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Results for “Environmental Exposure”

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PubMed1994

Biological monitoring of environmental exposure to polycyclic aromatic hydrocarbons; 1-hydroxypyrene in urine of people.

A biomarker of human exposure to chemical agents provides a valuable parameter for assessing the extent and significance of the uptake by giving a measurement that is direct and integrated over time and exposure routes. Urinary 1-hydroxypyrene is currently tested as a biomarker for the assessment of low level environmental exposure of people to polycyclic aromatic hydrocarbons (PAH). Five examples of the application of urinary 1-hydroxypyrene methodology in the assessment of environmental exposure to PAH are presented: inhalation of tobacco smoke; inhalation of urban outdoor air; windsurfers sailing on polluted water; absorption of contaminated food; exposure in an urban area with many heavy industries. The examples illustrate that the urinary 1-hydroxypyrene test is sufficiently sensitive. Urinary 1-hydroxypyrene is an effective biomarker for the assessment of human environmental exposure to PAH.

Adult↗

PubMed2004

[Pleural mesothelioma in women is associated with environmental exposure to asbestos].

OBJECTIVE: To determine whether local environmental exposure to asbestos in the community of Hof van Twente, The Netherlands (which houses a large asbestos cement facility and has a serious environmental asbestos pollution problem), is accompanied by an increased mortality due to pleural mesothelioma among women. DESIGN: A descriptive, ecologic-epidemiological study. METHOD: Twenty-nine women with a verified diagnosis of pleural mesothelioma were selected from 810 requests for compensation submitted to a specialised lawyers' office in the period 1990-2002. Information on asbestos exposure from occupational, household, environmental or unknown sources was obtained. The place of residence was compared to information on sources of asbestos in the immediate environment derived from the settlement 'Asbestos removal in the environment'. The expected number of cases of pleural mesothelioma among women was estimated on the basis of the observed mortality in The Netherlands in the period 1996-2002. A standardised mortality ratio (SMR) was calculated as the ratio of observed cases divided by the number of expected cases of pleural mesothelioma x 100. RESULTS: In total, 5 cases of pleural mesothelioma were identified among women without occupational or household exposure to asbestos. The age at diagnosis varied from 38 to 81 years. Each case was exposed to asbestos in the direct vicinity of the residence through walking and cycling over local roads metalled with asbestos cement scrap material. The expected number of cases of mortality due to pleural mesothelioma in the town of Hof van Twente for the period 1996-2002 was about 0.46. The SMR was 1090 (95% CI: 465-2551), indicating a 10-fold increase in risk. CONCLUSION: The increased mortality of pleural mesothelioma was most probably due to environmental exposure to asbestos. This finding agrees with comparable studies in other countries.

Adult↗

PubMedDate not supplied

Is histological subtype a marker for environmental exposures in acute myelogenous leukemia?

The association between occupational and other environmental exposures was evaluated in 60 acute myelogenous leukemia cases and controls. Odds ratios and 95% confidence intervals for prior cytotoxic therapy and benzene exposure, adjusted for age, sex, and race by logistic regression, were 3.7 (0.7, 19.9) and 2.6 (0.4, 15.2), respectively. No other work-related associations, including employment in electrical occupations, were present. Other associations were suggestive but may have been due to biases in control selection or small numbers of subjects. The risks for prior cytotoxic therapy (odds ratio = 10.2) and benzene exposure (odds ratio = 11.4) were concentrated in 13 patients with French-American-British M4 leukemia; no environmental exposures were associated with French-American-British subtypes M1 and M2. These findings support the concept that French-American-British histological subtypes of AML may have different etiologies.

Antineoplastic Agents↗

PubMed2001

[Environmental exposure of the Wroclaw inhabitants to nickel and assessment of its nephrotoxic effects].

The aim of the research was to evaluate the environmental exposure of Wroclaw inhabitants on nickel compounds and an assessment of their nephrotoxic effects. The study was realized in a group of 74 inhabitants of the Wroclaw's district Krzyki and compared with a group of 24 inhabitants of the countryfield Kobierzyce community located in the 20 km distance from Wroclaw. A nickel concentration was measured in morning urine of all the Wroclaw inhabitants, whereas nephrotoxicity indices were determined in the 26 inhabitants characterised by the increased nickel concentration (2.8 micrograms/l); in urine of 19 inhabitants this concentration was found to be normal. The average nickel concentration in the urine of the 74 Wroclaw inhabitants was equal to 2.85 +/- 0.22 micrograms/l. 40.5% of this group were characterised by the concentration higher than the physiological one, 4.05% of this group had that concentration higher than 7.9 micrograms/l which gives an evidence of the environmental exposure. In the Kobierzyce group the average nickel concentration in urine was 3.34 +/- 0.23 micrograms/l which is significantly higher (at p < or = 0.001) than that for the Wroclaw group. Moreover, in the Kobierzyce group, 62.5% inhabitants was higher the nickel concentration than the physiological one but still lower than the environmental exposure. Our results indicate that the Wroclaw inhabitants are not more exposed to nickel compounds in comparison with the countryside inhabitants. A nephrotoxic action of nickel was detected through the increased excretion of the sialic acid in urine which is an evidence of the reduced glomelural filtration. A positive correlation between the urine nickel concentration and the urine free sialic acid was found (r = 0.61). No increase in the urine N-acetyl-beta-D-glucosaminidase (NAG), isoenzyme NAG-B, beta 2-microglobulin (beta 2 M) and retinal binding protein (RBP) concentrations were found which could indicate a damage in kidney tubules.

Adult↗

PubMed2006

The effects of environmental exposure to DDT on the brain of a songbird: changes in structures associated with mating and song.

Dichlorodiphenyltrichloroethane (DDT) is a persistent organochlorine compound found worldwide that causes significant anatomical, physiological and behavioural abnormalities in humans and wildlife. However, little is known about whether environmental exposure to DDT affects the brain. Here, we show that environmental exposure to DDT alters the brains of American Robins (Turdus migratorius) in several ways. Increasing levels of DDT resulted in: (i) smaller brain and relative forebrain volumes; (ii) a reduction in the size of two song nuclei, nucleus robustus arcopallialis (RA) and HVC; and (iii) a drastic reduction in neuronal size and overall volume of nucleus intercollicularis (ICo), a structure that is critical for normal sexual behaviour. These changes likely result from stress, direct neurotoxicity and androgen receptor antagonism by the primary metabolite of DDT, p,p'-DDE and this is corroborated by analyses of brain region volumes and p,p'-DDE levels. Our results therefore demonstrate that environmental exposure to DDT is correlated with significant changes in the brain and specifically those structures related to mating and song. Given the magnitude of these changes in the brain and the fact that environmental DDT exposure was restricted to early development, we conclude that both humans and wildlife that live in DDT contaminated environments may be at risk of neurological damage.

Animals↗

PubMed2004

Methodologic and statistical approaches to studying human fertility and environmental exposure.

Although there has been growing concern about the effects of environmental exposures on human fertility, standard epidemiologic study designs may not collect sufficient data to identify subtle effects while properly adjusting for confounding. In particular, results from conventional time to pregnancy studies can be driven by the many sources of bias inherent in these studies. By prospectively collecting detailed records of menstrual bleeding, occurrences of intercourse, and a marker of ovulation day in each menstrual cycle, precise information on exposure effects can be obtained, adjusting for many of the primary sources of bias. This article provides an overview of the different types of study designs, focusing on the data required, the practical advantages and disadvantages of each design, and the statistical methods required to take full advantage of the available data. We conclude that detailed prospective studies allowing inferences on day-specific probabilities of conception should be considered as the gold standard for studying the effects of environmental exposures on fertility.

Data Collection↗

PubMedDate not supplied

Residence location as a measure of environmental exposure: a review of air pollution epidemiology studies.

Residence location has long been used to indicate environmental exposure in many epidemiological studies. This indicator is easy to establish, requires little exposure or monitoring data, and is potentially applicable to many types of investigations. The validity, accuracy and utility of residence location as an exposure indicator, however, is challenged by current concerns regarding multiple exposure pathways, persistent and toxic contaminants, and cumulative exposures from non-point, mobile and point sources. This paper reviews 45 epidemiological studies that use residence location to identify study populations and estimate air pollution exposures. Thirteen (29%) of the studies determined environmental exposures based on "proximity" measures, usually the distance from a subject's residence to a pollutant source. Other studies used "zones" presumed to have equal pollutant levels. Several studies combined zone and proximity approaches. Exposures were quantified using monitoring data in 27 (60%) studies and dispersion modeling in two (4%) studies. Sixteen (36%) studies did not use any environmental data to quantify exposure. A total of 31 (69%) of the studies reported significant associations between health endpoints and the pollutant exposures represented by residence location. In general, comprehensive and systematic approaches to identify and estimate population exposures were not used, and the exposure estimates were therefore deemed likely to have great uncertainty. Unless exposure levels among groups are verified, it cannot be determined whether nonsignificant associations between exposures and health endpoints indicate a lack of measurable health effects, or are merely a result of exposure misclassification. Site-specific and quantitative exposure assessments are needed to better quantify and confirm exposures within such studies, as well as to permit interpretations and comparisons across studies.

Air Pollution↗

PubMed2006

The influence of environmental exposure to complex mixtures including PAHs and lead on genotoxic effects in children living in Upper Silesia, Poland.

Environmental exposure is a complex mixture of hazardous compounds with different mechanisms of toxicity. In case of concomitant exposure to carcinogenic substances--such as polycyclic aromatic hydrocarbons (PAHs)--and to heavy metals--such as lead (Pb)--the level of DNA damage may be enhanced. Children are considered more vulnerable than adults to chemical toxicants because they take in more toxicants as a proportion of body mass and because of inherent biological growth and developmental factors. The objective of the study was to measure cytogenetic effects in Silesian children and to investigate their relation with the environmental exposure to PAHs and Pb. The examined population included 74 children 5-14-year-old who lived in two cities located in the most polluted centre of the Silesia province. Individual exposure to lead was assessed for each child by measuring lead in blood (PbB), and to PAH by measuring 1-hydroxypyrene in urine (1-OHP), urinary mutagenicity and DNA adducts in circulating lymphocytes. Biomarkers of genetic effects were assessed by measuring micronuclei (MN) and sister chromatid exchanges (SCE) in children's peripheral lymphocytes. The mean levels of biomarkers of exposure were as follows: PbB 7.69 microg/dl, DNA adducts 9.59 adducts per 10(8) nt, 1-OHP 0.54 micromol/mol creatinine, and urinary mutagenicity presented as the number of revertants per mmol of creatinine: 485 for TA 98 and 1318 for YG1024. Mean value of MN was 4.44 per 1000 binucleated cells and SCE frequency ranged between 6.24 and 10.06 with a mean value of 7.87. The results suggest the influence of exposure to environmental agents on the induction of cytogenetic effects in peripheral lymphocytes of children: namely Pb on MN and PAHs on SCE. The sources of that exposure may be outdoor and indoor. Emissions from coal-burning stoves are important contributors to the total exposure to PAHs and Pb in Silesian children.

Adolescent↗

PubMed2004

Signatures of environmental exposures using peripheral leukocyte gene expression: tobacco smoke.

Functional biological markers of environmental exposures are important in epidemiological studies of disease risk. Such markers not only provide a measure of the exposure, they also reflect the degree of physiological and biochemical response to the exposure. In an observational study, using DNA microarrays, we show that it is possible to distinguish between 85 individuals exposed and unexposed to tobacco smoke on the basis of mRNA expression in peripheral leukocytes. Furthermore, we show that active exposure to tobacco smoke is associated with a biologically relevant mRNA expression signature. These findings suggest that expression patterns can be used to identify a complex environmental exposure in humans.

Adult↗

PubMed2002

Environmental exposure to lead as a risk for prostate cancer.

OBJECTIVE: To evaluate the possible role of environmental exposure to lead as a risk factor for prostate pathology in patients suffering from prostate cancer (PCA) and benign prostate hyperplasia (BPH). METHODS: Blood lead (BPb) level was determined in PCA and BPH cases using a graphite furnace Atomic Absorption Spectrophotometer and compared with those in a control group living in the similar socioeconomic environment. RESULTS: BPb was significantly higher in PCA and BPH cases than in normals (P < 0.05). Blood levels of zinc and copper were significantly lower in PCA and BPH cases when compared with controls (P < 0.05). In all the three groups, a statistically significant positive correlation between lead and thiobarbituric acid reactive substances (TBARS) measured as malondialdehyde, and negative correlation between blood lead and antioxidant GSH level, indicative of possible generation of reactive oxygen species, were also observed after adjusting for age as a possible confounders. However, positive association between blood lead and TBARS was relatively higher in PCA patients (r = 0.77, P < 0.05) than in BPH (r = 0.32, P < 0.05) and normal (r = 0.30, P < 0.05). CONCLUSION: These results with limited power seem to suggest for the first time that environmental exposure of aging males to lead may be a risk factor for prostate cancer and/or benign prostate hyperplasia possibly through generation of reactive oxygen species and/or reducing the level of zinc which acts as a cellular growth protector.

Aged↗

PubMed2003

Validation of an environmental exposure unit for controlled human inhalation studies with grass pollen in patients with seasonal allergic rhinitis.

BACKGROUND: There is an increasing need for allergen inhalation systems to perform basic clinical research and test anti-allergic drugs under well-controlled conditions. This requires stability of environmental conditions like temperature and humidity, as well as allergen concentration and reproducible induction of allergic symptoms. OBJECTIVE: The aim of this study was to validate an environmental exposure unit for controlled human pollen inhalation studies in participants with seasonal allergic rhinitis. METHODS: Temperature, relative humidity, and air flow rate were kept constant with an air conditioning system. Pollen atmosphere was generated using a specially designed feeding system and monitored online by laser counter and offline using rotating rod samplers. Efficacy (total nasal symptom score, nasal air flow rate, nasal secretion) and safety (lung function) parameters were evaluated at different pollen concentrations and repeated allergen challenges. RESULTS: Temperature, humidity, and air flow rate in the environmental exposure unit remained constant within a range of <2%. The spatial distribution and the temporal stability of the pollen concentration varied only slightly over 4 h (+/-10% and <4%, respectively). Dose-dependent induction of allergic rhinitis symptoms, reduction in nasal air flow rate, and increase in nasal secretion were observed over time. These effects were reproducible from day to day. Lung function remained clinically normal at all concentrations and from day to day. CONCLUSIONS: Thus, pollen exposure in the environmental exposure unit is an effective, reproducible, safe, and suitable method for single-centre clinical studies on the efficacy of anti-allergic treatment or basic clinical research.

Adult↗

PubMed2006

Conjugal transformed mycosis fungoides: the unknown role of viral infection and environmental exposures in the development of cutaneous T-cell lymphoma.

The etiology of mycosis fungoides (MF) is uncertain, although infectious agents and other environmental exposures have been implicated. We describe what appears to be the first case in which both a husband and his wife were diagnosed with large-cell transformation of MF. After 10 years of having stage I MF, the wife developed tumors that showed sheets of large transformed cells with dysplastic nuclei on skin biopsies, leading to a diagnosis of transformed MF. Her husband was diagnosed 14 months later with transformed MF following a biopsy of his right arm and leg after a 15-year history of presumed psoriasis. The fact that this rare occurrence happened in a couple who had been married for more than 25 years points to a common environmental exposure. Future studies should aim to clarify the potential role of infectious agents, such as human T-lymphotropic virus I and II, cytomegalovirus, Epstein-Barr virus, and other environmental exposures, in the development of MF.

Aged↗

PubMed2006

Respiratory health in Turkish asbestos cement workers: the role of environmental exposure.

AIM: Benign and malignant pleural and lung diseases due to environmental asbestos exposure constitute an important health problem in Turkey. The country has widespread natural deposits of asbestos in rural parts of central and eastern regions. Few data exists about the respiratory health effects of occupational asbestos exposure in Turkey. A cross-sectional study was conducted to investigate respiratory health effects of occupational asbestos exposure and the contribution of environmental asbestos exposure. METHODS: Investigations included asbestos dust measurements in the workplace and application of an interviewer-administered questionnaire, a standard posteroanterior chest X-ray and spirometry. Information on birthplace of the workers was obtained in 406 workers and used to identify environmental exposure to asbestos, through a map of geographic locations with known asbestos exposure. RESULTS: Asbestos dust concentration in the ambient air of the work sites (fiber/ml) ranged between 0.2 and 0.76 (mean: 0.25, median: 0.22). Environmental exposure to asbestos was determined in 24.4% of the workers. After the adjustment for age, smoking, occupational asbestos exposure, and potential risk factors environmental asbestos exposure was associated with small irregular opacities grade > or = 1/0 (44.2% vs. 26.6%, P < 0.01), FVC% (97.8 vs. 104.5, P < 0.0001), and FEV1% (92.4 vs. 99.9, P < .0001). Occupational exposure to asbestos was associated with small irregular opacities grade > or = 1/0 (OR: 2.0, 95% CI: 1.3-3.1, per 1 unit increase in the natural logarithm of fiber/ml) and FEV1/FVC% (beta: 1.1, SEM: 0.54; P < 0.05, per 1 unit increase in the natural logarithm of fiber/ml). CONCLUSIONS: Environmental exposure to asbestos could increase the risk of asbestosis and lung function impairment in workers occupationally exposed to asbestos, independent from occupational exposure and smoking.

Adult↗

PubMed2025

Proteomic signatures and predictive modeling of cadmium-associated anxiety in middle-aged and elderly populations: an environmental exposure association study.

BACKGROUND: Emerging evidence implicates environmental contaminants such as cadmium (Cd) as modifiable risk factors for anxiety. Despite growing recognition of heavy metal toxicity in neuropsychiatric disorders, the molecular mechanisms linking environmental exposure to anxiety pathogenesis remain poorly understood. METHODS: Based on the established cohort of individuals with cognitive impairment in cadmium-contaminated areas, this cross-sectional association study enrolled 50 middle-aged and elderly hospitalized patients from these regions, adhering to the STROBE guidelines. Blood concentrations of cadmium (Cd), lead (Pb), and mercury (Hg) were analyzed in relation to anxiety severity assessed via the Hamilton Anxiety Rating Scale (HAMA). Plasma proteomic profiling was performed using data-independent acquisition (DIA) quantitative technology with an LC-MS/MS platform (timsTOF Pro, Bruker Daltonics), systematically characterizing 2,531 proteins across all samples. Machine learning techniques, specifically XGBoost and LASSO, were employed to identify biomarkers that were subsequently validated through mediation analysis and animal experiments, allowing for the screening of key protein signatures. Finally, clinical variables were integrated to construct a comprehensive model, which was then thoroughly evaluated. RESULTS: Anxious individuals exhibited significantly higher blood Cd levels than controls (β = 0.50, 95% CI: 0.07-0.93, p < 0.01), with anxiety positively correlating with depression (r = 0.62, p = 0.003) and inversely with ApoE3 genotype prevalence. Proteomics identified 120 differentially expressed proteins in anxious patients, enriched in oxidative phosphorylation and neurodegenerative pathways. CCDC126 emerged as a cadmium-associated biomarker, validated in rat models exposed to Cd. Combining CCDC126, blood Cd, Pb, and hypertension, a clinical prediction model achieved robust discrimination (AUC = 0.80, validation cohort). CONCLUSIONS: This first integrative environmental-proteomic study highlights cadmium's synergistic role in anxiety pathophysiology and psychiatric comorbidity. The predictive model offers translatable potential for early risk stratification, while CCDC126 provides mechanistic insights for targeted interventions in populations exposed to environmental pollutants.

Cadmium↗

PubMed1988

Extrapolation of laboratory findings to risks from environmental exposures: male reproductive effects of ethylene oxide.

The extrapolation of human risk from laboratory findings is based on physiologic and biochemical similarities between humans and test animals. While these extrapolations can be based on correlations and empiric relationships, such relationships must be derived for each agent and new set of exposure conditions. The complexity and diversity of environmental exposures severely limit the number of situations in which this may be done. An alternative approach is to use linked pharmacokinetic and pharmacodynamic models to estimate the tissue concentrations and subsequent effects associated with a given type of exposure. This approach has the advantage of allowing a determination of the tissue levels of the agent and of its effects for different time profiles of exposure and routes of entry. It permits comparisons of animal studies that use different experimental protocols. The utility of this approach was illustrated by quantitatively extrapolating from laboratory studies of male mice to mutational risk of male sterilizer operators exposed to ethylene oxide. This approach puts severe data demands on the researcher building models: extensive physiologic, biochemical and metabolic data must be available or estimable for body compartments; time-course and dose-response data must be available on the effects; and environmental exposure profiles must be available. However, it permits a degree of coordination of laboratory and epidemiologic studies that has rarely been possible. It also identifies potential new human risks, and a way of formulating testable hypotheses about human effects that are directly derived from laboratory data. Thus, this approach offers an exciting opportunity for better characterization of human effects and potential risks.

Animals↗

PubMed2004

Effect of environmental exposure to cadmium on pregnancy outcome and fetal growth: a study on healthy pregnant women in China.

The objective of the present study was to evaluate the potential effect of environmental exposure to cadmium on pregnancy outcome and fetal growth. Normal pregnant women were selected from Da-ye city of Hubei province, a cadmium-polluted area, from November 2002 through January 2003. Whole blood of pregnant women, cord blood, and placenta were collected and cadmium levels were determined by inductively coupled plasma emission mass spectroscopy. Incidence rate of preterm labor (gestational age < or = 37 weeks) and neonatal asphyxia, neonatal birth height, and birth weight were compared between lower and higher cadmium exposure level groups. Whole blood cadmium of 44 mothers ranged from 0.80 to 25.20 microg/L. Cadmium concentration in maternal blood was significantly higher than that in cord blood (t = 11.44, P < 0.01). Placenta cadmium ranged from 0.084 to 3.97 microg/g dry weight. After adjustment for maternal age, history of gestation, abortion and lactation, Logistic regression analysis showed that there was no significant association between cadmium exposure levels and pregnancy outcome (premature labor or neonatal asphyxia). Multiple linear regression analysis showed that, cord blood cadmium level, but not maternal blood cadmium and placenta cadmium, was significantly negatively associated with neonatal birth height (t= -2.33, P < 0.05). Compared with lower cord blood cadmium level (< or = 0.40 microg/L), higher level of cord blood cadmium (>0.40 microg/L) was associated with 2.24cm decrease in neonatal birth height. There was no significant association between cadmium exposure and birth weight. It was concluded that environmental exposure to cadmium significantly lower neonatal birth height.

Adult↗

PubMed2005

Interaction between genetic susceptibility and early-life environmental exposure determines tumor-suppressor-gene penetrance.

Gene-environment interactions are important determinants of cancer risk. Traditionally, gene-environment interactions are thought to contribute to tumor-suppressor-gene penetrance by facilitating or inhibiting the acquisition of additional somatic mutations required for tumorigenesis. Here, we demonstrate that a distinctive type of gene-environment interaction can occur during development to enhance the penetrance of a tumor-suppressor-gene defect in the adult. Using rats carrying a germ-line defect in the tuberous sclerosis complex 2 (Tsc-2) tumor-suppressor gene predisposed to uterine leiomyomas, we show that an early-life exposure to diethylstilbestrol during development of the uterus increased tumor-suppressor-gene penetrance from 65% to >90% and tumor multiplicity and size in genetically predisposed animals, but it failed to induce tumors in wild-type rats. This exposure was shown to impart a hormonal imprint on the developing uterine myometrium, causing an increase in expression of estrogen-responsive genes before the onset of tumors. Loss of function of the normal Tsc-2 allele remained the rate-limiting event for tumorigenesis; however, tumors that developed in exposed animals displayed an enhanced proliferative response to steroid hormones relative to tumors that developed in unexposed animals. These data suggest that exposure to environmental factors during development can permanently reprogram normal physiological tissue responses and thus lead to increased tumor-suppressor-gene penetrance in genetically susceptible individuals.

Animals↗

PubMed2005

Test-retest repeatability of self-reported environmental exposures in Parkinson's disease cases and healthy controls.

There is substantial disagreement among published epidemiological studies regarding environmental risk factors for Parkinson's disease (PD). Differences in the quality of measurement of environmental exposures may contribute to this variation. The current study examined the test-retest repeatability of self-report data on risk factors for PD obtained from a series of 32 PD cases recruited from neurology clinics and 29 healthy sex-, age- and residential suburb-matched controls. Exposure data were collected in face-to-face interviews using a structured questionnaire derived from previous epidemiological studies. High repeatability was demonstrated for 'lifestyle' exposures, such as smoking and coffee/tea consumption (kappas 0.70-1.00). Environmental exposures that involved some action by the person, such as pesticide application and use of solvents and metals, also showed high repeatability (kappas>0.78). Lower repeatability was seen for rural residency and bore water consumption (kappa 0.39-0.74). In general, we found that case and control participants provided similar rates of incongruent and missing responses for categorical and continuous occupational, domestic, lifestyle and medical exposures.

Aged↗