Plasma and water fluoride levels and hyperuricemia among adolescents: A cross-sectional study of a nationally representative sample of the United States for 2013-2016.

Exposure to excessive fluoride has been associated with a number of adverse health outcomes; however, there is a lack of evidence on the relation between fluoride exposure and serum uric acid levels, especially in human populations. The present study examined a potential relationship between fluoride exposure, measured as both plasma and water fluoride concentrations, and uric acid levels in an adolescent population. A nationally representative subsample of 1933 adolescents, aged 12-19 years, in the 2013-2016 National Health and Nutrition Examination Survey was analyzed for the association of fluoride concentrations with serum uric acid levels using multivariate general linear and logistic regression models, adjusting for potential confounders. Since uric acid levels change during development, hyperuricemia was defined in this study as over the mean plus one standard deviation for each sex and age group of adolescents. Of the study participants, 276 adolescents (weighted prevalence, 16.56%) had hyperuricemia. A significant and dose-dependent increase in prevalence of hyperuricemia was seen among the participants cross increasing quartiles of plasma fluoride (p-trend = 0.0017). After adjusting for potential confounders, we found that adolescents in the higher quartiles of plasma fluoride (≥0.32 µmol/L) and in the highest quartile of water fluoride (≥0.73 mg/L) had significantly increased odds of hyperuricemia compared with those in the lowest quartile. A 1.95-fold increased odds (95% CI: 1.37, 2.77) of hyperuricemia was also observed when analyzing plasma fluoride concentrations as continuous variable. A general linear model revealed that a 1 µmol/L increase in ln-plasma fluoride was associated with a 0.212 mg/dL (p < 0.0001) increased serum uric acid level. Furthermore, a positive relationship was observed between water and plasma fluoride concentrations (ß = 0.1907; p < 0.0001). Our study demonstrates a potential relation between fluoride exposure and hyperuricemia in adolescents. Further studies are warranted to overcome the limitations of this study to examine the impact of long-term exposure to low levels of fluoride during development on hyperuricemia and its related health outcomes.

Pet ownership and risk of dying from cancer: observation from a nationally representative cohort.

We longitudinally examined the relationship between pet ownership and risk of dying from cancer in a nationally representative cohort of 13,725 adults in the Third National Health and Nutrition Examination Survey, 1988-1994. The vital status was followed through 31 December 2010. Women who owned pets (any type) presented one-year shorter survival time (15.88 years) than non-pet owner (16.83 years). A larger difference of survival time was particularly seen in bird owners (13.01 years) compared to non-bird owners (16.82 years). After adjusting for potential confounders, hazard ratio (HR) of dying from cancer associated with any type of pets was 1.08 (95% CI = 0.77-1.50) for men and 1.40 (1.01-1.93) for women. The association in women was presumably driven by owning birds [HR 2.41 (1.34-4.31)] or cats [HR 1.48 (0.97-2.24)]. Keeping birds and cats in the household was associated with an increased risk of dying from cancer, especially in women.

Pet ownership and the risk of dying from lung cancer, findings from an 18 year follow-up of a US national cohort.

PURPOSE: In contrast to the popularity of pets, research on the health effects of living with pets, particularly, on the risk of cancer, is minimal and inconclusive. We longitudinally examined relationships between pet ownership and the risk of dying from lung cancer. METHODS: We analyzed nationally representative data of 13,725 adults aged ≥ 19 who answered the question about pet ownership in the Third National Health and Nutrition Examination Survey, 1988-1994, as the baseline survey. Vital status was followed through December 31st, 2010. RESULTS: About 43% of the study population owned pets, with 20.4% having cats and 4.6% having birds. A total of 213 lung cancer deaths were recorded by the end of 183,094 unweighted person-years of follow-up with a lung-cancer specific death rate of 1.00 per 1000 person-years. After adjustment for cigarette smoking, alcohol drinking, physical activity, body mass index, history of atopic conditions, and serum cotinine, owning a pet (any) was associated with a doubled mortality rate among women for lung cancer [hazard ratio (HR)= 2.31 (1.41-3.79)] over non-owners. This association was largely attributed to having a cat or a bird. The HR was 2.85 (1.62-5.01) for cats, and 2.67 (0.68-10.5) for birds. The HR for dogs was 1.01 (0.57-1.77). No significant patterns of association were observed among men either for any pets or for a subtype of pet. CONCLUSIONS: Living with a pet, especially, a cat or a bird, was significantly associated with elevated hazard of dying from lung cancer among women. The detrimental effect that pets conferred was not explained by confounding from cigarette smoking or atopic conditions.

Endocrine-disrupting metals in ambient air and female breast cancer incidence in US.

Metals could act as endocrine disruptors that mimic the actions of hormones, such as estrogens, and contribute to the development and progression of breast cancer. In this study, we examined the association between ambient air emissions of several endocrine-disrupting metals and the incidence of female breast cancer in the United States by analyzing county-level data from national datasets. Linear regression analysis was conducted to evaluate the association in unadjusted and adjusted models. Of the metals analyzed, air emissions of arsenic, cadmium, lead, and mercury, but not chromium VI, were significantly associated with the incidence of all breast cancers, after adjusting for potential confounders. Emissions of arsenic, lead, and mercury were found to be significantly associated with the incidence of estrogen receptor (ER)-positive breast cancer. Among these metals, air emissions of lead showed the strongest association with breast cancer incidence with the ß of 3756.66 (95% CI: 1660.29, 5853.03) for all breast cancers and 2433.85 (440.59, 4427.10) for ER-positive breast cancer. Our results demonstrate that exposure to endocrine-disrupting metals in ambient air may be associated with an increased incidence of breast cancer in the United States. Further studies are needed to explore these interactions and to elucidate mechanisms of action.

Para-Dichlorobenzene Exposure Is Associated with Thyroid Dysfunction in US Adolescents.

OBJECTIVE: To examine the association between exposure to para-dichlorobenzene, measured as urinary concentrations of 2,5-dichlorophenol (2,5-DCP), and thyroid function in US adolescents. STUDY DESIGN: A nationally representative subsample of 618 adolescents aged 12-19 years in the 2007-2008 and 2011-2012 National Health and Nutrition Examination Survey was analyzed for the association of urinary 2,5-DCP with serum thyroid function measures using multivariate logistic and general linear regression models. RESULTS: After adjusting for potential confounders, we found a significantly positive association between urinary concentrations of 2,5-DCP and serum levels of thyroid-stimulating hormone and thyroglobulin in adolescents. Furthermore, urinary 2,5-DCP was associated with an increased prevalence of hypothyroidism in the study population. CONCLUSIONS: This study demonstrates a potential relationship between para-dichlorobenzene exposure, measured as urinary 2,5-DCP, and thyroid dysfunction in adolescents; however, further studies are needed to confirm our findings and to elucidate mechanisms of action.

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.

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

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 ß = 0.568 (95 % CI: 0.209, 0.927); p = 0.004] and PM2.5 [adjusted ß = 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.

Decreased number of CD14+TLR4+ monocytes and their impaired cytokine responses to lipopolysaccharide in patients with chronic kidney disease.

This study aimed to examine the number of circulating Toll-like receptor 4 (TLR4) + CD14+ monocytes in patients with different stages of chronic kidney disease (CKD), their responses to lipopolysaccharide (LPS), and to explore the potential association of the number of TLR4+CD14+ monocytes with clinical laboratory measures. The numbers of TLR4+CD14+, LPS-stimulated TNF-α+CD14+ and interleukin (IL)-6+CD14+ monocytes were determined by flow cytometry in 9 patients with stage 3 CKD, 11 with stage 4 CKD, 16 with stage 5 CKD, and 19 healthy controls (HCs). Their laboratory tests were performed by routine methods and the potential association among these measures was analyzed by Pearson's correlation analysis. The numbers of CD14+, CD14+TLR4+, LPSstimulated TNF-α+CD14+ and IL-6+CD14+ monocytes in patients with CKD were significantly less than those of HCs (all P<0.05), and were negatively associated with patient disease severity. The number of CD14+TLR4+ monocytes was positively correlated with estimated glomerular filtration rate (eGFR, P<0.001) and the levels of hematocrit (P<0.01), but negatively correlated with the levels of blood urine nitrogen, serum creatinine, and C-reactive protein (P<0.001 for all), in the CKD patients. Our data indicate that significant reduction in the number of TLR4+ monocytes and their impaired responses to LPS may be associated with the progression of CKD in Chinese patients.

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.

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.

Exposure to p-dichlorobenzene and serum α-Klotho levels among US participants in their middle and late adulthood.

P-dichlorobenzene (p-DCB) is a volatile compound commonly used as pest repellent and air deodorant in the home and public buildings, leading to a widespread exposure in indoor environments. There has been an increasing concern about its metabolic and endocrine effects. In this study, we explored the relation between p-DCB exposure and serum levels of soluble α-Klotho, an anti-aging hormone, in US adults. A nationally representative subsample of 1485 adults 40-79 ages in the 2013-2016 National Health and Nutrition Examination Survey was analyzed for the association between p-DCB exposure, measured as urinary concentrations of 2,5-dichlorophenol (2,5-DCP), the major metabolite of p-DCB, and serum α-Klotho levels using multiple general linear models, adjusting for potential confounders. Age- and sex-specific analyses were further conducted. The weighted geometric mean of urinary 2,5-DCP was 2.43 µg/L and the weighted mean of serum α-Klotho was 831.97 pg/mL in the study participants during 2013-2016. After adjusting for potential confounders and urinary creatinine, urinary 2,5-DCP was significantly associated with decreased serum levels of α-Klotho (regression coefficient ß = -9.88; p = 0.0133) in the total study population. When age- and sex-specific analyses being conducted, a significantly inverse association was found in older adults aged 60-79 years (ß = -20.40; p = 0.0001) and in males (ß = -13.81; p = 0.0097), but not in the middle ages (40-59 years) and in females. The strongest association was observed in older (60-79 years) male participants, with a 25.43 pg/mL reduction of α-Klotho levels per 1-unit increase of 2,5-DCP concentrations (p = 0.0008). This is the first study demonstrating a relation between p-DCB exposure, measured as 2,5-DCP, and decreased α-Klotho levels in older males. Additional studies would further explore these interactions and elucidate the pathogenesis of the potential effects of p-DCB exposure on aging.

Urinary Concentrations of Endocrine-Disrupting Metals and Prevalent Breast Cancer in US Women.

The toxic metals cadmium, lead, and mercury are endocrine-disrupting agents that could produce estrogenic effects involving breast carcinogenesis. In this study, we further explored the relationship between exposure to these metals and prevalent breast cancer among female participants, aged 20 years or older, in the 2007-2016 National Health and Nutrition Examination Survey (NHANES). Exposure was determined by measuring urinary concentrations of metals using inductively coupled plasma mass spectrometry. Urine creatinine-corrected concentrations of metals were calculated for each study participant. Multivariate logistic regression models were constructed to examine the association between urinary metals and prevalent breast cancer, adjusting for potential confounders. Of the 3352 study participants, 106 had been diagnosed with breast cancer (weighted prevalence, 3.13%). The results show that women with breast cancer had significantly higher urinary concentrations of lead and cadmium (both p < 0.0001) than those without breast cancer. After adjusting for all the covariates included in the study, however, only urinary lead was shown to be significantly associated with increased prevalence of breast cancer, with an odds ratio of 2.95 (95% CI: 1.13, 7.70) in the highest quartile of urinary lead concentrations (≥ 0.71 µg/g creatinine) as compared with the lowest quartile. No statistically significant associations were observed between urine cadmium or mercury levels and breast cancer. This study demonstrates a potential association between lead exposure and prevalent breast cancer among US women. Prospective and mechanistic studies are warranted to further investigate this interaction and explore the role of lead in breast carcinogenesis.

Exposure to endocrine-disrupting metals and serum estrogen levels among US women.

Multiple factors could affect estrogen levels in the body; however, the impact of exposure to endocrine-disrupting chemicals on estrogen levels in humans remains inconclusive. This cross-sectional study was to assess the association between blood levels of endocrine-disrupting metals (including cadmium, lead, and mercury) and serum estradiol levels in 1618 women (aged ≥ 20 years) who participated in the 2013-2016 National Health and Nutrition Examination Survey. Using multiple general linear models, we estimated percent changes of estradiol levels in association with blood metal concentrations. Age-specific analysis was further conducted. The median level of blood cadmium, lead, and mercury was 0.31 µg/L (range: 0.07-7.23), 0.76 µg/dL (0.11-12.80), and 0.73 µg/L (0.20-36.90), respectively, and the median estradiol level was 31.10 pg/mL (range: 2.12-523.00) among women aged 20-80 years. After adjusting for potential confounders, a 10 % increase in blood cadmium and lead levels was associated with 1.43 % (95 % CI: 0.50, 2.37) increased levels and 1.45 % (- 2.17, - 0.11) decreased levels of estrogen, respectively, in the total study population. When stratified by age, the positive association with cadmium was only seen in women aged 20-49 years [1.47 % (0.39, 2.56) increased estradiol] and the inverse association with lead was seen among women aged 50-80 years [3.40 % (- 4.78, - 2.00) decreased estradiol]. Mercury was not significantly associated with estrogen levels. Our study demonstrates a potential relationship between exposure to endocrine-disrupting cadmium and lead and serum estrogen levels in US women. Age-specific associations were observed. Prospective and mechanistic studies are warranted to further explore these interactions and the associated reproductive toxicities.

Covariation between serum cotinine and blood lead levels among US pediatric populations: Trends from 1999 to 2018.

BACKGROUND: Tobacco smoke, including both active and passive smoke, can be an important source of lead exposure. However, the relationship between passive tobacco smoke exposure (PTSE) and blood lead levels (BLL), especially in vulnerable populations, needs to be further explored. The present study was to assess the covariation between serum cotinine, a measure of PTSE, and BLL in a pediatric population during 1999-2018. METHODS: Data on 21,817 children, aged 3-19 years, was extracted from the biennial nationally representative surveys. The trends of the prevalence of lead exposure (BLL ≥ 3.5 µg/dL) and PTSE (cotinine ≥ 1 ng/mL but < 10 ng/mL) were determined, and the covariation between BLL and cotinine was assessed. The population attributable fraction (PAF) of PTSE to the BLL was proxied using the partial R2 of the hierarchical linear regression. The association between PTSE and lead exposure was estimated using multivariate logistic regression. RESULTS: A parallel decreasing trend in the prevalence of lead exposure and PTSE was observed. Similarly, the means of both BLL and cotinine declined simultaneously. Overall, the PAF from PTSE towards blood lead was 7 %, doubling the PAF from race/ethnicity and family income combined. Stratified by race/ethnicity, PAF from PTSE was 8 % in Blacks and Whites and 4 % for Hispanics. The odds ratio of PTSE with lead exposure was 2.45 (95 % CI, 1.75, 3.44), 2.00 (1.21, 3.33), and 1.16 (0.64, 2.13) for Black, White, and Hispanic children, respectively. Cotinine mean remained two times higher in Blacks than non-Black children at the end of the study period. CONCLUSION: Serum cotinine and BLL may have a significant association in children that persists even as both have been steadily declining in recent years. The contribution from PTSE to blood lead variations could be greater than that from socioeconomic factors. Further reducing lead exposure might be achieved by eliminating PTSE, particularly for the Black pediatric population.

Exposure to p-dichlorobenzene and prevalent endocrine-related reproductive cancers among US women.

P-dichlorobenzene (p-DCB) is a pest repellent and air deodorant that is commonly found in the household and public buildings. Exposure to p-DCB has been suggested to have potential metabolic and endocrine effects. Little is known about its association with endocrine-related female cancers. In this cross-sectional study, a nationally representative subsample of 4459 women, aged 20 years or older, in the 2003-2016 National Health and Nutrition Examination Survey was analyzed for the association between p-DCB exposure, measured as urinary concentrations of 2,5-dichlorophenol (2,5-DCP), the primary metabolite of p-DCB, and prevalent endocrine-related female cancers (defined as breast, ovarian, and uterine cancers) using multivariate logistic regression models, adjusting for potential confounders. Of the study participants, 202 women (weighted prevalence, 4.20%) reported being diagnosed with any of these endocrine-related reproductive cancers. Women with reproductive cancers showed a statistically significant increase in urinary 2,5-DCP concentrations (weighted geometric mean, 7.97 vs. 5.84 µg/g creatinine; p < 0.0001), compared to women without these cancers. After adjusting for potential confounders, we found that women in the moderate (1.94- < 28.10 µg/g creatinine) and high level (≥ 28.10 µg/g creatinine) of 2,5-DCP had significantly increased odds of endocrine-related reproductive cancers (odds ratio of 1.66 (95% CI: 1.02, 2.71) and 1.89 (1.08, 3.29), respectively), as compared with those in the low exposure group (< 1.94 µg/g creatinine). This study demonstrates a potential relation between p-DCB exposure and prevalent endocrine-related reproductive cancers in US women. Prospective and mechanistic studies would further explore these interactions and elucidate the pathogenesis of endocrine-related female cancers potentially associated with p-DCB exposure.

Crossover Trends in Current Cigarette Smoking Between Racial and Ethnic Groups of US Adolescents Aged 12-19 Years Old, 1999-2018.

OBJECTIVE: To examine the racial difference and trends in cigarette smoking among adolescents from 1999 to 2018. METHODS: We analyzed the data of 10,760 adolescents aged 12-19 who participated in the National Health and Nutrition Examination Surveys (NHANES), 1999-2018. Current tobacco smoking (CTS) was defined as participants with serum cotinine ≥10 ng/mL. Adjusted biennial prevalence ratios (abiPR: the ratio associated with a two-year increase in time) were estimated. RESULTS: Diverging trends in CTS prevalence were revealed in adolescents. The steepest decrease occurred in Hispanics aged 12-17, with 15% declining every two calendar years [abiPR = 0.85(0.77, 0.94)]. The sharpest increase occurred with Blacks aged 18-19 years [abiPR = 1.06(0.99, 1.14)]. A crossover of prevalence trend between Blacks and Whites occurred in adolescents aged 18-19 years old due to the diverging trends. The average CTS prevalence was significantly higher in Whites than in Blacks in the early [(1999-2008, 13.65% (11.85%, 15.46%) vs. 8.80% (7.55%, 10.04%)], but Blacks had a higher average in recent years [(2009-2018, 8.32% (6.53%, 10.12%) vs. 7.77% (5.86%, 9.68%)]. For adolescents aged 18-19 years, the survey cycles or calendar years linearly explained 71% of the variations in the prevalence for Hispanics, 60% for Whites, but only 1% for Blacks. CONCLUSIONS: A crossover in the trend of current tobacco smoking occurred between 1999 and 2018 due to an increase in prevalence among Black adolescents and a significant decrease in prevalence among other racial groups.

The Diverging Trend in Exposure to Environmental Tobacco Smoke Among US Children.

OBJECTIVE: Environmental tobacco smoke exposure (ETSE) was race/ethnicity-specific, but how the race/ethnicity-specific ETSE has changed over time, diverging or converging, remains unclear. We examined ETSE trends by race/ethnicity in US children aged 3-11 years. METHODS: We analyzed the data of 9678 children who participated in the biennial National Health and Nutrition Examination Surveys, 1999-2018. ETSE was defined as serum cotinine ≥ 0.05 ng/ml, with ≥ 1 ng/ml as heavy exposure. For trend description, adjusted biennial prevalence ratios (abiPR: the ratio associated with a 2-year increase in time) were estimated by race/ethnicity. The prevalence ratios between races/ethnicities were used to quantify ethnoracial differences in different survey periods. Analyses were performed in 2021. RESULTS: The overall ETSE prevalence was cut by almost half, from 61.59% (95% confidence interval = 56.55%, 66.62%) in the 1999-2004 survey to 37.61% (33.90%, 41.31%) in 2013-2018, exceeding the national 2020 health target (47.0%). However, the decrease occurred unequally between races/ethnicities. Heavy ETSE declined significantly in white [abiPR = 0.80 (0.74, 0.86)] and Hispanic children [0.83 (0.74, 0.93)], but insignificantly in black children [0.97 (0.92, 1.03)]. Consequently, the adjusted prevalence ratio between black children and white children increased from 0.82 (0.47, 1.44) in 1999-2004 to 2.73 (1.51, 4.92) in 2013-2018 for heavy ETSE. Hispanic children remained at the lowest risk throughout the study period. CONCLUSION: Overall ETSE prevalence was cut by half between 1999 and 2018. However, due to uneven declines, the gaps between black children and others have expanded in heavy ETSE. Special vigilance is needed in preventive medicine practice with black children.

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.

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.

Ambient air emissions of endocrine-disrupting metals and the incidence of hormone receptor- and HER2-dependent female breast cancer in USA.

Limited evidence exists on the relationship between exposure to endocrine-disrupting metals in ambient air and hormone receptor- and HER2-dependent breast cancer. This study investigates the association between ambient air emissions of endocrine-disrupting metals and the incidence of female breast cancer of different receptor status. County-level data from the US national datasets were analyzed for the association between emissions of various metals including arsenic, cadmium, chromium VI, lead, and mercury, and the annual age-adjusted incidence of hormone receptor-dependent breast cancer for 1990-2016 and HER2-dependent breast cancer for 2010-2016 using adjusted linear regression models. Lead emissions showed the strongest association among the metals examined with the incidence of different receptor status breast cancers, including ER-positive, ER-negative, PR-negative, HER2-negative, and Triple-negative breast cancers, with the adjusted ß ranging from 917.26 for ER-negative to 3182.37 for HER2-negative breast cancer. Arsenic and mercury showed significant associations with the incidence of ER-positive, ER-negative, PR-positive, and PR-negative breast cancers. However, cadmium emissions were only significantly associated with ER-negative breast cancer. Moreover, chromium was not associated with any subtypes of breast cancer. Among all of the metals, only lead and mercury emissions showed significant associations with HER2-negative and Triple-negative breast cancer incidence. The results from this study suggest that increased exposure to endocrine-disrupting metals, especially lead, in ambient air could be associated with an increased incidence of female breast cancers with various receptor status in the US. Prospective studies are warranted to further explore this relationship.