Analysis of Postdeployment Serum Samples Identifies Potential Biomarkers of Exposure to Burn Pits and Other Environmental Hazards.

OBJECTIVE: The potential health risks of deployment to sites with open burn pits remain poorly understood, in part, because personal exposure monitoring was not performed. Here, we investigated whether postdeployment serum samples contain biomarkers associated with exposure to burn pits. METHODS: A total of 237 biomarkers were measured in 800 serum samples from deployed and never-deployed subjects. We used a regression model and a supervised vector machine to identify serum biomarkers with significant associations with exposures and deployment. RESULTS: We identified 101 serum biomarkers associated with polycyclic aromatic hydrocarbons, dioxins or furans, and 54 biomarkers associated with deployment. Twenty-six of these biomarkers were shared in common by the exposure and deployment groups. CONCLUSIONS: We identify a potential signature of exposure to open burn pits, and provide a framework for using postexposure sera to identify exposures when contemporaneous monitoring was inadequate.

Responses of serum chemokines to dramatic changes of air pollution levels, a panel study.

Background: Despite the in vitro and in vivo evidence, studies are limited in evaluating whether chemokines are potential inflammatory mediators in response to air pollution exposure in humans. Methods: We conducted a panel study coinciding with the Beijing Olympics, when temporary air pollution controls were implemented. We measured a suite of serum chemokines among healthy adults before, during and after the Olympics, respectively. Linear mixed-effect models were used to evaluate changes in chemokine levels over the three time periods. Results: In response to the 50% drop in air pollution levels during the games, levels of RANTES, MCP-2, and TARC decreased by 25.8%, 20.9% and 35.3%, respectively (p < 0.001) from pre-Olympics, and then increased by 45.8%, 34.9% and 61.5%, respectively (p < 0.001) after the games when air pollution levels went up again. Similar patterns were observed in subgroup analyses by sex, age, smoking and body mass index. GRO-α and IL-8 decreased significantly during the games (22.5% and 30.4%), and increased non-significantly after the games. Eotaxin-1 only increased significantly from during- to post-games. Conclusions: The strongest associations with air pollution levels were observed among RANTES, TARC and MCP-2. Those chemokines may play important roles in the air pollution-induced inflammatory pathway.

Modeling study of ozone source apportionment over the Pearl River Delta in 2015.

In recent years, the concentration of fine particulate matter has decreased gradually in the Pearl River Delta (PRD) region, but the ozone (O3) concentration remains high and has become the primary air pollutant. In this study, using a three-dimensional numerical model [nested air quality prediction modeling system (NAQPMS)] coupled with an on-line source apportionment module, the contribution of different source regions and source categories to the O3 concentration in the PRD region was quantified. A comparison with observation data confirmed that the NAQPMS adequately reproduced surface O3 concentrations in different seasons. Compared with biogenic emissions, anthropogenic precursors play a dominant role in O3 production. In Guangzhou city, among different source categories, mobile emission is the largest contributor (accounting for approximately 40%), followed by industry emissions (20%-24%). Regional control measures for solvent use and mobile emissions are effective for reducing O3 concentration. In the PRD region, self-contribution is more significant in daytime (∼40%) than in nighttime (∼10%) on average. Among the source regions outside PRD, the northern part of Guangdong province, Jiangxi province, and Fujian province are important contributors. Within the PRD region, the self-contribution of each city increases by 12%-32% during O3 episodes (>80 ppbv) compared with the annual mean contribution. The contribution of the entire PRD region and the entire Guangdong province is 46%-63% and 63%-74% in PRD cities during O3 episodes. These results indicate that regional collaboration on emission control within PRD or Guangdong province is effective for reducing O3 episodes in the PRD region. In addition, because long-range transport from regions outside Guangdong province played an important role in the O3 concentration in the PRD region, long-term emission control measures throughout China in subsequent years should be propitious to further reduce the annual O3 level and improve air quality in the PRD region.

Prenatal ambient air pollution exposure and SOD2 promoter methylation in maternal and cord blood.

The evidence is increasing that prenatal air pollutant exposure contributes to elevated oxidative stress in children, but the underlying mechanism is unclear. A pilot study was conducted in China to explore the associations between prenatal ambient air pollution exposure and superoxide dismutase 2 (SOD2) promoter methylation in maternal and cord blood. After detection and analyses, SOD2 promoter methylation levels in umbilical cord blood were elevated as maternal SOD2 promoter methylation levels increased. In addition, the SOD2 promoter methylation levels in umbilical cord blood were positively associated with the particulate matter 10 (PM10) exposure concentrations during the entire pregnancy and the second trimester. In maternal peripheral blood, the SOD2 promoter methylation levels were positively associated with the exposure concentrations of PM10 (during the entire pregnancy and the second trimester) and nitrogen dioxide (NO2) (during the first trimester of pregnancy), whereas the levels were negatively associated with the exposure concentrations of NO2 during the third trimester of pregnancy. Additionally, interaction analyses revealed that the maternal SOD2 promoter methylation level and sulfur dioxide (SO2) exposure (during the entire pregnancy and the third trimester), as well as NO2 exposure (during the third trimester of pregnancy), had an interaction effect on the SOD2 promoter methylation level in umbilical cord blood. Furthermore, mediation analysis revealed that the associations between SOD2 promoter methylation in umbilical cord blood and PM10 exposure during the entire pregnancy and the second trimester were partly mediated by maternal SOD2 promoter methylation. In conclusion, prenatal exposure to air pollutants was significantly associated with SOD2 promoter methylation levels in umbilical cord blood, and this association may be affected by SOD2 promoter methylation levels in maternal peripheral blood. These associations may be one of the mechanisms by which prenatal air pollutant exposure leads to oxidative stress in newborns.

Biological and environmental exposure monitoring of volatile organic compounds among nail technicians in the Greater Boston area.

Nail technicians are exposed to volatile organic compounds (VOCs) from nail products, but no studies have previously measured VOC biomarkers for these workers. This study of 10 nail technicians aimed to identify VOCs in nail salons and explore relationships between air concentrations and biomarkers. Personal and area air samples were collected using thermal desorption tubes during a work shift and analyzed using gas chromatography/mass spectrometry (GC/MS) for 71 VOCs. Whole blood samples were collected pre-shift and post-shift, and analyzed using GC/MS for 43 VOCs. Ventilation rates were determined using continuous CO2 measurements. Predominant air VOC levels were ethyl methacrylate (median 240 µg/m3 ), methyl methacrylate (median 205 µg/m3 ), toluene (median 100 µg/m3 ), and ethyl acetate (median 639 µg/m3 ). Blood levels were significantly higher post-shift than pre-shift for toluene (median pre-shift 0.158 µg/L and post-shift 0.360 µg/L) and ethyl acetate (median pre-shift <0.158 µg/L and post-shift 0.510 µg/L); methacrylates were not measured in blood because of their instability. Based on VOCs measured in these seven nail salons, we estimated that emissions from Greater Boston area nail salons may contribute to ambient VOCs. Ventilation rates did not always meet the ASHRAE guideline for nail salons. There is a need for changes in nail product formulation and better ventilation to reduce VOC occupational exposures.

Prevalence of childhood lead poisoning and respiratory disease associated with lead smelter emissions.

BACKGROUND: The city of Port Pirie in South Australia has been a world leading centre for lead and zinc smelting and processing since 1889 that continues to cause contamination of its environment and resident population. This study quantifies the effect of lead and SO2 emissions from Nyrstar Port Pirie Pty Ltd's smelter on blood lead and respiratory health outcomes, respectively, and establishes what air quality values are required to better protect human health. METHOD: Blood lead and emergency department presentation data collected by South Australia Health (SA Health) and lead in air and SO2 data collected by the South Australian Environment Protection Authority (SAEPA) were obtained and analysed to quantify health outcomes due to smelter emissions in Port Pirie. Regression analysis was used to assess the relationship between the concentration of lead in air and children's blood lead levels between the years of available data: 2003 to 2017. Ambient SO2 concentrations (SAEPA) measured continuously between 2008 and 2018 were 24-hour averaged and compared to daily local emergency department respiratory presentation rates (available from July 2012 to October 2018). Rates of emergency department respiratory presentations at Port Pirie and regional comparators were calculated as age-standardised rates. RESULTS: The data show that increases in ambient SO2 concentrations are associated with increased rates of emergency department respiratory presentations of Port Pirie residents, in which children are over-represented. The 30-day rolling average of respiratory presentations was significantly associated (p < 0.05) with incremental increases in SO2. Analysis of the relationship between lead in air and blood lead shows that annual geometric mean air lead concentrations need to be <0.11 µg/m3 to ensure the geometric mean blood lead of Port Pirie children under 5 years is ≤5 µg/dL. For children aged 24 months, lead in air needs to be no greater than 0.082 µg/m3 (annual geometric mean) to ensure geometric mean blood lead does not exceed 5 µg/dL. CONCLUSION: Current smelting emissions continue to pose a clear risk of harm to Port Pirie children. Allowable emissions must be lowered significantly to limit adverse childhood health outcomes including respiratory illness and IQ, academic achievement and socio-behavioural problems that are associated with lead exposure at levels experienced by Port Pirie children. Current SO2 levels are likely to be responsible for increased rates of emergency department respiratory presentations in Port Pirie compared with other South Australian locations. As a minimum, Australian SO2 air quality standards need to be enforced in Port Pirie to better protect human health. Lead in air needs to be approximately 80% lower than the current national standard (0.5 µg/m3) to ensure that the geometric blood lead of children under 5 years is less than or equal to 5 µg/dL.

Concentration of mercury species in hair, blood and urine of individuals occupationally exposed to gaseous elemental mercury in Asturias (Spain) and its comparison with individuals from a control group formed by close relatives.

Between November 19th, 2012 and December 3rd, 2012, 50 workers were intoxicated with gaseous Hg in San Juan de Nieva (Asturias, Spain) during the maintenance of a heat exchanger of a zinc manufacturer. We have quantified the concentration of methylmercury (MeHg), ethylmercury (EtHg) and Hg(II) in blood, hair and urine samples of those individuals taken three years after the accident. Blood, hair and urine of their closest relatives were also analyzed to assess whether the mercury burden present in the intoxicated individuals was due to the occupational exposure or to environmental or lifestyle-related factors. The determination of the mercury species in the samples was carried out applying multiple spiking Isotope Dilution GC-ICP-MS. This procedure corrects for possible interconversion reactions between the Hg species during the sample preparation procedure. Linear correlations were observed for both groups when plotting MeHg in blood vs MeHg in hair, and MeHg in hair vs Hg (II) in urine. The concentrations of Hg species in the intoxicated individuals were not significantly different from those obtained in the control group except for MeHg in blood. Significantly higher levels of MeHg in blood were obtained in some of the intoxicated individuals who had not consumed fish or seafood since the accident. A different correlation between MeHg in hair and MeHg in blood was obtained for these individuals compared to the control group who showed a hair-to-blood ratio consistent with the reported value for people exposed to Hg via fish consumption. Our results suggest that ingested MeHg followed the same pathway of deposition in hair in exposed and non-exposed individuals. However, the exposed individuals with high MeHg levels in blood showed a significantly different extent of MeHg deposition in hair compared to the control group.

Assessment of air pollution caused by illegal e-waste burning to evaluate the human health risk.

The onset of the 21st century has started a corresponding change in consumer lifestyles, resulting in the generation of a huge amount of the end-of-life electronics, known as e-waste. The e-waste recycling activities can pose a high risk to the environment and human health. We monitored air pollution levels (PM10) and heavy metal concentrations (Pb, Cu, Zn, Ni and Cr) in the air for three consecutive months in an area where illegal e-waste recycling was in operation and compared the results with other two residential sites. In addition, we measured the concentrations of the same heavy metals in human blood to find out if there exists any correlation between environmental and biological exposure. Hypoxemia and hypertension were also determined for the comparison of health status amongst the study population. The study design comprised of three sites, which were selected on the basis of different major activities in the respective areas. Air samples were collected with the help of RDS and subjected to heavy metals analysis by ICP-OES, whereas blood samples were analyzed by ICP-MS. Results showed that amongst all study sites significant highest mean concentration of PM10 (243.310 ±â€¯22.729 µg/m3) and its heavy metal was found at e-waste burning site (SIII). High levels of heavy metal in the air were responsible for the higher exposure to the residents of SIII. Therefore, the study concluded that e-waste burning by the informal sector has significantly contributed to the high levels of the air pollution, which in turn was responsible for the highest level of heavy metal exposure to the residents. This was also associated with the occurrence of cardiovascular morbidity namely hypertension amongst the inhabitants of SIII may indicate the effect of chronic exposure to the air pollution due to e-waste processing activities, which needs to be studied further.

Roadside Exposure and Inflammation Biomarkers among a Cohort of Traffic Police in Kathmandu, Nepal.

Air pollution is a major environmental problem in the Kathmandu Valley. Specifically, roadside and traffic-related air pollution exposure levels were found at very high levels exceeding Nepal air quality standards for daily PM2.5. In an exposure study involving traffic police officers, we collected 78 blood samples in a highly polluted spring season (16 February 2014⁻4 April 2014) and 63 blood samples in the less polluted summer season (20 July 2014⁻22 August 2014). Fourteen biomarkers, i.e., C-reactive protein (CRP), serum amyloid A (SAA), intracellular adhesion molecule (ICAM-1), vascular cell adhesion molecule (VCAM-1), interferon gamma (IFN-γ), interleukins (IL1-ß, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12, IL-13), and tumor necrosis factor (TNF-α) were analyzed in collected blood samples using proinflammatory panel 1 kits and vascular injury panel 2 kits. All the inflammatory biomarker levels were higher in the summer season than in the spring season, while particulate levels were higher in the spring season than in the summer season. We did not find significant association between 24-hour average PM2.5 or black carbon (BC) exposure levels with most of analyzed biomarkers for the traffic volunteers working and residing near busy roads in Kathmandu, Nepal, during 2014. Inflammation and vascular injury marker concentrations were generally higher in females, suggesting the important role of gender in inflammation biomarkers. Because of the small sample size of female subjects, further investigation with a larger sample size is required to confirm the role of gender in inflammation biomarkers.

Levels of phthalate acid esters and sex hormones and their possible sources in traffic-patrol policemen in Chongqing.

To investigate the correlation between the air phthalate acid ester (PAE) exposure and serum PAE concentration and the effects of PAE exposure on reproductive health among Chongqing traffic-patrol policemen. In 2013, 32 traffic-patrol policemen working in an area with poor air quality in Chongqing and 28 traffic-patrol policemen working in an area with good air quality were selected. Their blood levels of 14 PAEs and six reproductive hormones were determined. Air samples were collected from four traffic-patrol platforms. The concentrations of 14 PAEs in the air samples were evaluated. All 14 PAEs were detected in the blood samples. The concentrations of seven PAEs in the total suspended particulate, namely, dimethyl phthalate, diethyl phthalate, dibutyl phthalate, bis (2-ethox-yethyl) phthalate, dihexyl phthalate, benzyl butyl phthalate, and bis (2-n-butoxyethyl) phthalate, were positively and significantly associated with the blood levels of these PAEs in the participants. All the sex hormone levels measured here were significantly different between the participants from the two areas. The PAE concentrations in the blood samples were correlated with the reproductive hormone levels in the participants. Air PAE pollution may be a major source of PAE exposure in the traffic-patrol policemen of Chongqing.

A cross-sectional survey based on blood VOCs, hematological parameters and urine indicators in a population in Jilin, Northeast China.

The objective of this study was to examine whether long-term exposure to low-dose volatile organic compounds (VOCs) will have an effect on the health of non-occupational population. A total of 499 non-occupational participants aged more than 18 that live around Jilin Petrochemical Industrial Zone were chosen by stratified cluster random sampling. Their blood VOCs' levels, hematological parameters and urine indicators together with detailed questionnaire data were used to find possible relationships using binary logistic regression analysis. The detection rate of benzene in the blood was high in the non-occupational population around the industrial area, and it even reached 82.3% in males but no significant difference was recorded between male and female population. In addition, trichloroethane (male: 33.2% V female: 21.7%; p = 0.002), carbon tetrachloride (males: 20.3% V females: 7.5%; p < 0.001) and trichlorethylene (male: 34.9% V female: 24.7%; p = 0.004) all showed significant differences in gender, and without exception, the prevalence of males was higher in these three VOCs than of females. The changes in red blood cell (RBC), hematocrit (HCT) and basophils are correlated with carbon tetrachloride, trichloroethylene and chloroform, respectively. And RBC, HCT and basophils are statistically significant in male compared with female of the study population. The increase in trichlorethylene was associated with an increase of 1.723% (95% CI 1.058-2.806) in HCT. The increase in carbon tetrachloride showed a more significant correlation with an increase of 2.638% in RBC count (95% CI 1.169-5.953). And trichloromethane led to a 1.922% (95% CI 1.051-3.513) increase in basophils. The changes in urinary WBC, urine ketone (KET) and urinary bilirubin (BIL) showed significant correlation with benzene, carbon tetrachloride and dibromochloromethane, respectively. The correlation in females is more significant than in males. The increase of benzene in the female population increased urinary leukocyte count by 2.902% (95% CI 1.275-6.601). The effect of carbon tetrachloride on KET was particularly pronounced, resulting in an increase of 7.000% (95% CI 1.608-30.465). Simultaneously, an increase in dibromochloromethane caused an increase of 4.256% (95% CI 1.373-13.192) in BIL. The changes in RBC, HCT and basophils can only serve as an auxiliary indicator for disease diagnosis, so they have no significant clinical significance. However, the alteration of urinary WBC, KET and BIL has great clinical significances, and it is suggested that the monitoring of the above indicators from low-dose long-term exposure be strengthen in this area.

Incorporation of in vitro metabolism data and physiologically based pharmacokinetic modeling in a risk assessment for chloroprene.

Objective: To develop a physiologically based pharmacokinetic (PBPK) model for chloroprene in the mouse, rat and human, relying only on in vitro data to estimate tissue metabolism rates and partitioning, and to apply the model to calculate an inhalation unit risk (IUR) for chloroprene.Materials and methods: Female B6C3F1 mice were the most sensitive species/gender for lung tumors in the 2-year bioassay conducted with chloroprene. The PBPK model included tissue metabolism rate constants for chloroprene estimated from results of in vitro gas uptake studies using liver and lung microsomes. To assess the validity of the PBPK model, a 6-hr, nose-only chloroprene inhalation study was conducted with female B6C3F1 mice in which both chloroprene blood concentrations and ventilation rates were measured. The PBPK model was then used to predict dose measures - amounts of chloroprene metabolized in lungs per unit time - in mice and humans.Results: The mouse PBPK model accurately predicted in vivo pharmacokinetic data from the 6-hr, nose-only chloroprene inhalation study. The PBPK model was used to conduct a cancer risk assessment based on metabolism of chloroprene to reactive epoxides in the lung, the target tissue in mice. The IUR was over100-fold lower than the IUR from the EPA Integrated Risk Information System (IRIS), which was based on inhaled chloroprene concentration. The different result from the PBPK model risk assessment arises from use of the more relevant tissue dose metric, amount metabolized, rather than inhaled concentrationDiscussion and conclusions: The revised chloroprene PBPK model is based on the best available science, including new test animal in vivo validation, updated literature review and a Markov-Chain Monte Carlo analysis to assess parameter uncertainty. Relying on both mouse and human metabolism data also provides an important advancement in the use of quantitative in vitro to in vivo extrapolation (QIVIVE). Inclusion of the best available science is especially important when deriving a toxicity value based on species extrapolation for the potential carcinogenicity of a reactive metabolite.

POPs' effect on cardiometabolic and inflammatory profile in a sample of women with obesity and hypertension.

Persistent organic pollutants (POPs) are man-made compounds with metabolic disruption impact. We investigated the effect of POP exposure in the cardiometabolic and inflammatory profile in a population of women with obesity and hypertension. In 43 premenopausal women (22 treated vs. 21 nontreated) undergoing bariatric surgery, blood and adipose tissue samples (visceral (vAT) and abdominal subcutaneous (scAT)) were collected. Median concentrations of ∑HCH and ∑POPs in vAT were significantly higher in treated women. VAT ∑HCH and scAT ∑HCH and ∑POPs concentrations were positively correlated with systolic blood pressure in the non-treated group. Our findings suggest that exposure to POPs and its accumulation in vAT and circulating in plasma may be associated to a higher cardiovascular risk in women with obesity and hypertension, with or without antihypertensive treatment.

Serum metabolomics analysis of mice that received repeated airway exposure to a water-soluble PM2.5 extract.

BACKGROUND: Air pollutant exposure negatively affects human health; however, the molecular mechanisms causing disease remain largely unclear. OBJECTIVES: To explore the effects of respiratory particulate matter (PM2.5) exposure on the serum metabolome and to identify biomarkers for risk assessment of PM2.5 exposure. METHODS: PM2.5 from Nanjing, China, was collected, and its water-soluble extract was subjected to component analysis. BALB/c mice received acute or prolonged exposure to insoluble PM2.5 particles or its water-soluble extract, and lung tissue was submitted to histopathological analyses. Serum samples were collected pre- and post-PM2.5 exposure and analyzed by liquid chromatography/mass spectrometry. RESULTS: Component analysis revealed that metals and inorganic ions were the most abundant components in the soluble PM2.5 samples. Acute exposure to insoluble PM2.5 particles and prolonged exposure to the water-soluble PM2.5 extract both induced severe lung injury, and the lung histopathological scores were significantly associated with PM2.5 exposure. Metabolomics analysis showed that prolonged exposure to the water-soluble PM2.5 extract was associated with statistically significant metabolite changes; the serum concentrations of 30 known metabolites, including metabolites of phospholipids, amino acids and sphingolipids, differed significantly between the control and PM2.5 exposure group. Pathway analysis identified an association of the tricarboxylic acid cycle (TCA) and the phospholipase metabolism pathway with PM2.5 exposure. The most influential metabolites for discriminating between the PM2.5-exposure group serum and the control serum were LysoPE, LysoPC, LGPC, citric acid, PAF C-18, NeuAcalpha2-3Galbeta-Cer, Lyso-PAF C-16, ganglioside GA2, 1-sn-glycero-3-phosphocholine, PC and L-tryptophan. CONCLUSIONS: Respiratory exposure to water-soluble PM2.5 extract has developmental consequences affecting not only the respiratory system but also metabolism.

Metals and oxidative potential in urban particulate matter influence systemic inflammatory and neural biomarkers: A controlled exposure study.

BACKGROUND: Oxidative stress and inflammation are considered to be important pathways leading to particulate matter (PM)-associated disease. In this exploratory study, we examined the effects of metals and oxidative potential (OP) in urban PM on biomarkers of systemic inflammation, oxidative stress and neural function. METHODS: Fifty-three healthy non-smoking volunteers (mean age 28 years, twenty-eight females) were exposed to coarse (2.5-10 µm, mean 213 µg/m3), fine (0.15-2.5 µm, 238 µg/m3), and/or ultrafine concentrated ambient PM (<0.3 µm, 136 µg/m3). Exposures lasted 130 min, separated by ≥2 weeks. Metal concentrations and OP (measured by ascorbate and glutathione depletion in synthetic airway fluid) in PM were analyzed. Blood and urine samples were collected pre-exposure, and 1-h and 21-h post exposure for assessment of biomarkers. We used mixed-regression models to analyze associations adjusting for PM size and mass concentration. RESULTS: Results for metals were expressed as change (%) from daily pre-exposure biomarker levels after exposure to a metal at a level equivalent to the mean concentration. Exposure to various metals (silver, aluminum, barium, copper, iron, potassium, lithium, nickel, tin, and/or vanadium) was significantly associated with increased levels of various blood or urinary biomarkers. For example, the blood inflammatory marker vascular endothelia growth factor (VEGF) increased 5.3% (95% confidence interval: 0.3%, 10.2%) 1-h post exposure to nickel; the traumatic brain injury marker ubiquitin C-terminal hydrolase L1 (UCHL1) increased 11% (1.2%, 21%) and 14% (0.3%, 29%) 1-h and 21-h post exposure to barium, respectively; and the systemic stress marker cortisol increased 1.5% (0%, 2.9%) and 1.5% (0.5%, 2.8%) 1-h and 21-h post exposure to silver, respectively. Urinary DNA oxidation marker 8­hydroxy­deoxy­guanosine increased 14% (6.4%, 21%) 1-h post exposure to copper; urinary neural marker vanillylmandelic acid increased 29% (3%, 54%) 1-h post exposure to aluminum; and urinary cortisol increased 88% (0.9%, 176%) 1-h post exposure to vanadium. Results for OP were expressed as change (%) from daily pre-exposure biomarker levels after exposure to ascorbate-related OP at a level equivalent to the mean concentration, or for exposure to glutathione-related OP at a level above the limit of detection. Exposure to ascorbate- or glutathione-related OP was significantly associated with increased inflammatory and neural biomarkers including interleukin-6, VEGF, UCHL1, and S100 calcium-binding protein B in blood, and malondialdehyde and 8-hydroxy-deoxy-guanosine in urine. For example, UCHL1 increased 9.4% (1.8%, 17%) in blood 21-h post exposure to ascorbate-related OP, while urinary malondialdehyde increased 19% (3.6%, 35%) and 8-hydroxy-deoxy-guanosine increased 24% (2.9%, 48%) 21-h post exposure to ascorbate- and glutathione-related OP, respectively. CONCLUSION: Our results from this exploratory study suggest that metal constituents and OP in ambient PM may influence biomarker levels associated with systemic inflammation, oxidative stress, perturbations of neural function, and systemic physiological stress.

Relationship of Time-Activity-Adjusted Particle Number Concentration with Blood Pressure.

Emerging evidence suggests long-term exposure to ultrafine particulate matter (UFP, aerodynamic diameter < 0.1 µm) is associated with adverse cardiovascular outcomes. We investigated whether annual average UFP exposure was associated with measured systolic blood pressure (SBP), diastolic blood pressure (DBP), pulse pressure (PP), and hypertension prevalence among 409 adults participating in the cross-sectional Community Assessment of Freeway Exposure and Health (CAFEH) study. We used measurements of particle number concentration (PNC, a proxy for UFP) obtained from mobile monitoring campaigns in three near-highway and three urban background areas in and near Boston, Massachusetts to develop PNC regression models (20-m spatial and hourly temporal resolution). Individual modeled estimates were adjusted for time spent in different micro-environments (time-activity-adjusted PNC, TAA-PNC). Mean TAA-PNC was 22,000 particles/cm³ (sd = 6500). In linear models (logistic for hypertension) adjusted for the minimally sufficient set of covariates indicated by a directed acyclic graph (DAG), we found positive, non-significant associations between natural log-transformed TAA-PNC and SBP (ß = 5.23, 95%CI: -0.68, 11.14 mmHg), PP (ß = 4.27, 95%CI: -0.79, 9.32 mmHg), and hypertension (OR = 1.81, 95%CI: 0.94, 3.48), but not DBP (ß = 0.96, 95%CI: -2.08, 4.00 mmHg). Associations were stronger among non-Hispanic white participants and among diabetics in analyses stratified by race/ethnicity and, separately, by health status.

Association of Maternal Insecticide Levels With Autism in Offspring From a National Birth Cohort.

OBJECTIVE: Autism is a complex neurodevelopmental disorder with a largely unknown etiology. To date, few studies have investigated prenatal exposure to toxins and risk of autism by using maternal biomarkers of exposure. Persistent organic pollutants are lipophilic halogenated organic compounds and include the insecticide dichlorodiphenyltrichloroethane (DDT), as well as its metabolite p,p'-dichlorodiphenyl dichloroethylene (p,p'-DDE), and polychlorinated biphenyls (PCBs). The objective of this study was to test whether elevated maternal levels of persistent organic pollutants are associated with autism among offspring. METHOD: The investigation was derived from the Finnish Prenatal Study of Autism, a national birth cohort study based on a nested case-control design. Cases of autism among children born between 1987 and 2005 were ascertained by national registry linkages. In cases of childhood autism and matched control subjects (778 matched case-control pairs), maternal serum specimens from early pregnancy were assayed for levels of p,p'-DDE and total levels of PCBs. RESULTS: The odds of autism among offspring were significantly increased with maternal p,p'-DDE levels that were in the highest 75th percentile, with adjustment for maternal age, parity, and history of psychiatric disorders (odds ratio=1.32, 95% CI=1.02, 1.71). The odds of autism with intellectual disability were increased by greater than twofold with maternal p,p'-DDE levels above this threshold (odds ratio=2.21, 95% CI=1.32, 3.69). There was no association between total levels of maternal PCBs and autism. CONCLUSIONS: These findings provide the first biomarker-based evidence that maternal exposure to insecticides is associated with autism among offspring. Although further research is necessary to replicate this finding, this study has implications for the prevention of autism and may provide a better understanding of its pathogenesis.

Acute changes in DNA methylation in relation to 24 h personal air pollution exposure measurements: A panel study in four European countries.

BACKGROUND: One of the potential mechanisms linking air pollution to health effects is through changes in DNA-methylation, which so far has mainly been analyzed globally or at candidate sites. OBJECTIVE: We investigated the association of personal and ambient air pollution exposure measures with genome-wide DNA-methylation changes. METHODS: We collected repeated 24-hour personal and ambient exposure measurements of particulate matter (PM2.5), PM2.5 absorbance, and ultrafine particles (UFP) and peripheral blood samples from a panel of 157 healthy non-smoking adults living in four European countries. We applied univariate mixed-effects models to investigate the association between air pollution and genome-wide DNA-methylation perturbations at single CpG (cytosine-guanine dinucleotide) sites and in Differentially Methylated Regions (DMRs). Subsequently, we explored the association of air pollution-induced methylation alterations with gene expression and serum immune marker levels measured in the same subjects. RESULTS: Personal exposure to PM2.5 was associated with methylation changes at 13 CpG sites and 69 DMRs. Two of the 13 identified CpG sites (mapped to genes KNDC1 and FAM50B) were located within these DMRs. In addition, 42 DMRs were associated with personal PM2.5 absorbance exposure, 16 DMRs with personal exposure to UFP, 4 DMRs with ambient exposure to PM2.5, 16 DMRs with ambient PM2.5 absorbance exposure, and 15 DMRs with ambient UFP exposure. Correlation between methylation levels at identified CpG sites and gene expression and immune markers was generally moderate. CONCLUSION: This study provides evidence for an association between 24-hour exposure to air pollution and DNA-methylation at single sites and regional clusters of CpGs. Analysis of differentially methylated regions provides a promising avenue to further explore the subtle impact of environmental exposures on DNA-methylation.

Low internal exposure and absence of adverse effects in workers exposed to high air levels of inorganic selenium.

Selenium is an essential trace element for humans, but adverse health effects may occur after elevated intake. The margin between it is small. This study aimed to assess external and internal exposure in workers of a selenium-processing plant, in which elemental and inorganic selenium occurred. Selenium was analyzed in the form of the selenium concentration in plasma (Se-P), in erythrocytes (Se-RBC) and in personal air samples (Setotal-Air) of 17 exposed workers. Internal exposure was compared to 20 controls without occupational selenium exposure. For potential effects, glucose, HbA1c, proinsulin, prothrombin time and GPX were determined. Setotal-Air had a maximum of 2394 µg/m3 (median 319 µg/m3), containing a small water-soluble fraction (median 12.7 µg/m3, range 0.07-975 µg/m3). Se-P of the exposed ranged from 62 to 123 µg/L (median 105 µg/L), whereas the median of Se-RBC was 63.4 µg/L blood (range 51.9-92.7 µg/L). Both were significantly higher than the controls. No significant difference was found for the effect parameters. Biological effect monitoring of employees occupationally exposed to very high levels of selenium and inorganic selenium compounds did not show any indication of adverse health effects. The moderate increase of the internal selenium exposure compared to the high ambient exposure to selenium and its compounds suggests an efficient air protection or an extremely low resorption of elemental and inorganic species of selenium via inhalation.

Elevated biomarkers of sympatho-adrenomedullary activity linked to e-waste air pollutant exposure in preschool children.

Air pollution is a risk factor for cardiovascular disease (CVD), and cardiovascular regulatory changes in childhood contribute to the development and progression of cardiovascular events at older ages. The aim of the study was to investigate the effect of air pollutant exposure on the child sympatho-adrenomedullary (SAM) system, which plays a vital role in regulating and controlling the cardiovascular system. Two plasma biomarkers (plasma epinephrine and norepinephrine) of SAM activity and heart rate were measured in preschool children (n = 228) living in Guiyu, and native (n = 104) and non-native children (n = 91) living in a reference area (Haojiang) for >1 year. Air pollution data, over the 4-months before the health examination, was also collected. Environmental PM2.5, PM10, SO2, NO2 and CO, plasma norepinephrine and heart rate of the e-waste recycling area were significantly higher than for the non-e-waste recycling area. However, there was no difference in plasma norepinephrine and heart rate between native children living in the non-e-waste recycling area and non-native children living in the non-e-waste recycling area. PM2.5, PM10, SO2 and NO2 data, over the 30-day and the 4-month average of pollution before the health examination, showed a positive association with plasma norepinephrine level. PM2.5, PM10, SO2, NO2 and CO concentrations, over the 24 h of the day of the health examination, the 3 previous 24-hour periods before the health examination, and the 24 h after the health examination, were related to increase in heart rate. At the same time, plasma norepinephrine and heart rate on children in the high air pollution level group (≤50-m radius of family-run workshops) were higher than those in the low air pollution level group. Our results suggest that air pollution exposure in e-waste recycling areas could result in an increase in heart rate and plasma norepinephrine, implying e-waste air pollutant exposure impairs the SAM system in children.