SEARCH · PubMed Health

Results for “Environmental Exposure”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources

PubMed2003

How environmental exposures influence the development and exacerbation of asthma.

Environmental exposures may increase a child's risk of developing asthma and also may increase the risk of asthma exacerbations. This article reviews several environmental exposures and suggests whether they contribute to asthma prevalence, asthma exacerbations, or both. Outdoor air exposures and violence are not likely to cause the increase in asthma prevalence. Exposure to outdoor air pollutants primarily leads to increased exacerbations, sometimes manifested as asthma clusters. Clinicians should be alert for space-time clusters of asthma exacerbations in the community, because these clusters may suggest a modifiable point-source exposure. Indoor air exposures are more strongly linked to the increase in asthma prevalence. Exposure to dust mites and tobacco smoke are risk factors for the development of asthma and may also exacerbate existing asthma. Effective measures to prevent exposures to these pollutants are available. With proper management, the amount of environmental exposures can be decreased. Whether decreasing these exposures will result in decreases in asthma prevalence and exacerbations is not yet documented.

Air Pollution↗

PubMed2002

Chronic effects of toxic environmental exposures on children's health.

Children have unusual patterns of exposure to environmental chemicals, and they have vulnerabilities that are quite distinct from those of adults. Increasingly, children's exposures to chemicals in the environment are understood to contribute to the causation and exacerbation of certain chronic, disabling diseases in children including asthma, cancer, birth defects, and neurobehavioral dysfunction. The protection of children against environmental toxins is a major challenge to modern society.

Asthma↗

PubMedDate not supplied

Environmental exposure and lifestyle predictors of lead, cadmium, PCB, and DDT levels in Great Lakes fish eaters.

A previously characterized cohort of 115 Great Lakes fish eaters and 95 non-fish-eating regional controls was reexamined in 1989. Levels of blood lead and cadmium and serum PCB and DDT were measured. Lifestyle characteristics, including recent and historic fish consumption, were evaluated as predictors of contaminant levels using multivariate regression analysis. Significantly elevated serum PCB and DDT levels were observed in fish eaters, compared with controls. Historic fish consumption, rather than recent consumption, was identified as the primary predictor of current serum levels. Mean blood lead and cadmium were also significantly higher in fish eaters than in controls. However, the primary predictors of lead and cadmium were behavioral exposures--specifically smoking and self-reported occupational and recreational exposure-rather than fish consumption. These findings illustrate the importance of evaluating a variety of possible sources when investigating human exposure to environmental contaminants.

Adult↗

PubMed2002

DNA methylation and environmental exposures in human hepatocellular carcinoma.

BACKGROUND: Hypermethylation of a CpG-rich promoter (CpG island) blocks expression of the corresponding gene. The CpG island methylator phenotype (CIMP), defined as a variable pattern of hypermethylation of CpG islands in tumor suppressor genes, may be associated with carcinogenesis. To determine whether CIMP is associated with the development of hepatocellular carcinoma (HCC) and with exposure to environmental agents, we examined the methylation status of CpG islands in HCCs from countries with various HCC risks. METHODS: We examined the methylation status of 12 CpG islands (eight for known genes) in 85 HCC tumors from various geographic locations by use of bisulfite-polymerase chain reaction methylation assays and analyzed results with univariate and multivariable methods. All statistical tests were two-sided. RESULTS: Eight CpG islands were hypermethylated. The frequency of hypermethylation in the 85 tumors was 62% for the estrogen receptor (ER), 42% for p16, 18% for cyclooxygenase-2, 21% for the T-type calcium channel gene, 38% for MINT31, 28% for MINT1, 15% for MINT27, and 11% for MINT2 (the latter four CpG islands are not yet associated with genes). Methylation levels of the eight frequently methylated CpG islands were positively correlated (from R =.2 [P =.05] to R =.6 [P<.001]), supporting the presence of CIMP. p16 methylation had statistically significant geographic variation (34.4% in tumors from China and Egypt versus 12.2% in tumors from the United States and Europe, difference = 22.2%; 95% confidence interval [CI] = 11.2% to 33.2%; P<.001). Similar geographic variations were observed for ER methylation and CIMP. This observation was partly related to higher methylation in tumors from patients with cirrhosis (33.6% for patients with cirrhosis versus 11.7% for those without it; difference = 21.9%; 95% CI = 10.9% to 32.8%; P<.001) or hepatitis (34.2% for patients with hepatitis versus 6.2% for those without it; difference = 28%; 95% CI = 18.3% to 37.6%; P<.001). CONCLUSION: Geographic variations in the methylation status of various CpG islands indicate that environmental factors may influence the frequent and concordant degree of hypermethylation in multiple genes in HCC tumors.

Aflatoxins↗

PubMed1991

Altitude and allergy to house-dust mites. A paradigm of the influence of environmental exposure on allergic sensitization.

To further investigate the possibility of a cause and effect relationship between exposure to house-dust mite (HDM) allergens and respiratory disease associated with dust mite sensitivity, we compared schoolchildren living in the Alps, where exposure to HDM is low, with those living at sea level, where it is high. The study included 933 schoolchildren from the fourth and fifth grades. The protocol included the standardized 1978 American Thoracic Society (ATS) questionnaire for children, skin testing using common aero-allergens and controls, and antigenic measurements of dust samples from mattresses (Group I antigen). The prevalence of asthma with positive skin test to HDM and the overall prevalence of positive skin test to HDM were significantly lower in mountain schoolchildren. The mean geometric HDM antigenic level in mattresses was much lower in the Alps (0.36 micrograms/g dust) than at sea level (15.8 micrograms/g dust). In contrast, the prevalence of hay fever and positive skin test to grass pollens as well as the overall prevalence of positive skin tests to grass pollens were significantly higher in the Alps. These data illustrate a striking relationship between exposure to environmental allergens and atopic sensitization.

Altitude↗

PubMedDate not supplied

Estimating environmental exposures to sulfur dioxide from multiple industrial sources for a case-control study.

This paper first discusses how population exposures to environmental pollutants are estimated from environmental monitoring data and the problems that are encountered in estimating risk from pollutants on the basis of ecologic studies. We then present a technique of estimating individualized exposures to an atmospheric pollutant, sulfur dioxide (SO2), through atmospheric transport modeling for a case-control study. The transport model uses the quantities of SO2 released from 30 geographically identified industrial facilities and meteorological data (wind speed and direction) to predict the downwind ground-level concentrations of SO2 at geographically identified residences, receptors, of 797 study subjects. A distribution of facility SO2 emissions, uncertainties in effective stack height, and model uncertainty are incorporated to examine the uncertainty in the predicted versus ambient monitoring SO2 levels, and to generate an exposure uncertainty distribution for both the cases and controls. The transport model's accuracy is evaluated by comparing recorded ambient measurements of SO2 with the model's predicted SO2 estimates at geographically identified ambient monitoring stations.

Air Pollutants↗

PubMed1997

Urinary chromium as a biological marker of environmental exposure: what are the limitations?

Public concern has mounted recently about environmental exposures to chromium in soil, tap water, and ambient air. In response, agencies charged with protecting public health have attempted to study exposure by monitoring urinary chromium levels among potentially exposed populations. While urinary biomonitoring of occupationally exposed workers has been successfully used to assess high-level inhalation exposures in the workplace, evaluating low-level environmental exposures has been problematic. Due to these problems, before an extensive biological monitoring study is conducted of those exposed to low levels of environmental chromium, several issues must be resolved. First, exposures to chromium must occur at the same time as sampling, because the biological half-life of chromium in urine is very short (less than 2 days). Second, reduced bioavailability and bioaccessibility via the oral and dermal routes of exposure limit the capacity of urinary monitoring to measure environmental exposures (e.g., systemic dose is too small to be measured). Third, the dose of chromium must be sufficient such that it may be reliably measured above background levels in urine (range of 0.2 to 2 microg/liter) and above the analytical limit of detection (0.2 microg/liter). Fourth, the inter- and intrapersonal variability in background levels of urinary chromium is known to be significant and influenced by food and beverage intake, smoking, and exercise. Thus, the role of each factor must be carefully understood. Finally, it is imperative to have developed a complete understanding of the clinical significance of elevated urinary chromium levels before a study is performed, because higher than background levels, in and of themselves, are not indicative of a significant health concern. The route of exposure, valence of chromium to which people were exposed, exposure time, and duration must all be understood before the biological data can be implemented. We have conducted a total of nine human exposure studies over the past 3 years in an attempt to understand the kinetics of chromium and the impact on urinary, red blood cell (RBC), and plasma biomonitoring programs. The results of these studies are described here and our recommendations are offered for how to design and implement a urinary chromium biomonitoring study. In our view, given some evidence that the dose of hexavalent chromium [Cr(VI)] is sufficient to be measurable above background concentrations of total chromium [Cr(III) and Cr(VI)], duplicated measurements of chromium in plasma and RBCs are, in most cases, a more definitive gauge of environmental exposure than urinary biomonitoring.

Biological Availability↗

PubMed2006

Improving environmental exposure analysis using cumulative distribution functions and individual geocoding.

BACKGROUND: Assessments of environmental exposure and health risks that utilize Geographic Information Systems (GIS) often make simplifying assumptions when using: (a) one or more discrete buffer distances to define the spatial extent of impacted regions, and (b) aggregated demographic data at the level of census enumeration units to derive the characteristics of the potentially exposed population. A case-study of school children in Orange County, Florida, is used to demonstrate how these limitations can be overcome by the application of cumulative distribution functions (CDFs) and individual geocoded locations. Exposure potential for 159,923 school children was determined at the childrens' home residences and at school locations by determining the distance to the nearest gasoline station, stationary air pollution source, and industrial facility listed in the Toxic Release Inventory (TRI). Errors and biases introduced by the use of discrete buffer distances and data aggregation were examined. RESULTS: The use of discrete buffers distances in proximity-based exposure analysis introduced substantial bias in terms of determining the potentially exposed population, and the results are strongly dependent on the choice of buffer distance(s). Comparisons of exposure potential between home and school locations indicated that different buffer distances yield different results and contradictory conclusions. The use of a CDF provided a much more meaningful representation and is not based on the a-priori assumption that any particular distance is more relevant than another. The use of individual geocoded locations also provided a more accurate characterization of the exposed population and allowed for more reliable comparisons among sub-groups. In the comparison of children's home residences and school locations, the use of data aggregated at the census block group and tract level introduced variability as well as bias, leading to incorrect conclusions as to whether exposure potential was higher at school or at home. CONCLUSION: The use of CDFs in distance-based environmental exposure assessment provides more robust results than the use of discrete buffer distances. Unless specific circumstances warrant the use of discrete buffer distances, their applcation should be discouraged in favor of CDFs. The use of aggregated data at the census tract or block group level introduces substantial bias in environmental exposure assessment, which can be reduced through individual geocoding. The use of aggregation should be minimized when individual-level data are available. Existing GIS analysis techniques are well suited to determine CDFs as well as reliably geocode large datasets, and computational issues do not present a barrier for their more widespread use in environmental exposure and risk assessment.

Child↗

PubMed1993

Occupational and environmental exposures reported to poison centers.

This analysis of 25,368 occupational and 7,565 environmental exposure cases characterizes the occupational and environmental exposures reported to the American Association of Poison Control Centers Toxic Exposure Surveillance System. Compared with other poisonings, occupational and environmental exposures were predominantly inhalation exposures rather than ingestions, were more often subacute or chronic, and demonstrated greater morbidity, mortality, and increased use of health care resources. As regional poison centers evolve to fill a critical information void in the management and assessment of environmental and occupational exposures, the American Association of Poison Control Centers Toxic Exposure Surveillance System provides an important, untapped passive surveillance mechanism.

Air Pollutants↗

PubMed2004

Comparative clinical efficacy, onset and duration of action of levocetirizine and desloratadine for symptoms of seasonal allergic rhinitis in subjects evaluated in the Environmental Exposure Unit (EEU).

The Environmental Exposure Unit, an indoor pollen challenge system to test anti-allergic medications, was used to compare the onset and duration of action and the efficacy of levocetirizine and desloratadine, two recently developed H1-antagonists. In this double-blind, placebo-controlled, parallel-group study, qualified subjects were randomised to once-daily levocetirizine 5 mg (n = 141), desloratadine 5 mg (n = 140) or placebo (n = 92) and exposed to ragweed pollen on two consecutive days (7 h and 6 h). Symptoms were self-rated every 30 min. On both days, levocetirizine produced a greater improvement in the major symptom complex score (primary efficacy variable) than desloratadine (p = 0.015); both were better than placebo (p < 0.001). Levocetirizine acted earlier (1 h vs. 3 h) and produced greater symptom relief at 24 h than desloratadine (p = 0.003). Levocetirizine also alleviated nasal obstruction better than desloratadine (p = 0.007) on day 1; and better than placebo (p = 0.014) after the second dose on day 2, which was not observed with desloratadine. Levocetirizine and desloratadine were safe and well tolerated.

Adolescent↗

PubMedDate not supplied

Environmental exposure and occupational asthma.

Environmental exposure in relation to occupational asthma (OA) concerns the exposure of subjects in the work-place. There are qualitative and quantitative differences in occupational exposures which may influence the development and/or the course of OA. Although more than 300 different agents have been described causing OA, 5-6 groups of substances are sufficient to explain more than 80% of all cases of OA. In addition, a variant of occupational asthma without latency period may occur after an acute inhalation of massive concentrations of irritants, and exacerbations of a pre-existent asthma may be due to products or conditions in the work-place. Despite our increased knowledge of the etiology and pathophysiology of OA, its prevalence in the industrialised world has been relatively steady over the last decade. Therefore, the transfer of knowledge has not been sufficiently effective in the prevention of the disease. The results of studies on the exposure-response relationship for several high molecular weight chemicals (and fewer low molecular weight) indicate that sensitisation may be prevented in large part by reducing work-place concentrations of these agents. These data give support to the attempt to develop Threshold Limit Values (TLV) for sensitisers.

Asthma↗

PubMedDate not supplied

Identifying environmental health priorities for a whole nation: the use of principal environmental exposure pathways in the Philippines.

This paper presents a novel approach to establishing environmental health priorities for a large society, based upon the concept of principal environmental exposure pathways (PEEPs). Principal environmental exposure pathways extend the concept of a causal pathway backward from health outcome to exposure, then to the industrial, transportation, commercial, or living conditions that gave rise to the pollution of interest. In the Philippines, where the method was developed and used, five PEEPs were identified: an urban air-pollution pathway; a community water-supply pathway; an urban solid-waste pathway; a rural "point-source" pathway; and a pathway whereby fertilizers and pesticides affect food, worker health, and rural water supplies. Characterizing the PEEPs involved pinpointing the populations at risk necessary to estimate the burden of morbidity and mortality related to each as well as identifying the health outcomes that were experienced by those exposed along each pathway or that they could be expected to experience; determining where adequate health-outcome information was available or absent; where exposure sources were or were not adequately identified; where there were significant gaps in agency responsibilities; where new data flows were needed; and where things could have been improved by improving inter-agency cooperation. The most important success of the PEEP method was to reduce the "problem of everything" in a complex country of 65 million people to a small and manageable number of priority environmental exposures.

Air Pollution↗

PubMed1996

Biomarkers of environmental benzene exposure.

Environmental exposures to benzene result in increases in body burden that are reflected in various biomarkers of exposure, including benzene in exhaled breath, benzene in blood and urinary trans-trans-muconic acid and S-phenylmercapturic acid. A review of the literature indicates that these biomarkers can be used to distinguish populations with different levels of exposure (such as smokers from nonsmokers and occupationally exposed from environmentally exposed populations) and to determine differences in metabolism. Biomarkers in humans have shown that the percentage of benzene metabolized by the ring-opening pathway is greater at environmental exposures than that at higher occupational exposures, a trend similar to that found in animal studies. This suggests that the dose-response curve is nonlinear; that potential different metabolic mechanisms exist at high and low doses; and that the validity of a linear extrapolation of adverse effects measured at high doses to a population exposed to lower, environmental levels of benzene is uncertain. Time-series measurements of the biomarker, exhaled breath, were used to evaluate a physiologically based pharmacokinetic (PBPK) model. Biases were identified between the PBPK model predictions and experimental data that were adequately described using an empirical compartmental model. It is suggested that a mapping of the PBPK model to a compartmental model can be done to optimize the parameters in the PBPK model to provide a future framework for developing a population physiologically based pharmacokinetic model.

Air Pollutants↗

PubMed1995

Genetic factors in individual responses to environmental exposures.

Individual susceptibility to lung cancer due to occupational and environmental exposures to carcinogenic agents has been shown to be modulated by host-specific factors. The underlying principle of these factors is the differences that confer sensitivity or resistance to the disease. Since the majority of chemical carcinogens are not capable of causing hazardous effects per se, the metabolism of these compounds is a crucial part of the initial host response to the environmental exposure. Disturbances in the balance between activation and detoxification may thus explain the individual variations in responses to exposures to carcinogens. Many of the metabolic enzymes have recently been shown to express genetic polymorphisms in the population, and an association has been found between cigarette smoke-induced lung cancer and CYP1A1, CYP2D6, and GSTM1 genes. In addition, GSTM1 and NAT2 polymorphisms have been associated with susceptibility to bladder cancer. Since substantial ethnic differences exist in the distribution of altered and normal alleles, and findings in one ethnic group are not necessarily applicable to others, these biomarkers are still in the validation stage. However, as more information emerges on the specific features that lead to enhanced susceptibility they can undoubtedly be used to determine risks of environmental exposures to susceptible individuals and populations.

Arylamine N-Acetyltransferase↗

PubMedDate not supplied

Assessing environmental exposure in children: immunotoxicology screening.

Environmental exposure to a number of xenobiotics, including pesticides, can have serious effects on the immune system of children, thus rendering them susceptible to infections or other disease states. To study this problem, a recycling chromatographic system for assessing cytokine profiles in humans has been developed and used for the measurement of immune system function in children with documented exposure to residential pesticides. The system is capable of measuring 30 different analytes in a single sample thus enabling the same time examination of representative markers of immune differentiation and function. In the present study, a cohort of 25 exposed children were examined and shown to exhibit a number of features; all subjects demonstrated some abnormalities in cytokines associated with hematopoiesis. Additionally, elevations in pro-inflammatory cytokines and neuropeptides indicated a state of generalized and neurogenic inflammation. Further analysis indicated that a depression of the cellular arm of the immune system that correlated with clinical indicators of lowered host resistance to infection could also be detected in a subgroup of the exposed subjects. All exposed children demonstrated evidence of hyperstimulation of the humoral immune system as indicated by elevated IL-5 concentrations and clinical allergy. The degree of immune dysregulation in the exposed children was found to be quite marked when compared to similar studies performed on age-matched controls.

Biomarkers↗

PubMed2005

I PREPARE: development and clinical utility of an environmental exposure history mnemonic.

The I PREPARE environmental exposure history mnemonic is a quick reference tool created for primary care providers. Health care providers (N = 159) were asked to evaluate a prototype mnemonic, to suggest new health history questions, and to propose the deletion of less relevant questions. The goal of this evaluation was to create a practical and clinically relevant mnemonic, rather than to obtain quantitative estimates of validity. The final I PREPARE mnemonic cues the provider to "Investigate potential exposures;" ask questions related to "Present work," "Residence," "Environmental concerns," "Past work," and "Activities;" provide "Referrals and resources;" and "Educate" the patient by reviewing a checklist of strategies to prevent or minimize exposures. The sequence of I PREPARE makes intuitive sense by cueing the provider to ask specific questions and provide educational materials to the patient. National improvements in the quality of environmental exposure history data are predicated in part on the creation of simple and convenient tools for use in clinical practice.

Adult↗

PubMed1990

Environmental exposures with decreased risks for lung cancer?

The case for a decreased risk of lung cancer after exposure to environmental agents is evaluated using toxicological and epidemiological data. Experimental evidence demonstrates that exposure to substances which produce an inflammatory response in the lung, such as bacterial endotoxins, causes an increase in the secretion of inflammatory mediators and substances with a particular effect on tumour cells such as tumour necrosis factor (TNF). Other irritant agents, such as tobacco smoke, may also induce an activation of macrophages at low levels of exposure. Epidemiological evidence from several studies suggests that people exposed to dusts containing bacterial endotoxins have a lower lung cancer incidence than those who are unexposed. There are also some data suggesting that in certain ethnic groups, females smoking a small number of cigarettes/day, might have a lower risk for lung cancer than non-smokers. These data provide support for a hypothesis that low-dose exposures to some air pollutants might result in a decreased risk of lung cancer.

Cause of Death↗

PubMedDate not supplied

A linear model relating breath concentrations to environmental exposures: application to a chamber study of four volunteers exposed to volatile organic chemicals.

A linear model relating levels of volatile organic chemicals (VOCs) in exhaled breath to personal exposures at environmental (parts per billion) levels has been developed and evaluated in a chamber study of four human volunteers. The purpose of the model is to allow estimation of VOC concentrations in the body from measurements of exposure, or conversely to estimate previous exposure from a measurement of exhaled breath. The model differs from previous models in considering long-term inhalation at low or moderate concentrations rather than instantaneous intake (as in drug administration) or intermittent exposure at high concentrations (as in occupational situations). The model is based on a mass balance approach using one or more compartments to represent distribution of the chemical in the body. The main observable parameters in the model are the residence times tau 1 in the compartments, their "capacities" Ai, and the fraction f of the parent compound that is exhaled under equilibrium conditions. The basic equations for the one-, two-, three-, and n-compartment cases are derived. Solutions to these equations for the cases of a sudden constant high exposure, a sudden constant low exposure, and a linearly increasing exposure are provided. These solutions can be readily applied to more complex exposure scenarios. The chamber study suggests residence times on the order of a few minutes in the blood and 1-2 hr in the vessel-rich group of tissues. The design of the chamber study did not allow an estimate of the model parameters for fat; a subsequent chamber study has provided initial estimates of 50-100 hr. Field studies of personal exposures and breath concentrations of several hundred persons suggest values of f ranging from 0.1 for xylenes and ethylbenzene to about 0.9 for tetrachloroethylene.

Atmosphere Exposure Chambers↗