Source Of Environmental Exposure Research Articles

Determination of Three Carcinogenic Aromatic Amines in Urine of Smokers and Nonsmokers

Aromatic amines (arylamines) such as o-toluidine, 2-aminonaphthalene, and 4-aminobiphenyl occur in the environment and are constituents of tobacco smoke. Human exposure to these aromatic amines has long been associated with an elevated risk of bladder cancer. A validated, specific, and sensitive method for measuring o-toluidine, 2-aminonaphthalene, and 4-aminobiphenyl in cigarette smokers and nonsmokers was developed. The method uses acid hydrolysis of the arylamine conjugates in urine, extraction with n-hexane, derivatization with pentafluoropropionic anhydride, and subsequent analysis with gas chromatography combined with mass spectrometry using negative ion chemical ionization. The limits of detection were 4 ng/L for o-toluidine and 1 ng/L for 2-aminonaphthalene and 4-aminobiphenyl. Smokers (N = 10) excreted significantly higher amounts of o-toluidine (204 versus 104 ng/24 h), 2-aminonaphthalene (20.8 versus 10.7 ng/24 h), and 4-aminobiphenyl (15.3 versus 9.6 ng/24 h) than nonsmokers (N = 10). Urinary arylamine excretion in smokers was associated with the extent of smoking as assessed by daily cigarette consumption, urinary excretion of nicotine equivalents (nicotine plus its five major metabolites), cotinine in saliva, and carbon monoxide in exhaled breath. All nonsmokers investigated had quantifiable amounts of o-toluidine, 2-aminonaphthalene, and 4-aminobiphenyl in their urine, confirming that other environmental sources of exposure to these compounds also occur. In conclusion, the analytical method is suitable for measuring short-term exposure to arylamines in urine of non-occupationally exposed smokers and nonsmokers.

Polybrominated diphenyl ethers and traditional organochlorine pollutants in fulmars ( Fulmarus glacialis) from the Faroe Islands

The observed high-level burdens of organohalogens among the residents of the Faroe Islands, needs to be explained. Long-finned pilot whale ( Globicephala melas) blubber and meat are known sources of environmental exposure. The present study focus on the organohalogen contamination of the fulmar ( Fulmarus glacialis). The compounds quantified in fulmar muscle, fat, and egg are PCBs, DDTs, hexachlorobenzene (HCB), and polybrominated diphenyl ethers (PBDEs). The dominating pollutants are the 4,4′-DDT metabolite 4,4′-DDE and the two PCB congeners, CB-153 and CB-180, which are present in geometric mean concentrations of 7100, 4700 and 2500 ng/g lipid weight (l.w.), respectively, in adult fulmar muscle. 4,4′-DDT and HCB concentrations are approximately 250 ng/g l.w., each. Concentrations in the eggs are about 50% of the fulmar muscle levels, due to differences in lipid amounts, 4% in muscle and 10% in the eggs, the exposure contribution on a fresh weight basis is almost the same. As a result, both the egg and the adult fulmar muscle may lead to a significant exposure risk, if consumed by humans. BDE-153, the most abundant PBDE congener in fulmar muscle, with a geometric mean concentration of 6.5 ng/g l.w., is much lower than the individual PCB congeners and 4,4′-DDE concentrations. In the adult fulmar muscle, the relative PBDE congener pattern is different from that previously observed in biota, with BDE-153 and BDE-154 as the dominating congeners, rather than BDE-47. In contrast, BDE-47 is the most abundant congener in juvenile muscle and subcutaneous fat. The ∑PBDE concentrations are almost the same in egg, muscle (adult and juvenile) and subcutaneous fat (juvenile). For the polybrominated biphenyl (BB-153) the concentrations are considerably higher in the adult bird and egg than in the juvenile bird; this is also seen for the PCB and 4,4′-DDE concentrations. PCB concentrations found in fulmar egg and muscle are in the same range as seen in the pilot whale, i.e. 590–5700 ng/g l.w. for CB-153. Hence humans are also exposed to PCBs at a reasonable degree via intake of fulmar and/or fulmar egg and not only via pilot whale blubber.

Environmental Cardiology: Getting to the Heart of the Matter

Cardiovascular disease (CVD) is the leading killer in many developed countries, and is soon expected to be the leading killer in all countries. A number of factors have raised CVD to this unsavory stature, among them lack of exercise, poor diet, and smoking. But evidence has slowly been building to indicate that exposures to chemicals and other environmental substances also can have a profound impact on heart health. The link between environmental agents and CVD was once considered tenuous by much of the medical and scientific establishment. But after watching the evidence accumulate over the years, with a surge in the past five years, more and more scientists, doctors, and organizations are acknowledging the importance of a field that some are calling environmental cardiology. One group that is beginning to embrace environmental cardiology is the American Heart Association (AHA), an 80-year-old organization that has traditionally focused on risk factors such as poor diet and lack of exercise as some of the most important contributors to CVD. In the 1 June 2004 issue of Circulation, an expert panel of 11 researchers and physicians published an AHA Scientific Statement that concluded that air pollutants, one of the major environmental exposure sources under investigation by environmental cardiologists, pose a “serious public health problem” for CVD. This is the first official AHA acknowledgment of such links. The group’s decision was based on the breadth and depth of the accumulating information. “There was no single major study that prompted the writing of this paper,” says Sidney Smith, past president of the AHA and a professor of medicine at the University of North Carolina at Chapel Hill. “It was the gathering body of evidence that connected air pollution with cardiovascular diseases, extending well beyond cigarette smoke.” The AHA paper was a very positive development in the eyes of some of the researchers who have been involved in the field for many years. “That’s pretty amazing,” says C. Arden Pope III, an environmental epidemiologist at Brigham Young University. “It’s taken the research out of the fringes and made it part of the mainstream.” Less than two months after the release of the AHA statement, the U.S. Environmental Protection Agency (EPA) gave a clue to how seriously it takes this issue, awarding the largest scientific research grant in its history, $30 million, to study links between air pollution and CVD. The research team will be headed by associate environmental and occupational health professor Joel Kaufman of the University of Washington, and includes scientists from nine other universities and medical centers. A few other government agencies, such as the National Heart, Lung, and Blood Institute (NHLBI), have also begun to address the links between environmental agents and CVD, as have advocacy organizations such as the American Lung Association and the Natural Resources Defense Council. And the NIEHS, one of the original players in the environmental cardiology arena, has ramped up its efforts to explore this area of research. There is still a ways to go before environmental cardiology is fully embraced as a medical paradigm. Many major public health organizations, such as the World Health Organization (WHO) and the Centers for Disease Control and Prevention (CDC), have yet to fold this concept into their prevention efforts in any significant way. And there is very little trickle-down into the typical doctor–patient relationship. Nonetheless, environmental cardiology shows signs of increasingly becoming a factor in research, public policy discussion, and pollutant regulation, as its presence spreads into journals, conferences, textbooks, e-mail discussion groups, and continuing medical education courses. Even The Weather Channel is getting into the act with a new feature that advises viewers on daily levels of pollutants that can affect heart health.

Estimate of uncertainty of measurement from a single-laboratory validation study: application to the determination of lead in blood.

Lead is an environmental pollutant, and human exposure is assessed by monitoring lead concentrations in blood. Because the main source of environmental exposure has been the use of leaded gasoline, its phase-out has led to decreased lead concentrations in the general population. Therefore, validated analytical methods for the determination of lower lead concentrations in blood (<150 microg/L) are needed. In addition, new ISO standards require that laboratories determine and specify the uncertainty of their results. We validated a method to determine lead in blood at concentrations up to 150 microg/L by electrothermal atomic absorption spectrometry with Zeeman background correction according to EURACHEM guidelines. Blood samples were diluted (1:1 by volume) with 2 mL/L Triton X-100. NH4H2PO4 (5 g/L) and Mg(NO3)2 (0.5 g/L) were used as modifiers. Matrix-matched standards were used for calibration. We determined the limits of detection (3.1 microg/L) and quantification (9.4 microg/L). Repeatability and intermediate imprecision within the range 35-150 microg/L were <5.5% and <6.0%, respectively. We assessed trueness by use of certified reference materials, by recovery tests, and by comparison with target values of other reference materials (candidate external quality assessment samples). The expanded uncertainty ranged from 20% to 16% (with a confidence level of 95%) depending on concentration. This study provides a working example of the estimate of uncertainty from method performance data according to the EURACHEM/CITAC guidelines. The estimated uncertainty is compatible with quality specifications for the analysis of lead in blood adopted in the US and the European Union.

Study of human exposure to particulate PAHs using personal air samplers.

Three common sources of environmental exposure to particulate polycyclic aromatic hydrocarbons (PAHs) in Taiwan were chosen for this study. They are smoke of incense burning, exhausts of motor vehicles, and fumes of charcoal burning. The campus environment without any specific PAH sources (nonpoint sources) was chosen as the control. The particulate PAH concentrations in the air samples containing smoke of incense burning were only slightly higher than those in the control. However, the total concentration of particulate PAHs in the air samples with exhausts of motor vehicles and fumes of charcoal burning was about 7.5 times and 22 times higher than those observed in the control, respectively. The mean inhalation amounts of particulate PAHs per unit time are very high both in samples with exhausts of motor vehicles (13.9 ng/min) and fumes of charcoal burning (38.1 ng/min). The exposure dose of 22 PAHs per day ranged from 3.18 to 18.0 microg/day under four exposure conditions. Moreover, the personal inhalation BaP(eq) levels are in the range of 0.4 to 1.55 microg/day.

Hair and toenail arsenic concentrations of residents living in areas with high environmental arsenic concentrations.

Surface soil and groundwater in Australia have been found to contain high concentrations of arsenic. The relative importance of long-term human exposure to these sources has not been established. Several studies have investigated long-term exposure to environmental arsenic concentrations using hair and toenails as the measure of exposure. Few have compared the difference in these measures of environmental sources of exposure. In this study we aimed to investigate risk factors for elevated hair and toenail arsenic concentrations in populations exposed to a range of environmental arsenic concentrations in both drinking water and soil as well as in a control population with low arsenic concentrations in both drinking water and soil. In this study, we recruited 153 participants from areas with elevated arsenic concentrations in drinking water and residential soil, as well as a control population with no anticipated arsenic exposures. The median drinking water arsenic concentrations in the exposed population were 43.8 micro g/L (range, 16.0-73 micro g/L) and median soil arsenic concentrations were 92.0 mg/kg (range, 9.1-9,900 mg/kg). In the control group, the median drinking water arsenic concentration was below the limit of detection, and the median soil arsenic concentration was 3.3 mg/kg. Participants were categorized based on household drinking water and residential soil arsenic concentrations. The geometric mean hair arsenic concentrations were 5.52 mg/kg for the drinking water exposure group and 3.31 mg/kg for the soil exposure group. The geometric mean toenail arsenic concentrations were 21.7 mg/kg for the drinking water exposure group and 32.1 mg/kg for the high-soil exposure group. Toenail arsenic concentrations were more strongly correlated with both drinking water and soil arsenic concentrations; however, there is a strong likelihood of significant external contamination. Measures of residential exposure were better predictors of hair and toenail arsenic concentrations than were local environmental concentrations.

Public health, GIS, and spatial analytic tools.

We review literature that uses spatial analytic tools in contexts where Geographic Information Systems (GIS) is the organizing system for health data or where the methods discussed will likely be incorporated in GIS-based analyses in the future. We conclude the review with the point of view that this literature is moving toward the development and use of systems of analysis that integrate the information geo-coding and data base functions of GISystems with the geo-information processing functions of GIScience. The rapidity of this projected development will depend on the perceived needs of the public health community for spatial analysis methods to provide decision support. Recent advances in the analysis of disease maps have been influenced by and benefited from the adoption of new practices for georeferencing health data and new ways of linking such data geographically to potential sources of environmental exposures, the locations of health resources and the geodemographic characteristics of populations. This review focuses on these advances.

Blood lead levels of primary school children in Dhaka, Bangladesh.

Dhaka, Bangladesh, has one of the highest air lead levels in the world. In February 2000, we evaluated children at five primary schools in Dhaka to determine blood lead (BPb) levels, sources of environmental exposure, and potential risk factors for lead poisoning. Selected schools represented a range of geographic and socioeconomic strata. A total of 779 students 4-12 years of age participated. The mean BPb level was 15.0 microg/dL (range 4.2-63.1 microg/dL). Most students (87.4%) had BPb levels above the Centers for Disease Control and Prevention's level of concern (10 microg/dL). Elevated BPb levels correlated with soil eating [odds ratio (OR) = 3.31; 95% confidence interval (CI), 1.30-8.39], low parental education (OR = 2.72; 95% CI, 1.97-3.75), living close to major roads (OR = 2.30; 95% CI, 1.23-4.29), and increasing age (OR = 1.11; 95% CI, 1.06-1.16). BPb levels measured were similar to those in other countries that use leaded gasoline. No other potential sources of lead exposure were consistently identified. Combustion of leaded gasoline is the main source of lead exposure in Dhaka, resulting in ubiquitous contamination of the environment. The increase in BPb levels with age, a finding contrary to observations in the United States and Australia, may be related to increased outdoor activities. The Bangladeshi government recently announced a plan to eliminate leaded gasoline. Baseline BPb surveys are critical to develop and evaluate intervention policies. Strategies to reduce BPb levels need to address variations in socioeconomic status, construction type and location of housing, and levels of hygiene.

Background lead and cadmium exposure of adult women in Xian City and two farming villages in Shaanxi Province, China

The objectives of the present study are: (a) to clarify the current levels of environmental exposure to lead (Pb) and cadmium (Cd) in Shaanxi Province in China in comparison with levels in other parts of mainland China; (b) to examine if there is any urban–rural difference in Pb and Cd exposure; and (c) to quantify the role of cereals as the dietary source of environmental exposure to these metals. For this purpose, triplet surveys on lead and cadmium exposure were conducted in the provincial capital of Xian and two farming villages A and B in Shaanxi Province, China in 1997. The grand geometric mean for lead (Pb) intake via foods (Pb-F), Pb in blood (Pb-B) and Pb in urine as corrected for creatinine concentration (Pb-Ucr) were 30 μg/day, 33 μg/l and 5 μg/g creatinine, respectively, with significant differences among the survey sites, e.g. Pb-B being higher in Xian (43 μg/l) than in the two villages (38 and 22 μg/l). The counterpart values for cadmium (Cd) intake via foods (Cd-F), Cd in blood (Cd-B) and Cd in urine (Cd-Ucr) were 6.1 μg/day, 0.46 μg/l and 2.8 μg/g creatinine, respectively, with no substantial inter-survey site difference. Thus, it was possible to conclude that, from comparison with the values reported in 1990s literature, the exposure of Shaanxi people to Pb and Cd is no higher than, and even possibly lower than, the levels reported for people in other parts of mainland China. The exposure to Cd was almost exclusively from foods, whereas the exposure to air-borne Pb was large enough in Xian to explain higher Pb-B and Pb-Ucr than the level in Village B despite lower Pb-F in Xian than in Village B. Cereals (wheat, rice, maize and foxtail millet) contributed 26 and 84% of dietary Pb and Cd intake, respectively.

Conference reports

The objectives of the present study are: (a) to clarify the current levels of environmental exposure to lead (Pb) and cadmium (Cd) in Shaanxi Province in China in comparison with levels in other parts of mainland China; (b) to examine if there is any urban–rural difference in Pb and Cd exposure; and (c) to quantify the role of cereals as the dietary source of environmental exposure to these metals. For this purpose, triplet surveys on lead and cadmium exposure were conducted in the provincial capital of Xian and two farming villages A and B in Shaanxi Province, China in 1997. The grand geometric mean for lead (Pb) intake via foods (Pb-F), Pb in blood (Pb-B) and Pb in urine as corrected for creatinine concentration (Pb-Ucr) were 30 μg/day, 33 μg/l and 5 μg/g creatinine, respectively, with significant differences among the survey sites, e.g. Pb-B being higher in Xian (43 μg/l) than in the two villages (38 and 22 μg/l). The counterpart values for cadmium (Cd) intake via foods (Cd-F), Cd in blood (Cd-B) and Cd in urine (Cd-Ucr) were 6.1 μg/day, 0.46 μg/l and 2.8 μg/g creatinine, respectively, with no substantial inter-survey site difference. Thus, it was possible to conclude that, from comparison with the values reported in 1990s literature, the exposure of Shaanxi people to Pb and Cd is no higher than, and even possibly lower than, the levels reported for people in other parts of mainland China. The exposure to Cd was almost exclusively from foods, whereas the exposure to air-borne Pb was large enough in Xian to explain higher Pb-B and Pb-Ucr than the level in Village B despite lower Pb-F in Xian than in Village B. Cereals (wheat, rice, maize and foxtail millet) contributed 26 and 84% of dietary Pb and Cd intake, respectively.

Urinary antimony in infancy

OBJECTIVETo determine whether antimony may be detected in the urine during infancy and early childhood and its association with passive exposure to tobacco smoke, as assessed by urinary cotinine.DESIGNAnalysis of...

Dioxins, dibenzofurans, dioxin-like PCBs, and DDE in U.S. fast food, 1995

Food, especially dairy products, meat, and fish, is the primary source of environmental exposure to dioxins in the general population. Little data exists on dioxin levels in the popular and widely consumed “fast foods”. Data presented in a previously published pilot study was limited to measuring only the levels of dioxins and dibenzofurans in three types of U.S. fast food. This study adds to the previous paper by presenting data, in addition to dioxins and dibenzofurans, on the closely related dioxin-like polychlorinated biphenyls (PCBs), and the persistent metabolite of DDT, 1,1-dichloro-2,2- bis ( p-chlorophenyl) ethylene (DDE), in four types of popular U.S. fast food. These include McDonald's Big Mac Hamburger®, Pizza Hut's Personal Pan Pizza Supreme®, Kentucky Fried Chicken® (KFC) three piece original recipe mixed dark and white meat luncheon package, and Häagen-Daz® chocolate-chocolate chip ice cream. Dioxin plus dibenzofuran dioxin toxic equivalents (TEQ) ranged from 0.03 to 0.28 TEQ pg/g wet or whole weight for the Big Mac, from 0.03 to 0.29 for the Pizza, from 0.01 to 0.31 for the KFC, and from 0.03 to 0.49 TEQ pg/g for the ice cream. Daily TEQ consumption per kilogram body weight (kg/BW), assuming an average 65 kg adult and a 20 kg child, from one serving of each of these fast food ranged between 0.046 and 1.556 pg/kg in adults whereas in children the values were between 0.15 and 5.05 pg/kg. Total measured PCDD/Fs in the Big Mac, Personal Pan Pizza, KFC, and the Häagen-Daz ice cream varied from 0.58 to 9.31 pg/g. Measured DDE levels in the fast foods ranged from 180 to 3170 pg/g. Total mono-ortho PCB levels ranged up to 500 pg/g or 1.28 TEQ pg/g for the KFC and for di-ortho PCBs up to 740 pg/g or 0.014 TEQ pg/g for the pizza sample. Total PCB values in the four samples ranged up to 1170 pg/g or 1.29 TEQ pg/g for the chicken sample.

A Side-by-Side Comparison of Dust Collection Methods for Sampling Lead-Contaminated House Dust

The Environmental Protection Agency is required to set a standard for lead-contaminated house dust, but whether dust lead loading (μg/ft 2) or concentration (μg/g) is more predictive of children′s blood lead levels, which dust collection method should be used, and which surfaces should be sampled are unknown. Using a random sample of sequential births, we enrolled 205 urban children, 12 to 30 months of age, who had lived in the same house since at least 6 months of age. Samples of dust were obtained from predetermined surfaces in each child′s residence using a wipe method and two vacuum methods, the Baltimore repair and maintenance method (BRM) and the dust vacuum method (DVM). Other potential sources of environmental exposure also were analyzed for lead, including soil, water, and paint. In general, dust lead loading is more predictive of children′s blood lead levels than is dust lead concentration. Dust lead loading as measured with the BRM sampler explained more of the variation in children′s blood lead levels than did wipe loading and DVM loading (13.7, 10.1, and 5.9%, respectively, adjusted for other significant predictors). The partial correlation between BRM lead loading and children′s blood lead was significantly different than that for DVM lead loading, but it was not significantly different than that for wipe lead loading. Of the four surfaces measured, noncarpeted floors and interior window sills or wells were significantly associated with children′s blood lead levels in multiple regression models. These data indicate that dust lead loading is more predictive of children′s blood lead levels than is dust lead concentration and that, to determine if a housing unit is safe for children, noncarpeted floors and interior window sills or window wells should be measured using either the BRM or wipe sampling method.

Hair mineral analysis and behavior: an analysis of 51 studies.

An attempt was made to compile and summarize all available studies on the relationship between hair mineral levels and various aspects of human behavior. The 51 studies located covered a wide range of behaviors: learning disabilities (10 studies); retardation (7); hyperactivity (5); criminality and delinquency (5); “behaviorally disturbed” (4); autism (4); schizophrenia (3); anorexia, hypoglycemia (2 each); fatigue, anxiety, allergy, senility, and phenylketonuria (1 each); giftedness and intelligence (4). High levels of certain minerals, especially lead and cadmium, and low levels of other minerals, especially potassium and sodium, tend to be associated with undesirable behavior. There is a need for vigorous attempts to eliminate sources of environmental exposure to heavy metals and for further study of the role of mineral excesses and deficiencies in human health and behavior.

Lead-Cadmium Interaction: Effects on Viral-Induced Mortality and Tissue Residues in Mice

Simultaneous exposure to lead and cadmium is highly probable due to common environmental sources of exposure. Mice were exposed simultaneously for 10 wek to lead and cadmium and effects were observed on accumulation of the metals in tissues and susceptibility to viral challenge. The incidence of viral-induced mortality was enhanced in all groups of mice exposed to lead and suppressed in groups of mice treated with cadmium. Mice exposed to both lead and cadmium had mortality rates intermediate to those observed after exposure to the individual metals. Lead and cadmium residues in tissues of mice exposed to both metals, as compared to residues in tissues of mice which received lead or cadmium only, indciated that interaction occurs in regard to metabolism, storage, and excretion of these elements. Chronic coexposure to lead and cadmium appears to alter certain effects produced by exposure to each metal alone.

Comparison of chlorinated hydrocarbon pesticides in maternal blood and placental tissues

Fifty-three paired placental and maternal blood specimens were collected from women in a general population and analyzed for the chlorinated hydrocarbon pesticides. All specimens were analyzed by electron gas liquid chromatography. Chlorinated hydrocarbons, previously reported in human adipose and blood specimens (DDT, DDE, DDD, dieldrin, aldrin, BHC, lindane, and heptachlor epoxide), were detected in the placental and maternal blood specimens. DDE, DDT and lindane were detected more frequently. No marked differences were observed among residence, age, or race because the population group sampled was fairly homogeneous with similar environmental sources of exposure to the chlorinated hydrocarbon pesticides. To our knowledge, this is the first reported comparison of the chlorinated hydrocarbon levels detected in placental and maternal blood specimens, as well as the detection of aldrin and heptachlor in placental and blood specimens collected from women in a general population, i.e., without occupational or accidental exposure to these pesticides.