Yudan Wei

Ambient air pollution is associated with the increased incidence of breast cancer in US

Women in the United States have among the highest incidence rates of breast cancer. The reasons behind this are not fully understood. In this study we analyzed US ecological data to examine the effect of ambient air pollution on breast cancer incidence. Time trends and regional variations in breast cancer incidence were assessed in relation to emissions of air pollutants. A statistically significant increase in the incidence of female breast cancer in US was observed during 1986–2002, which could occur following the increased emissions of air pollutants as a result of industrial development and automobile use. Emissions of nitrogen oxides, carbon monoxide, sulfur dioxide, and volatile organic compounds were shown to be positively associated with breast cancer incidence with r = 0.89, 0.82, 0.71, and 0.68, respectively (p < 0.001). A higher incidence rate of breast cancer was found in high emission regions and metropolitan areas. This study suggests a possible association between air pollution and female breast cancer in US.

Rice consumption and urinary concentrations of arsenic in US adults

Exposure to inorganic arsenic in the general population occurs mainly from drinking water and food sources. This study examined the association between rice consumption and urinary concentrations of arsenic in US adults, aged 20–85 years, in the 2003–2006 National Health and Nutrition Examination Survey. Significantly higher geometric means of creatinine-corrected urinary concentrations of total arsenic (TAs) and dimethylarsinic acid (DMA) were found in participants who consumed rice more than twice per week, compared to the reference group. Multivariate logistic regression analysis revealed a statistically significant association between rice consumption and urinary concentrations of TAs [odds ratio (OR) = 1.51 (1.08, 2.09)] and DMA [OR = 2.24 (1.57, 3.21)] after adjustment for demographic variables, seafood intake (the main source of organic arsenic), and source of drinking water. Furthermore, significant variations in rice consumption and urinary concentrations of arsenic were observed in different racial groups. This study demonstrated that rice consumption contributed to inorganic arsenic exposure in US adults.

Urinary concentrations of dichlorophenol pesticides and obesity among adult participants in the U.S. National Health and Nutrition Examination Survey (NHANES) 2005–2008

Accumulating evidence from recent studies has suggested a possible link between exposure to environmental pesticides and obesity. In this study, we assessed the potential associations between exposure to dichlorophenol pesticides and obesity in adults. Study participants aged 20-85 years were selected from the 2005 to 2006 and 2007 to 2008 U.S. National Health and Nutrition Examination Survey, and were categorized as obese and non-obese based on body mass index. Creatinine-corrected urinary concentrations of dichlorophenols were determined to assess level of exposure to environmental pesticides. Multivariate logistic regression was performed using SAS 9.3 to assess the association between 2,4-dichlorophenol (2,4-DCP) and 2,5-dichlorophenol (2,5-DCP) levels in urine and obesity with adjustment for potential confounders. Significantly higher geometric means of urinary concentrations of both 2,5-DCP (p<0.0001) and 2,4-DCP (p=0.0170) were seen in obese adults, compared to that in non-obese adults. A dose-dependent increase in the prevalence of obesity was observed in the study participants across increasing levels of urinary 2,5-DCP (p-trend<0.0001). Urinary concentrations of 2,5-DCP were significantly associated with obesity among the second (AOR: 1.47, 95% CI: 1.12, 1.93), third (AOR: 1.41, 95% CI: 1.07, 1.87), and fourth (AOR: 1.62, 95% CI: 1.21, 2.17) inter-quartiles after adjustment for age, gender, race, education, total fat intake, and physical activity. A statistically significant association was not seen between urinary 2,4-DCP and obesity. Our findings suggest a potential relationship between exposure to the fumigant insecticide paradichlorobenzene, measured as urinary concentrations of 2,5-DCP, and obesity in adults. Because we cannot rule out the possibility of reverse causality in our study, prospective studies measuring exposure during etiologically relevant periods are warranted.

Fluoride Decreased Osteoclastic Bone Resorption Through the Inhibition of NFATc1 Gene Expression

Over the past two decades, fluoride effects on osteoclasts have been evaluated; however, its molecular mechanisms remain unclear. In this study, we investigated the effect of fluoride on osteoclast formation, function, and regulation using osteoclasts formed from mice bone marrow macrophages treated with the receptor activator of NF‐κB ligand and macrophage colony‐stimulating factor. Our data showed that fluoride levels ≤ 8 mg/L had no effect on osteoclast formation; however, it significantly reduced osteoclast resorption at 0.5 mg/L. Fluoride activity on bone resorption occurred through the inhibition of nuclear factor of active T cells (NFAT) c1 expression. Furthermore, the expression of its downstream genes, including the dendritic cell‐specific transmembrane protein, c‐Src, the d2 isoform of vacuolar (H+) ATPase v0 domain, matrix metalloproteinase 9, and cathepsin K were decreased, leading to impaired osteoclast acidification, reduced secretion of proteolytic enzymes, and decreased bone resorption. In summary, our results suggested that fluoride has different roles in osteoclast formation and function. Fluoride ≤ 8 mg/L did not impact osteoclast formation; however, it significantly decreased the resorption activity of newly formed osteoclasts. The molecular mechanism of fluoride action may involve inhibition of NFATc1 and its downstream genes.

The association between urinary concentrations of dichlorophenol pesticides and obesity in children.

Abstract Background: Increasing prevalence of childhood obesity has been seen in the United States and other parts of the world. Environmental chemical exposures might play a role in the worldwide obesity epidemic. Objective: This study was conducted to assess the association of exposure to environmental pesticides with childhood obesity. Methods: A total of 6770 subjects aged 6–19 years were selected from the 2003–2004 and 2005–2006 National Health and Nutrition Examination Survey (NHANES). Exposure to environmental pesticides was determined based on the concentrations of pesticide residues in urine. Multivariate logistic regression was performed using SAS 9.1.3 to assess the association between pesticide levels in urine and childhood obesity with the adjustment of potential confounders, including age, gender, race, income, and total fat intake. Results: A dose-dependent increase in prevalence of obesity was observed in the groups with inter-quartile urinary concentrations of 2,5-dichlorophenol (2,5-DCP). Logistic regression revealed a significant association between adjusted third (Q3) (AOR: 1.47; 95% CI: 1.09, 1.97) and fourth (Q4) (AOR: 1.44; 95% CI: 1.06, 1.95) inter-quartile urinary 2,5-DCP levels and childhood obesity. However, urinary concentrations of 2,4-dichlorophenol were not shown to be significantly associated with childhood obesity. Conclusion: This study suggests a possible relationship between exposure to 2,5-DCP and obesity in children.

Serum proteomic profiling analysis of chronic arsenic exposure by using SELDI-TOF-MS technology

This study was to investigate the differences in serum proteomic profiling among subjects exposed to different levels of arsenic in drinking water and to identify proteins related to arsenicosis. A total of 148 subjects from endemic regions of China were selected and divided into low (0-8.30 microg/L), medium (16.30-37.60 microg/L) and high (140.88-273.67 microg/L) exposure groups. High exposure group consisted of subjects with and without skin lesions. Serum proteomic profiling was analyzed by surface-enhanced laser desorption/ionization time-of-flight mass spectrometry (SELDI-TOF-MS) technology. Twenty proteins were found significantly different among three groups. Further multivariate logistic regression revealed that no different proteins existed in medium versus low exposure group. A panel of five proteins, including m/z of 15167.7, 7783.1, 7580.7, 2952.6 and 2237.4, was seen in high versus low exposure group, with a sensitivity of 93.0% and specificity of 87.5%. The same panel was found in high versus a combination of low and medium exposure groups but with somewhat lower predicting power. Only one protein was significantly different between high exposure group with and without skin lesions. The results indicate that high levels of arsenic exposure could significantly change human serum proteomic profiling, which can be detected before skin lesions occur.

Changes in serum thioredoxin among individuals chronically exposed to arsenic in drinking water

It is well known that oxidative damage plays a key role in the development of chronic arsenicosis. There is a complex set of mechanisms of redox cycling in vivo to protect cells from the damage. In this study, we examined the differences in the levels of serum thioredoxin1 (TRX1) among individuals exposed to different levels of arsenic in drinking water and detected early biomarkers of arsenic poisoning before the appearance of skin lesions. A total of 157 subjects from endemic regions of China were selected and divided into arsenicosis group with skin lesions (total intake of arsenic: 8.68-45.71mg-year) and non-arsenicosis group without skin lesions, which further divided into low (0.00-1.06mg-year), medium (1.37-3.55mg-year), and high (4.26-48.13mg-year) arsenic exposure groups. Concentrations of serum TRX1 were analyzed by an ELISA method. Levels of water arsenic and urinary speciated arsenics, including inorganic arsenic (iAs), monomethylated arsenic (MMA), and dimethylated arsenic (DMA), were determined by hydride generation atomic absorption spectrometry. Our results showed that the levels of serum TRX1 in arsenicosis patients were significantly higher than that of the subjects who were chronically exposed to arsenic, but without skin lesions. A positive correlation was seen between the levels of serum TRX1 and the total water arsenic intake or the levels of urinary arsenic species. The results of this study indicate that arsenic exposure could significantly change the levels of human serum TRX1, which can be detected before arsenic-specific dermatological symptoms occur. This study provides further evidence on revealing the mechanism of arsenic toxicity.

Biomarkers of renal toxicity caused by exposure to arsenic in drinking water.

This study is intended to explore effective and sensitive biomarkers for kidney damage after low level arsenic (As) exposure and to provide scientific evidence on cut-off values of arsenic concentrations in drinking water. The levels of α1-MG detected in urine samples were found to have statistically significant differences between high As group (As>0.05 mg/L) and a combination of low and medium As exposure groups (As<0.05 mg/L, p=0.018), as well as between the patient and high As groups (As in two group were both higher than 0.05 mg/L, p<0.001). After the logistic regression analysis the AUC values of α1-MG between two comparisons were 0.613 and 0.701, and p value was less than 0.05. The present data demonstrate the potential value of α1-MG excretion as a biomarker of renal toxicity, which could contribute to the enforcement of the maximum limit of 0.05 mg/L arsenic in drinking water for non-central water supply in rural areas.

PAHs and PM2.5 emissions and female breast cancer incidence in metro Atlanta and rural Georgia

Abstract Environmental chemical exposure could be an important etiologic factor for geographic differences in breast cancer incidence. In this study, we examined emissions of polycyclic aromatic hydrocarbons (PAHs) and PM2.5 in relation to breast cancer incidence in metro Atlanta and rural Georgia by analyzing data from the Surveillance, Epidemiology, and End Results Program and the Environmental Protection Agency. The results showed that metro Atlanta had a significantly higher age-adjusted annual incidence rate of female breast cancer than rural Georgia (132.6 vs. 113.7 per 100,000) for 1992–2011. Emissions of both PAHs [adjusted β = 0.568 (95 % CI: 0.209, 0.927); p = 0.004] and PM2.5 [adjusted β = 2.964 (95 % CI: 0.468, 5.459); p = 0.023] were significantly associated with breast cancer incidence in metro Atlanta area. This study suggests that ambient air pollution, especially PAHs and PM2.5, could have a significant impact on the increased incidence of female breast cancer in urban areas.

Maternal exposure to ambient PM2.5 and term low birthweight in the State of Georgia

A growing body of evidence suggests that ambient air pollution could be associated with low birthweight (LBW). In this study, we examined pregnancy exposure to ambient PM2.5 and the risk of LBW in the State of Georgia. The study population consisted of 48,172 full-term live births between 1 January 2004 and 31 December 2004 in nine counties of Georgia, which was obtained from the national natality dataset. County-level air quality index data obtained from the U.S. Environmental Protection Agency was used to estimate exposure to ambient levels of PM2.5. Multivariate logistic regression revealed that infants with maternal exposure to PM2.5 falling within 75 to < 95th percentiles were at increased risk of LBW (OR: 1.36; 95 % CI: 1.03, 1.79), after adjusting for potential confounders. This study provided more evidence on the role of PM2.5 in LBW. Reducing exposure for pregnant women would be necessary to improve the health of infants.