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PubMed2003

The relationship between human semen parameters and environmental exposure to polychlorinated biphenyls and p,p'-DDE.

Scientific and public concern exists about potential reproductive health effects of persistent chlorinated organic chemicals, such as polychlorinated biphenyls (PCBs), dichlorodiphenyltrichloroethane (DDT), and dichlorodiphenyldichloroethylene (DDE, the most stable daughter compound of DDT). To explore the hypothesis that environmental exposures to PCBs and DDE are associated with altered semen parameters, we conducted a cross-sectional study of 212 male partners of subfertile couples who presented to the Massachusetts General Hospital Andrology Laboratory. Semen parameters were analyzed as both a continuous measure and dichotomized based on World Health Organization reference values for sperm concentration (< 20 million/mL), motility (< 50% motile), and Kruger strict criteria for morphology (< 4% normal). The comparison group for the dichotomized analysis was men with all three semen parameters above the reference values. In serum, 57 PCB congeners and p,p -DDE were measured by congener-specific analysis using gas chromatography with electron capture detection. There were dose-response relationships among PCB-138 and sperm motility (odds ratio per tertile, adjusted for age, abstinence, and smoking, and p-value for trend were, respectively, 1.00, 1.68, 2.35, and p-value = 0.03) and morphology (1.00, 1.36, 2.53, p-value = 0.04). There was limited evidence of an inverse relationship between sum of PCBs, as well as those PCBs classified as cytochrome P450 enzyme inducers, with sperm motility and sperm morphology, as well as limited evidence of an inverse association between p,p -DDE and sperm motility. The lack of a consistent relationship among semen parameters and other individual PCB congeners and groupings of congeners may indicate a difference in spermatotoxicity between congeners.

Adult↗

PubMed1991

Thrombocytopenia associated with environmental exposure to polyurethane.

Few chemicals in the environment have been implicated as causes of isolated thrombocytopenia, and the evidence is usually less than convincing because the patients were not rechallenged with the chemical in vivo. In the present paper, a child is reported with the onset of thrombocytopenia in temporal association with environmental exposure to polyurethane. Five years after the initial thrombocytopenia had resolved, an inadvertent in vivo rechallenge with environmental polyurethane resulted in recurrence of the thrombocytopenia. This recurrence, together with the fact that only 1-4% of cases of idiopathic thrombocytopenic purpura in children recur, provided strong evidence for a causal role for the polyurethane exposure in this patient's thrombocytopenia. In summary, environmental exposure to polyurethane should be considered in the differential diagnosis of acquired thrombocytopenia in childhood.

Child, Preschool↗

PubMed2004

Variability of environmental exposures to volatile organic compounds.

Although studies of occupational exposure to volatile organic compounds (VOCs) often partition variability across groups, and between and within persons, those of environmental exposure to VOCs have not involved such partitioning. Using data from the Environmental Protection Agency's total exposure assessment methodology (TEAM) studies, we partitioned exposure variability across cities, and between and within persons for nine VOCs. The estimated variance components decreased in the order: within-person > between-person > across city. Despite their smaller magnitudes, estimates of between-person and across-city variance components were sufficiently large to provide reasonable contrast for informative epidemiology studies of most VOCs. Estimates of between-person variance components for environmental VOCs were similar to those published for occupational VOCs (groups defined by job and factory). However, estimates of within-person variance components were much greater for environmental VOCs, probably due to the greater diversity of locations (including the workplace) visited by the general public over time. For benzene and perchloroethylene, we used a simple model to calculate numbers of personal measurements required to relate the exposure level to health outcome statistically. About 10 times more personal measurements would be required to investigate perchloroethylene exposure as compared to benzene exposure; this disparity reflects the greater within-subject variability of perchloroethylene data compared to benzene data. We conclude that variability should be partitioned for environmental VOC exposures in much the same manner as for occupational exposures. There should be sufficient variability in the levels of most VOCs across cities and between subjects to provide reasonable contrast for informative epidemiology studies, as we illustrate for exposures to benzene. Yet, epidemiologists should be wary of investigating environmental VOCs without preliminary data with which to estimate the variance structure of exposure variables.

Air Pollutants↗

PubMedDate not supplied

Incorporating molecular genetic variation and environmental exposures into epidemiologic studies of congenital anomalies.

Epidemiologic studies of congenital anomalies rarely incorporate measurements of both environmental and genetic factors. Given the suspected etiologic heterogeneity that exists among congenital anomalies, focusing on only environmental or on only genetic factors may substantially decrease the likelihood for identifying either type of factor as a contributor to the risk of congenital anomalies. Incorporating information on genotypic variation into an epidemiologic study of environmental exposures may potentially lead to improvements in case classification with accompanying potential improvements in risk estimation. Such genotypic information may also lead to a clearer understanding of the underlying pathogenesis and etiology of congenital anomalies. Using recent research findings on congenital anomalies, we illustrated the issues of case classification and how a clearer impression of the underlying pathogenesis can be achieved with the addition of genotypic information to epidemiologic studies of congenital anomalies.

Adult↗

PubMed1997

trans,trans-muconic acid as a biomarker of non-occupational environmental exposure to benzene.

Excretion of trans,trans-muconic acid (2,4-hexadienedioic acid; t,t-MA), a potential biomarker of low-level exposure to benzene, was determined in 32 smokers and 82 nonsmokers. In smokers the median background excretion of t,t-MA was 0.13 (0.06-0.39) mg/g creatinine and was significantly higher (P < 0.05) than the value of 0.065 (0.02-0.59) mg g creatinine in nonsmokers. For nonsmokers, the correlation between t,t-MA excretion and environmental exposure to benzene in ambient air, which was determined during the 8-day study period by personal diffusion samplers, was not significant (r = 0.164, P = 0.18). Nonsmokers living in the city tended to have higher t,t-MA excretion rates than nonsmokers living in the suburbs. However, the difference was only significant for nonsmokers from nonsmoking homes. For the same location (suburb or city), smoking at home leads to a marginal increase in t,t-MA excretion of the nonsmoking members of the household. In a further study with eight nonsmokers we found that dietary supplementation with 500 mg sorbic acid significantly increased (P < 0.001) the mean urinary t,t-MA excretion from 0.08 (0.04-0.12) to 0.88 (0.57-1.48) mg/24 h. Under study conditions 0.12% of the sorbic acid dose was excreted in urine as t,t-MA, thereby indicating that a typical dietary intake of 6-30 mg/day sorbic acid accounts for 10-50% of the background t,t-MA excretion in nonsmokers, and for 5-25% in smokers. As a consequence, sorbic acid in the diet is a significant confounding factor in assessing low-level benzene exposure if t,t-MA excretion in urine is used as a biomarker.

Benzene↗

PubMed1999

Double exposure. Environmental tobacco smoke.

One study after another is finding strong associations between a variety of human illness and exposure to environmental tobacco smoke (ETS). A 1986 report by the U.S. Surgeon General concluded that ETS is a cause of disease, including lung cancer, in healthy nonsmokers. Other reports have documented causal associations between ETS and lower respiratory tract infections, middle ear disease and exacerbation of asthma in children, heart disease, retardation of fetal growth, sudden infant death syndrome, and nasal sinus cancer. However, the findings from many of these studies remain controversial. A number of scientists remain skeptical about the association between ETS and serious illness in nonsmokers, charging that scientific journals either fail to publish pro-tobacco findings and meta-analyses or disregard those that are published. They also claim that many epidemiological studies declare causal associations based on marginal odds ratios.

Air Pollution, Indoor↗

PubMed1999

Communicating their individual results to participants in an environmental exposure study: insights from clinical ethics.

The objective of this study was to formulate a framework for determining what information to communicate to individual subjects of a study measuring biomarkers of exposure, consistent with the principles of ethical clinical and research practice. Methods consisted of review of the scope of environmental exposure studies, including the use of biomarker measurement in clinical medicine and environmental research and the relevant principles of clinical ethics and research practice. An exposure biomarker study is designed to elucidate constitutional, behavioral, and environmental determinants of tissue concentrations of exogenous substances. Of itself, it is not designed to measure risk relations, those being the relation between biomarker levels and health outcomes. In many settings, measured tissue biomarker concentrations fall below those known or reasonably predicted to cause disease. Ethical clinical and research practice, aiming to maximize autonomy and beneficence and to minimize harm, requires that study findings concerning the determinants of exposure be communicated to study participants. In addition, investigators should reference clinical action levels beyond which individual biomarker results are routinely communicated to participants. When biomarkers have no known relation to risk, or when levels fall below action levels, it may be preferable not to communicate individual results, if this arrangement has been formalized at the time of informed consent.

Biomarkers↗

PubMed1992

Both inherited susceptibility and environmental exposure determine the low-density lipoprotein-subfraction pattern distribution in healthy Dutch families.

A lipoprotein profile characterized by a predominance of small, dense, low-density lipoprotein (LDL) particles has been associated with an increased risk of atherosclerosis. To investigate whether genetic factors are involved in determining this heavy LDL subfraction pattern, this study was undertaken with the aim of resolving the effects that major genes, multifactorial heritability, and environmental exposures have on the LDL subfraction pattern. In a random sample of 19 healthy Dutch families including 162 individuals, the distribution of the LDL subfraction pattern was determined by density gradient ultracentrifugation. For each subject a specific LDL subfraction profile was observed, characterized by the relative contribution of the three major LDL subfractions--LDL1 (d = 1.030-1.033 g/ml), LDL2 (d = 1.033-1.040 g/ml), and LDL3 (d = 1.040-1.045 g/ml)--to total LDL. A continuous variable, parameter K, was defined to characterize each individual LDL subfraction pattern. Complex segregation analysis of this quantitative trait, under a model which includes a major locus, polygenes, and both common and random environment, was applied to analyze the distribution of the LDL subfraction pattern in these families. The results indicate that the LDL subfraction pattern, described by parameter K, is controlled by a major autosomal, highly penetrant, recessive allele with a population frequency of .19 and an additional multifactorial inheritance component. The penetrance of the more dense LDL subfraction patterns, characterized by values of K < 0, was dependent on age, gender, and, in women, on oral contraceptive use and postmenopausal status. Furthermore, multiple regression analysis revealed that approximately 60% of the variation in the LDL subfraction pattern could be accounted for by alterations in age, gender, relative body weight, smoking habits, hormonal status in women, and lipid and lipoprotein levels. In conclusion, our results indicate that genetic influences as well as environmental exposure, sex, age and hormonal status in women are important in determining the distribution of the LDL subfraction patterns in this population and that these influences may contribute to the explanation of familial clustering of coronary heart disease.

Adult↗

PubMed2001

The rationale for a national prospective cohort study of environmental exposure and childhood development.

Evidence is growing that pre- and perinatal exposures and factors play a role in not only childhood but adulthood disorders. Therefore, there is a compelling need to undertake a national cohort study to evaluate the effects of such factors, ideally through adult life. Several recent developments, including advancements in computer technology, the management, storage, and analysis of biological specimens, and the rapid growth of genetic markers, facilitate the evaluation of the influence of environmental exposures on the subsequent risk of developmental abnormalities and disease. The rationale behind the establishment of such a cohort is discussed.

Adolescent↗

PubMed2006

Environmental exposure assessment of pesticides in farmworker homes.

Farmworkers and their families are exposed to pesticides both at work and in their homes. Environmental exposure assessment provides a means to evaluate pesticides in the environment and human contact with these chemicals through identification of sources and routes of exposure. To date, a variety of methods have been used to assess pesticide exposure among farmworker families, mostly focusing on dust and handwipe samples. While many of the methods are similar, differences in the collection, chemical analysis, and statistical analysis, can limit the comparability of results from farmworker studies. This mini-monograph discusses the strategies used to assess pesticide exposures, presents limitations in the available data for farmworkers, and suggests research needs for future studies of pesticide exposure among farmworker families.

Agriculture↗

PubMed2004

Impact of environmental exposures on the mutagenicity/carcinogenicity of heterocyclic amines.

Carcinogenic heterocyclic amines are produced from overcooked foods and are highly mutagenic in most short-term test systems. One of the most abundant of these amines, 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), induces breast, colon and prostate tumors in rats. Human dietary epidemiology studies suggest a strong correlation between either meat consumption or well-done muscle meat consumption and cancers of the colon, breast, stomach, lung and esophagus. For over 20 years our laboratory has helped define the human exposure to these dietary carcinogens. In this report we describe how various environmental exposures may modulate the risk from exposure to heterocyclic amines, especially PhIP. To assess the impact of foods on PhIP metabolism in humans, we developed an LC/MS/MS method to analyze the four major PhIP urinary metabolites following the consumption of a single portion of grilled chicken. Adding broccoli to the volunteers' diet altered the kinetics of PhIP metabolism. At the cellular level we have found that PhIP itself stimulates a significant estrogenic response in MCF-7 cells, but even more interestingly, co-incubation of the cells with herbal teas appear to enhance the response. Numerous environmental chemicals found in food or the atmosphere can impact the exposure, metabolism, and cell proliferation response of heterocyclic amines.

Animals↗

PubMed2001

[Application of the interaction models between the polymorphism(s) of metabolic gene(s) and environmental exposure].

OBJECTIVE: Taking GST M1 as an example to introduce analytic method of interaction models between the polymorphism(s) of metabolic gene(s) and environmental exposure in stomach cancer susceptibility. METHODS: Using community-based case-control design, combined with molecular biological techniques (PCR) and multiple variables logistic regression models, we analyzed 112 intestinal types of stomach cancer cases with endoscopy and pathology diagnosis in the Yangzhong City Hospital during January 1997 and December 1998. A total of 675 controls were selected from persons who had no history of digestive system cancers. RESULTS: After adjustment of confounding variables with both GST M1 null genotype and history of ever tobacco smoking, the results showed a significant types of 4 gene-environment interaction. Interaction index (gamma) value was 3.38 and OR(eg) value was 8.40, suggesting that a super multiplicative interaction occurred. The results also showed that GST M1 null genotype had a high exposure-gene effect interaction with tobacco smoking (pack year), while gamma values were 0.995, 2.085 and 2.157 respectively. A low exposure-gene effect interaction was found in GST M1 null genotype with the amount of (kg x year) alcohol consumption while gamma values were 1.01 and 0.97 respectively. CONCLUSION: Logistic regression model can be used to evaluate gene-environment interaction and dose-response of exposure-gene effect.

Alcohol Drinking↗

PubMed2004

Acute childhood leukaemia and environmental exposure to potential sources of benzene and other hydrocarbons; a case-control study.

AIM: To analyse the association between potential environmental exposure to hydrocarbons and the risk of acute childhood leukaemia. METHODS: A hospital based multicentre case control study, stratified on centre, age, and sex, with 280 leukaemia cases and 285 controls was carried out. Data were collected by a standardised interview of the mothers. RESULTS: No clear association was seen between maternal occupational exposure to hydrocarbons during pregnancy and leukaemia, or between residential traffic density and leukaemia. There was an association between dwellings neighbouring a petrol station or a repair garage during childhood and the risk of childhood leukaemia (OR 4.0, 95% CI 1.5 to 10.3), with a duration trend. The association, which appeared particularly strong for acute non-lymphocytic leukaemia (OR 7.7, 95% CI 1.7 to 34.3), was not altered by adjustment for potential confounding factors. CONCLUSIONS: Results showed an association between acute childhood leukaemia and dwellings neighbouring auto repair garages and petrol stations, which are benzene emitting sources. These findings could be due to chance, although the strength of the association and the duration trend are arguments for a causal association.

Benzene↗

PubMed2000

Neurological effects of environmental exposure to arsenic in dust and soil among humans.

Persons living in a small town in Georgia, USA, were studied because of known environmental exposure to arsenic-containing dust. To assess the effects of this exposure on the nervous system, a cross-sectional epidemiological study was performed. The health outcome assessments of the study were based on a priori selected clinical examination results and quantitative electrophysiologic and behavioral outcome measures. Because the primary goal was to identify cases of peripheral neuropathy, a clinically relevant case definition, based on results of these outcomes was created. Historical exposure reconstructions were performed on a subset of the exposed subjects for whom such information was available. Of the 238 persons enrolled in the study, 133 were classified as non-exposed (i.e., did not reside in the area of known exposure) and 105 were classified as exposed (i.e., did reside in the area of known exposure). Following exclusions of persons with occupational exposure to neurotoxicants, pre-existing conditions associated with peripheral nerve impairment, or age below 18 years, 118 unexposed subjects and 85 exposed subjects were available for inclusion in the analyses of peripheral nerve outcomes. A total of 4 (3.4%) of the unexposed subjects and 13 (15.3%) of the exposed subjects met the case definitions for peripheral neuropathy (OR=5.1; p=0.004). Comparison of three exposure groups (none, low, high) did not yield statistically significant differences. Statistically significant exposure group differences were observed on quantitative tests of standing steadiness, vibrotactile threshold and tremor intensity but not for nerve conduction measures. These results demonstrate a strong association between community arsenic containing dust exposure and peripheral neuropathy among participants in this investigation.

Adult↗

PubMed2001

Significance of cadmium concentrations in blood and hair as an indicator of dose 15 years after the reduction of environmental exposure to cadmium.

To evaluate the significance of cadmium (Cd) concentrations in blood (B-Cd) and hair (H-Cd) as an indicator of dose, a cross-sectional study was performed on 40 residents in a Cd-polluted area, Nagasaki Prefecture, Japan, in 1996. In the study area, soil replacement of Cd-polluted rice fields ended in 1981. B-Cd and H-Cd were significantly higher in the study population than in the control subjects. B-Cd was positively correlated with urinary Cd (U-Cd) (Spearman r=0.50, P=0.06 for males and r=0.72, P=0.0001 for females), while H-Cd was weakly or moderately correlated with U-Cd. After adjustment for gender using logistic regression analysis, log(B-Cd) and log(U-Cd), but not log(H-Cd), were significantly associated with the prevalence of increased urinary beta2-microglobulin (P for trend <0.05). These findings suggest that B-Cd is a good indicator of cumulative dose many years after the reduction of environmental exposure to Cd. H-Cd may be weakly or moderately correlated with body burden.

Adult↗

PubMedDate not supplied

European multicentric case control study on risk for mesothelioma after non-occupational (domestic and environmental) exposure to asbestos.

The paper presents the European multicentric case-control study on risk for mesothelioma after non-occupational (domestic and environmental) exposure to asbestos. The study includes eight centres in seven European countries (Belgium, Denmark, Greece, Italy, Spain, Sweden and Switzerland). It is focused on the measurement of mesothelioma risk in relation to low intensity exposure to asbestos and to exposure to MMMF and other agents. It includes incident cases of pleural malignant mesothelioma (histologically diagnosed and verified) and a random sample of the population.

Asbestos↗

PubMed1999

Personal monitoring of 218Po and 214Po radionuclide deposition onto individuals under normal environmental exposure conditions.

Personal dosemeters have been utilized to monitor the deposition of the radon decay products 218Po and 214Po onto individuals under normal environmental exposure conditions. Each detector consists of TASTRAK alpha-sensitive plastic incorporated into an ordinary working wristwatch. Subsequent analysis provides energy discrimination of the detected alpha-particle decays, and allows events from the individual radon decay products 218Po and 214Po, attached to the detector surface, to be uniquely identified. Assuming similar deposition onto skin and detector surfaces, the activity per unit area of deposited radionuclides can be determined for exposed skin. Forty-one personal dosemeters were issued to volunteers selected through the hospital medical physics departments at Reading, Northampton, Exeter and Plymouth. Each volunteer was also issued with a personal radon dosemeter to determine their individual radon exposure. The volunteers wore the two dosemeters simultaneously and continuously for a period of around one month. Correlations were observed between the radon exposure of the individual and the activity per unit area of 218Po and 214Po on the detector surface. From these correlations it can be estimated that at the UK average radon exposure of 20 Bq m(-3), the number of decays/cm2/year on continuously exposed skin surface is between 3500 and 28,000 for 218Po, and between 7000 and 21,000 for 214Po. These results can be combined with theoretical modelling of the dose distribution in the skin to yield the alpha-particle radiation dose to any identified target cells.

Environmental Exposure↗

PubMed2006

Low-level environmental exposure to lead and progressive chronic kidney diseases.

PURPOSE: To determine whether low-normal body lead burden (BLB) accelerates progressive renal insufficiency in nondiabetic patients with chronic kidney diseases (CKD). METHODS: One hundred eight CKD patients (serum creatinine between 1.5 and 2.9 mg/dL) with low-normal BLB (<80 microg) and no lead exposure history were observed for 24 months. Following the observation, 32 patients with low-normal BLB (> or =20 microg and <80 microg) were randomly assigned to chelation and control groups. The chelation group patients were given edetate calcium disodium (EDTA) chelation therapy for 3 months and repeated chelation therapy during the following 24 months to maintain their BLB below 20 mug, while the control group patients underwent placebo therapy. The primary endpoint was an increased serum creatinine level to 1.25 times the baseline value. The secondary endpoint was temporal changes in renal function. RESULTS: The primary endpoint occurred in 14 patients in the observation period. Baseline BLB was the important risk factor in determining progressive renal insufficiency. The mean glomerular filtration rate (GFR) change in the chelation group patients was 6.6+/-10.7 mL/min/1.73m(2), compared with -4.6+/-4.3 mL/min/1.73 m2 in control group patients (P <.001) at the end of the intervention period. The mean decrease in GFR per year of chelation group patients was lower than that of control group patients during the repeated chelation period. CONCLUSION: Environmental exposure to lead, even at low level, may accelerate progressive renal insufficiency of nondiabetic patients with CKD.

Adult↗