites, pulmonary function and plasma CRP, and PRODCLIN program to evaluate the mediating role of CRP. We observed that urinary acrylamide metabolites were inversely and dose-dependently related to lung function (P trend<0.05). Each 1-unit increment in log-transformed level of AAMA, GAMA, or AAMA+GAMA (ΣUAAM) was significantly (P < 0.05) related to a 59.9-, 64.2-, or 64.3-mL reduction in FVC, and a 53.9-, 59.7-, or 58.5-mL reduction in FEV1, respectively. Such relationships were independent of smoking, and were significant in physically inactive rather than physically active participants. AAMA (ß = 0.10), GAMA (ß = 0.16) and ΣUAAM (ß = 0.12) were significantly (P < 0.05) related to increased CRP, which was significantly (P < 0.05) related to reduced FVC (ß = -55.3) and FEV1 (ß = -40.6). We further found that increased CRP significantly (P < 0.05) mediated 6.34-11.1% of the urinary acrylamide metabolites-associated lung function reductions. For the first time, our findings suggested that exposure to acrylamide in daily life was related to reduced lung function and increased systemic inflammation in general population, and systemic inflammation further mediated acrylamide-associated lung function reduction, indicating a potential mechanistic role of systemic inflammation underlying pulmonary dysfunction from acrylamide exposure.

The association between urinary aluminum and lung function among an urban adult population: A repeated-measure longitudinal study.

OBJECTIVES: To investigate the cross-sectional and longitudinal associations between aluminum exposure and lung function and the risk of chronic obstructive pulmonary disease (COPD). METHODS: The repeated-measure study was developed with 3917 adults from the Wuhan-Zhuhai cohort and they were followed-up after 3 years and 6 years. Urinary aluminum and lung function were measured at each period. Linear mixed models were used to estimate the exposure-response relationship between urinary aluminum and lung function. COX regression models were used to evaluate the association of urinary aluminum with the risk of COPD. RESULTS: A total of 6996 observations including 2251 (32.2%) males with a mean age of 54.8 years were included. In the cross-sectional analyses, each 1-unit increase in log-transformed urinary aluminum was associated with a -33.34 mL (95% confidence interval (CI) -45.71 to -20.96) change in forced vital capacity (FVC) and a -17.89 mL (-27.80 to -7.97) change in forced expiratory volume in 1 s (FEV1). The follow-up analyses detected a negative association between urinary aluminum and the annual change of FVC (-6.73 mL/year, 95% CI -10.92 to -2.54), while the association of annual decline of FEV1 with urinary aluminum was statistically insignificant (-2.26 mL/year, -5.76 to 1.23). In the adjusted COX regression model, each 1-unit increase in log-transformed urinary aluminum was associated with a 29% increase in the incident risk of COPD (hazard ratio 1.29, 95% CI 1.04-1.62). INCLUSION: Increased urinary aluminum was associated with lung function reduction and the increased risk of COPD in a general urban population.

Sources of 24-h personal exposure to PM2.5-bound metals: results from a panel study in Wuhan, China.

Atmospheric PM2.5-bound metals have been widely addressed, but research on the exposure levels and sources of personal PM2.5-bound metals among urban community residents is limited. The aim of this study is to explore the exposure levels and sources of 24-h personal PM2.5-bound metals among community inhabitants in Wuhan, China. We conducted a penal study of 216 observations with measurements of 16 metals bounded to 24-h personal PM2.5 samples in April-May, 2014, 2017. Analyses of covariance were used to compare PM2.5-bound metal levels across different living habits and ambient conditions. Principal component analysis (PCA) with varimax rotation was performed to explore PM2.5-bound metal sources. Personal PM2.5-bound aluminum (Al) (113.41 ng/m3) showed the highest geometric mean (GM) concentration, followed by lead (Pb) (90.89 ng/m3), zinc (Zn) (67.71 ng/m3), and iron (Fe) (51.85 ng/m3). The elevated levels of PM2.5-bound Al, vanadium (V), manganese (Mn), arsenic (As), rubidium (Rb), cadmium (Cd), and thallium (Tl) were found in participants with cigarette smoke exposure, compared with those without. The concentrations of Rb and strontium (Sr) were positively associated with the time spent outdoors. The increased concentration of nickel (Ni) was found in individuals who spent > 30 min/day in traffic. The elevated levels of V, Mn, and cobalt (Co) were associated with a short distance from dwellings to the main road. The results of PCA showed that PM2.5-bound metals might come from five sources: As, selenium (Se), Rb, Cd, Tl, and Pb from cigarette smoke exposure; Al, V, Mn, Fe, and Sr from crustal dust; copper (Cu) and antimony (Sb) from industrial activities; Ni and Co from traffic emission; and Zn from coal combustion. The concentrations of PM2.5-bound metals in this study were at moderate levels. Cigarette smoke exposure, industrial activities, traffic emission, and coal combustion might be major anthropogenic sources of personal PM2.5-bound metal exposures in Wuhan, China.

Polycyclic aromatic hydrocarbon exposure and atherosclerotic cardiovascular disease risk in urban adults: The mediating role of oxidatively damaged DNA.

Polycyclic aromatic hydrocarbon (PAH) exposure has been considered a risk factor for cardiovascular diseases (CVD), whereas possible mechanisms for this association have not been fully understood. This study focused on exploring the potential effect of oxidatively damaged DNA on the relationships between PAH exposure and the 10-year atherosclerotic CVD (ASCVD) risk. Urinary levels of monohydroxy PAH metabolites (OH-PAHs) and 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG, the typical biomarker for oxidatively damaged DNA) were measured among 3052 subjects in the baseline of the Wuhan-Zhuhai cohort. The relationships between urinary OH-PAHs, 8-oxodG and 10-year risk of ASCVD were analyzed by linear mixed models and logistic regression models, respectively. The mediation analysis was further applied to explore the role of 8-oxodG in the relationship between urinary OH-PAHs and 10-year ASCVD risk. After controlling for potential confounders, the log-transformed level of total urinary low molecular weight OH-PAHs (∑LMW OH-PAHs) was significantly associated with an elevated risk of 10-year ASCVD [odds ratio (OR) = 1.222, 95% confidence interval (CI): 1.065-1.402]. More specifically, significantly positive dose-response relationships between total urinary hydroxynaphthalene (∑OHNa), hydroxyfluorene (∑OHFlu), hydroxyphenanthrene (∑OHPh) and 10-year ASCVD risk were observed (all P for trend <0.05). We also found positive relationships between urinary OH-PAH levels and 8-oxodG, as well as between urinary 8-oxodG levels and 10-year risk of ASCVD. Moreover, mediation analyses indicated that urinary 8-oxodG mediated 14.49%, 12.62% and 10.55% of the associations between urinary ∑LMW OH-PAHs, ∑OHNa, ∑OHFlu and 10-year ASCVD risk, respectively. These findings suggest that the oxidatively damaged DNA pathway may be a possible mechanism underlying PAH-associated ASCVD risk elevation.

Exposure to acrylamide and reduced heart rate variability: The mediating role of transforming growth factor-ß.

The potential adverse health effects of acrylamide have drawn worldwide attention and the World Health Organization has urged further urgent studies on its health threat. Herein we explored the exposure-response relationship and underlying mechanism between internal acrylamide exposure and heart rate variability (HRV) alteration, a marker of cardiac autonomic dysfunction. We measured six HRV indices and two urinary acrylamide metabolites (N-Acetyl-S-(2-carbamoylethyl)-l-cysteine, AAMA; N-Acetyl-S-(2-carbamoyl-2-hydroxyethyl)-l-cysteine, GAMA) for 2997 general Chinese adults from the Wuhan-Zhuhai cohort, of whom 2414 had data on plasma transforming growth factor-ß1 (TGF-ß1). The associations among urinary acrylamide metabolites, HRV and TGF-ß1 were evaluated by linear mixed models and restricted cubic spline models. The mediating role of TGF-ß1 was investigated by conducting mediation analysis. We found significantly negative dose-response relationships of all urinary acrylamide metabolites and TGF-ß1 with all six HRV indices after adjusting for potential confounders (all P < 0.05). Urinary GAMA (ß=0.074, P < 0.05) rather than AAMA (ß=0.024, P > 0.05) was positively and dose-dependently associated with TGF-ß1, which in turn significantly mediated 5.71-7.41 % of the GAMA-associated HRV reduction. Our findings suggest for the first time that daily exposure of general population to acrylamide is associated with cardiac autonomic dysfunction, where a mechanism involving TGF-ß pathway may be involved.

The trends of mortality and years of life lost of cancers in urban and rural areas in China, 1990-2017.

BACKGROUND: With the rapid development of the socioeconomic status, the mortality of several cancers has been changed in China during the past 30 years. We aimed to estimate the trends of mortality and years of life lost (YLLs) of various cancers in urban and rural areas of China from 1990 to 2017. METHODS: The mortality data were collected from Chinese yearbooks and the age structure of population from the Chinese sixth population census were used as reference to calculate age-standardized mortality rates (ASMRs) and YLLs rates. Joinpoint regression analysis was implemented to calculate the annual percent change (APC) of mortality rates and YLL rates for cancers. YLLs owing to premature death were calculated as age-specific cancer deaths multiplied by the reference life expectancy at birth of 80 years for male and 82.5 years for female. RESULTS: The ASMRs of all cancers showed significant decreasing trends for urban residents from 1990 to 2017, such downward trend without significance was also observed among rural residents. Interestingly, ASMRs of lung cancer and breast cancer have raised continuously in rural areas since 1990. The age-standardized YYL rates for urban and rural residents decreased with 1.02% and 0.85% per year, respectively. YLLs in rural areas were higher than those in urban areas, whereas YLLs of urban outstripped those of rural finally with the increasing in YLLs of urban areas (216.71% for men and 207.87% for women). CONCLUSION: The ASMRs and YLL rates of all cancers have declined in urban and rural areas from 1990 to 2017. YLLs increased in urban areas and remained higher level in rural areas after 2014 year. Preventive measures should be strengthened to against cancer, especially for lung cancer.

Association between urinary polycyclic aromatic hydrocarbon metabolites and dyslipidemias in the Chinese general population: A cross-sectional study.

BACKGROUND: Exposure to polycyclic aromatic hydrocarbons (PAHs) has been associated with metabolic diseases. However, relationships between PAH exposures and dyslipidemias have not been well addressed. OBJECTIVES: To investigate associations between urinary PAH metabolite concentrations and dyslipidemias in the general population. METHODS: Twelve urinary PAH metabolites and four serum lipid profiles were measured in 3640 Chinese adults from the Wuhan-Zhuhai cohort. Dyslipidemias, including hyper-total cholesterol (HyperTC), hyper-triglyceride (HyperTG), hyper-low density lipoprotein cholesterol (HyperLDL-C), and hypo-high density lipoprotein cholesterol (HypoHDL-C) were classified according to the levels of serum lipids. Multiple logistic regression models were used to estimate the associations between urinary PAH metabolites and the prevalence of dyslipidemias. The effects of PAH exposure routes on dyslipidemias were further estimated by stratified analysis. RESULTS: We found positive exposure-response relationships between urinary PAH metabolites and the prevalence of dyslipidemias. Compared with the lowest tertile of urinary PAH metabolites, increased risk of HyperTC were observed in those in the highest tertiles; The odds ratios (ORs) and 95% confidence intervals were 1.23 (1.03, 1.47), 1.44 (1.21, 1.71), 1.19 (1.01, 1.42), and 1.43 (1.20, 1.71) for 1-OHNa, 9-OHFlu, 1-OHPh, and 4-OHPh, respectively. Participants in the highest tertiles of 1-OHNa and 2-OHFlu had higher risk for HyperLDL-C, and the ORs were 1.21 (1.01, 1.45) and 1.18 (0.98, 1.42), respectively. Among smokers, only urinary 1-OHNa was associated with increased risk of HyperTC (1.36, 1.08-1.73) and HyperLDL-C (1.33, 1.01-1.74). While the increasing urinary levels of 9-OHFlu, 1-OHPh, and 4-OHPh were significantly associated with increased risk of HyperTC among non-smokers. In addition, the associations between urinary PAH metabolites and dyslipidemias were more pronounced among non-smokers who are cooked for themselves and had long-term traffic exposure. CONCLUSION: Elevated urinary PAH metabolites were associated with increased risks of HyperTC and HyperLDL-C. The source of PAH exposure could modify PAH species that affect dyslipidemias.