PubMed Health⌕ Search

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 55 records · Page 3Linked to original sources

An aggregate public health indicator to represent the impact of multiple environmental exposures.

We present a framework to aggregate divergent health impacts associated with different types of environmental exposures, such as air pollution, residential noise, and large technologic risks. From the policy maker's point of view, there are at least three good reasons for this type of aggregation: comparative risk evaluation (for example, setting priorities), evaluation of the efficiency of environmental policies in terms of health gain, and characterizing health risk associated with geographical accumulation of multiple environmental exposures. The proposed impact measure integrates three important dimensions of public health: life expectancy, quality of life, and number of people affected. Time is the unit of measurement. "Healthy life years" are either lost by premature death or by loss of quality of life, measured as discounted life years within a population. Severity weights (0 for perfect health, 1 for death) are assigned to discount the time spent with conditions associated with environmental exposures. We combined information on population exposure distribution, exposure response relations, incidence, and prevalence rates to estimate annual numbers of people affected and the duration of the condition, including premature death. Using data from the fourth Dutch National Environmental Outlook, we estimated that the long-term effects of particulate air pollution account for almost 60% of the total environment-related health loss in the Netherlands as modeled here. Environmental noise accounts for 24%, indoor air pollution (environmental tobacco smoke, radon, and dampness, as well as lead in drinking water) for around 6%, and food poisoning (or infection) for more than 3%. The contribution of this set of environmental exposures to the total annual burden of disease in the Netherlands is less than 5%.

Cost of Illness↗

Approaches to environmental exposure assessment in children.

An improved understanding of the contribution made by environmental exposures to disease burden in children is essential, given current increasing rates of childhood illnesses such asthma and cancer. Children must be routinely included in environmental research. Exposure assessment, both external (e.g., air, water) and internal dose (e.g., biomarkers), is an integral component of such research. Biomarker measurement has some advantages that are unique in children. These include assessment of potentially increased absorption because of behaviors that differ from adults (i.e., hand-to-mouth activity); metabolite measurement, which can help identify age-related susceptibility differences; and improved assessment of dermal exposure, an important exposure route in children. Environmental exposure assessment in children will require adaption of techniques that are currently applied in adult studies as well as development of tools and validation of strategies that are unique for children. Designs that focus on parent-child study units provide adult comparison data and allow the parent to assist with more complex study designs. Use of equipment that is sized appropriately for children, such as small air pumps and badge monitors, is also important. When biomarkers are used, biologic specimens that can be obtained noninvasively are preferable. Although the current need is primarily for small focused studies to address specific questions and optimize research tools, the future will require establishment of large prospective cohorts. Urban children are an important study cohort because of relatively high morbidity observed in the urban environment. Finally, examples of completed or possible future studies utilizing these techniques are discussed for specific exposures such as benzene, environmental tobacco smoke, aflatoxin, volatile organic compounds, and polycyclic aromatic hydrocarbons.

Age Factors↗

National Children's Study: environmental exposures in Waukesha County.

The National Children's Study (NCS), launched in September of 2005, will investigate the effects of environmental exposures and children's health and development. Waukesha County, Wis was selected as 1 of 7 sites to spearhead this ambitious undertaking. Residents of Waukesha County may experience different kinds of environmental exposures from water, land, and air based on where they live, work, and play. A selected number of Waukesha County's environmental exposures described briefly in this report will serve the NCS well with their heterogeneity of potential exposures: from private well water and community water supplies that obtain water from both surface and groundwater; from the variable exposures to ambient air pollution from mobile sources, local industrial sources, and distant sources (ozone); and the different levels of exposures from soil and dust depending on the prevalence of pesticide use and lead-based paints. By combining data gathered from Waukesha County's participants with other study sites, a holistic picture of environmental exposures in the United States can be evaluated as it influences the health of our nation's children.

Child↗

Normal liver function in women in the general Japanese population subjected to environmental exposure to cadmium at various levels.

OBJECTIVES: Whereas it is well established that environmental exposure to cadmium (Cd) may induce kidney dysfunction, less attention has been paid to the possible disturbance of liver function by Cd exposure. The possibility that liver function is adversely affected by current levels of environmental exposure to Cd as investigated in women in the general population in Japan, where the background level of exposure to Cd is known to be high. METHODS: From 1991 to 1997, 24-h food duplicate, peripheral blood and morning spot urine samples were collected from 607 non-smoking and non-habitually drinking women (age range 19-78 years) at 30 survey sites (with no known environmental pollution from heavy metals) throughout Japan. Liver function parameters in serum were examined by conventional methods. After wet-ashing, the food duplicate, blood and urine samples were analyzed for Cd intake via food (Cd-F), Cd in blood (Cd-B), and Cd in urine (Cd-U) by inductively-coupled plasma mass spectrometry. RESULTS: The geometric mean values for Cd-F, Cd-B, and Cd-U were 24.7 (27.1) microg/day, 1.76 (2.07) microg/l, and 3.94 (4.61) microg/g creatinine (values in parentheses for 41- to 60-year-old women), respectively. It as found that the three parameters of ALP, ALT, and AST activity were positively and significantly related to the age of the subjects (whereas no association as detected in cases of gamma-GTP, LAP, and albumin). Accordingly, a further analysis as made with 367 women selected by age (41-60 years; about 60% of the total population). Essentially, no Cd dose-dependent changes in liver function parameters were observed in the selected population of this narrower age range. CONCLUSIONS: Overall, it seemed prudent to conclude that liver function as not disturbed by the current environmental exposure to Cd in Japan.

Adult↗

Environmental exposure to tobacco smoke and lung function in young adults.

The relationship between lung function and environmental exposure to tobacco smoke (passive smoking) was studied in 293 nonsmoking young men and women, 15 to 35 yr of age. A self-administered mailed questionnaire was used to assess the lifetime environmental exposure to cigarette smoke at home and at work for each subject. Lung function information used here had been gathered in the course of a previous study of the determinants of lung function in early adulthood. In men, maximal midexpiratory flow rate (FEF25-75) decreased in relation to an index of cumulative lifetime environmental exposure to tobacco smoke at home, after taking into account the effects of cumulative exposure at work as well as age, height, body size, respiratory pressures, and cooking fuels used at home. The components of this exposure index most closely related to the reduction in FEF25-75 were maternal smoking habits and exposure to second-hand smoke during childhood. In women, the diffusing capacity of the lung (DLCO) decreased in relation to cumulative exposure to tobacco smoke at work, after accounting for the effects of cumulative lifetime exposure at home and the other factors mentioned above. These findings contribute to the gathering evidence that environmental exposure to tobacco smoke is harmful to respiratory health, and suggest that the effects are not insignificant. For instance, the FEF25-75 of a young man 20 yr of age who had never smoked and always lived at home would be 800 ml less if both his parents smoked than if they did not.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Public health implications of environmental exposure to cadmium and lead: an overview of epidemiological studies in Belgium. Working Groups.

The CadmiBel Study was a cross-sectional population study that investigated the health effects of environmental exposure to cadmium and lead. The 2327 participants constituted a random sample of the population of four Belgian districts, chosen in order to provide a wide range of environmental exposure to cadmium. After adjustment for confounding factors, such as smoking and occupational exposure, the urinary cadmium excretion, a measure of lifetime exposure, was nearly 30% higher in the polluted areas. The CadmiBel Study produced evidence inconsistent with the hypothesis that environmental exposure to cadmium and lead would lead to an increase in blood pressure and to a higher prevalence of hypertension and other cardiovascular diseases. On the other hand, the serum alkaline phosphatase activity and the urinary excretion of calcium were significantly and positively correlated with urinary cadmium in both sexes. These findings suggested that the homeostasis of calcium was gradually affected as cadmium accumulated in the body. Furthermore, several markers of renal tubular dysfunction (urinary excretion of retinol-binding-protein, N-acetyl-beta-glucosaminidase, beta 2-microglobulin and amino acids) were significantly and positively associated with urinary cadmium. Across 10 small areas of which six were polluted with cadmium, an inverse association existed between the creatinine clearance and several indexes of environmental exposure to cadmium (cadmium concentration in the soil, cadmium content of locally grown vegetables, the inhabitants' 24 h urinary cadmium excretion). In the CadmiBel Study, the creatinine clearance was also inversely correlated with the concentrations of lead and zinc protoporphyrin in the blood. Thus, environmental exposure to cadmium and lead was associated with alterations in renal function. The significance in terms of morbidity and mortality of the functional disturbances observed in the CadmiBel Study, and the possible strategies to prevent the transfer of cadmium from the environment to man are under investigation in the prospective PheeCad Study in which half of the Cadmibel participants have been enrolled (participation rate 80%).

Adult↗

The relationship between blood pressure and environmental exposure to lead and cadmium in Belgium.

The question whether in the general population environmental exposure to lead and cadmium influences blood pressure after controlling for confounding factors remains debated. The environmental exposure of the Belgian population to both lead and cadmium is high as compared with other countries. The Cadmibel Cooperative Study was therefore designed to elucidate whether environmental exposure to lead and cadmium has any effect on blood pressure and renal function in the population at large. Before embarking on the large Cadmibel project, a small study was conducted. Blood pressure and the 24-hr urinary excretion of cadmium (CdU) and lead (PbU) were determined in a random 4% sample of the population of a small Belgian town. CdU averaged 0.27 micrograms/24 hr in 46 youths (mean age 14 +/- 3 years, +/- SD), increased with age, and was higher in 57 adult men (age 41 +/- 14 years), as compared with 59 adult women (age 39 +/- 14 years) (1.05 vs. 0.81 micrograms/24 hr; p less than 0.01). PbU averaged 5.8 micrograms/24 hr in youths and similarly increased with age; adult men excreted more lead than women (13.3 vs. 8.3 micrograms/24 hr; p less than 0.001). Among men, manual workers excreted more cadmium (1.4 vs. 0.8 micrograms/24 hr; p less than 0.05) but a similar amount of lead (7.0 vs. 6.9 micrograms/24 hr) as compared with office workers. In simple regression analysis, CdU was positively correlated with both systolic (r = 0.30; p less than 0.05) and diastolic (r = 0.38; p less than 0.01) blood pressure in women.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Effects of environmental exposure to polychlorinated biphenyls and dioxins on birth size and growth in Dutch children.

Lower birth weight and growth retardation has been found in studies with laboratory animals, in children born of mothers exposed to accidental high levels of polychlorinated biphenyls (PCBs) and related compounds, and in children born of mothers who consumed PCB-contaminated fish. The effect of background exposure to PCBs and dioxins on birth size and growth in human newborns, however, is still unknown. This study examined birth size and postnatal growth of term newborns in relation to their background PCB and dioxin exposure. Birth weight and weight, length, and head circumference were measured at 10 d and 3, 7, 18, and 42 mo of age in 207 children, of whom 105 were breast-fed and 102 were formula-fed during infancy. The effect of in utero exposure to PCBs on birth size, assessed by cord and maternal plasma PCB levels, was investigated in the whole group. The effect of prenatal PCB exposure on postnatal growth was studied in the formula-fed group, whereas the effect of prenatal as well as lactational exposure to PCBs and dioxins on postnatal growth was studied in the breast-fed group. After adjustment for covariates, cord and maternal plasma PCB levels where both negatively associated with birth weight. Infants with high cord plasma PCB levels (P90 = 0.80 microL) weighed 165 g less compared with infants with low cord plasma PCB levels (P10 = 0.20 microg/L). Cord and maternal plasma PCB levels where both significantly associated with lower growth rate, defined as change in SD score (SDS) of weight, length, and head circumference from birth to 3 mo in the formula-fed group (all p values <0.05). No negative effects of prenatal PCB exposure on growth rate were found from 3 to 42 months of age. Postnatal PCB and dioxin exposure was not negatively associated with growth rate in the breast-fed group. In utero exposure to environmental levels of PCBs is negatively associated with birth weight and postnatal growth until 3 mo of age. Although this growth delay was described in healthy term born infants, intrauterine and postnatal growth retardation are potentially harmful to the developing human and should be avoided by reducing maternal PCB and dioxin body burden, and consequently fetal exposure to these pollutants.

Adult↗

Environmental exposures to lead and urban children's blood lead levels.

Lead-contaminated water, soil, and paint have been recognized as potential sources of children's lead exposure for decades, but their contributions to lead intake among urban children remain poorly defined. This analysis was undertaken to estimate the relationship of environmental lead exposures to lead intake among a random sample of urban children, adjusted for exposure to lead-contaminated house dust. Analyses of 183 urban children enrolled in a random sample, cross sectional study were conducted. Children's blood and multiple measures of household dust, water, soil, and paint were analyzed for lead, and interviews were conducted to ascertain risk factors for childhood lead exposure. Environmental sources of lead, including house-dust, soil lead, and water lead, were independently associated with children's blood lead levels. In contrast, paint lead levels did not have a significant effect on blood lead levels after adjusting for other environmental exposures. An increase in water lead concentration from background levels to 0.015 mg/L, the current EPA water lead standard, was associated with an increase of 13.7% in the percentage of children estimated to have a blood lead concentration exceeding 10 micrograms/dL; increasing soil lead concentration from background to 400 micrograms/g was estimated to produce an increase of 11.6% in the percentage of children estimated to have a blood lead level exceeding 10 micrograms/dL, and increasing dust lead loading from background to 200 micrograms/ft2 is estimated to produce an increase of 23.3% in the percentage of children estimated to have a blood lead level exceeding 10 micrograms/dL. These data support the promulgation of health-based standards for lead-contaminated dust and soil and the progressive lowering of standards for lead-contaminated water as the definition of undue lead exposure has been modified.

Child, Preschool↗

Environmental exposures in cytogenetically defined subsets of acute nonlymphocytic leukemia.

Three previous investigations have reported a relationship between clonal chromosome abnormalities in marrow of patients with acute nonlymphocytic leukemia and employment in occupations involving mutagenic chemicals, but the effects of other exposures were not described. Environmental exposure profiles, gathered by questionnaire, were therefore compared using a case-control study design in 235 newly diagnosed patients with acute nonlymphocytic leukemia: 126 with abnormal and 109 with normal karyotypes. The univariate odds ratio for occupation at diagnosis was 4.6, which, when adjusted for demographic and other exposures by logistic regression, was reduced to 2.5 (95% confidence interval, 0.5 to 12.8). Adjusted point estimates for other exposures were 4.3 (1.4 to 13.3) for prior cytotoxic therapy, 1.7 (0.9 to 3.1) for cigarette smoking, and 1.9 (1.0 to 3.4) for alcohol use. Dose-response relationships were present for both tobacco and alcohol consumption. Associations between specific abnormalities (+8, -7I-7q, [corrected] inv16, t[8;21]) and certain exposures were also present. These results suggest that life-style exposures may be associated with cytogenetic lesions in persons with acute nonlymphocytic leukemia.

Alcohol Drinking↗

Biomarkers for assessing environmental exposure to carcinogens in the diet.

The major sources of human exposure to environmental carcinogens are through inhalation, ingestion, and percutaneous absorption. Food-borne carcinogens constitute the primary source of ingested carcinogens. Epidemiological analyses indicate that 20-50% of all human cancer is due to dietary causes, unfortunately, few specific etiologic agents have been identified. The use of chemical-specific molecular biomarkers in studies of several classes of carcinogens to which humans are exposed through the ingestion of food may provide the necessary data to identify these etiologic agents. These molecular biological markers can be classified into several categories: markers of exposure reflecting dose of toxic agents, markers of effect indicating a biological response to an exposure, and markers of susceptibility providing information about the inherent sensitivity of an individual to the toxic agent. By definition some of these markers are chemical-agent specific, such as a carcinogen-DNA or carcinogen-protein adduct, whereas others are biological process-specific such as the altered expression of a gene. In the future, information obtained from studies of molecular biomarkers in humans and experimental animals can be used for a range of public health applications from primary and secondary prevention to the design of clinical therapies. Aflatoxins have been extensively studied with validated biomarkers, and, currently, dietary polycyclic aromatic hydrocarbons (PAH) and heterocyclic amines (HA) derived from cooking meats and other staples are being intensively investigated. This article reviews some of the recent information on aflatoxins and describes future potential of PAH and HA biomarkers.

Aflatoxins↗

Exposure to cadmium and conventional and ambulatory blood pressures in a prospective population study. Public Health and Environmental Exposure to Cadmium Study Group.

This prospective population study investigated in a random sample of 692 subjects (age 20-83 years) how changing environmental exposure to cadmium influenced blood pressure (BP) and the incidence of hypertension. At baseline (1985 to 1989; participation rate, 78%) and follow-up (1991 to 1995; re-examination rate, 81%), blood pressure was measured by conventional sphygmomanometry (CBP; 15 readings in total) and, at follow-up, also by 24-h ambulatory blood pressure monitoring (ABP). Systolic/diastolic CBP at baseline averaged 128.4/77.3 mm Hg. At baseline, blood cadmium concentration (B-Cd) and urinary cadmium excretion (U-Cd) averaged (geometric means) 11.1 nmol/L and 10.2 nmol/24 h. Over 5.2 years (median follow-up), B-Cd fell by 29.6% and U-Cd by 15.2%. B-Cd fell less in subjects living closer to three zinc smelters and in premenopausal women. During follow-up, systolic CBP decreased by 2.2 mm Hg in men and remained unchanged in women, and diastolic CBP increased by 1.8 mm Hg in both sexes. No relationship could be demonstrated between the secular trends in CBP and B-Cd or U-Cd or between B-Cd or U-Cd at baseline and the incidence of hypertension. In addition, in cross-sectional analyses involving the average of all available CBP measurements in each participant or 24-h ABP at follow-up (mean, 119.1/71.4 mm Hg), blood pressure was not correlated with B-Cd or U-Cd. In conclusion, environmental exposure to cadmium was not associated with higher CBP or 24-h ABP or with increased risk for hypertension. The lesser fall in B-Cd in the residents living closer to the zinc smelters or in premenopausal women underscores the necessity to sanitize cadmium-polluted areas and to systematically reinforce the preventive measures to be adopted by exposed communities to reduce cadmium uptake.

Adult↗

Environmental exposure and birth outcomes.

The influence of environmental hazards on the health of children is one of the major current concerns in environmental health. Scientific investigations are now focusing on identifying and understanding the role of environmental hazards in the development of birth outcomes that result from in utero exposure to environmental contaminants. This paper reviews the published literature with provided evidence concerning the impact of environmental exposures to chemicals on the incidence of birth outcomes in the areas of environmental pollution originating from various sources. In spite of methodological limitations in a number of reviewed studies, the present body of knowledge calls for a precautionary approach and for preventive measures in order to reduce the risk of environmental exposures to chemicals with a recognized or suspected potential to cause birth outcomes.

Environmental Exposure↗

Adjusting occupational exposure limits for moonlighting, overtime, and environmental exposures.

A mathematical model is used to predict relative body burdens of inhaled contaminants in workers who work two jobs or overtime, or who experience off-the-job exposure to air contaminants. Expected "peak" or maximum body burdens from multiple exposures are compared to those expected from the "normal" occupational exposure on which TLVs and Permissible Exposure Limits (PELs) arebased (five 8-hour days per week with zero off-the-job exposure). The model is designed to predict what adjustments to the TLVs and PELs are necessary to avoid accumulation of excess peak body burdens of contaminants from the additional exposures incurred. The general application of models to determine occupational exposure limits is reviewed, and several models are compared.

Air Pollutants↗

Human leukocyte antigen class II genes and Helicobacter pylori infection: does genotype overwhelm environmental exposure?

OBJECTIVE: We investigated associations between human leukocyte antigen class II genes, environmental exposures, and Helicobacter pylori infection. METHODS: Sixty-eight subjects with histologically confirmed H. pylori and intestinal metaplasia (cases) and 70 healthy subjects without H. pylori (controls) matched for age, sex, and year of birth were included in this study. All patients answered a detailed questionnaire designed to collect sociodemographic characteristics, smoking, alcohol drinking, and dietary habits. Human leukocyte antigen class II genes were typed with genomic DNA. The cytotoxins CagA and VacA were investigated with serology. Odds ratios and corresponding 95% confidence intervals were estimated from multivariate conditional logistic regression. Multiple correspondence analysis was used to represent the interrelationships of a multiple contingency table. RESULTS: Human leukocyte antigen DRB1, DQA1, and DQB1 genotypes were not significantly associated with H. pylori infection and intestinal metaplasia. No significant association with blood group or Lewis antigen system was found. However, multiple correspondence analysis clearly associated H. pylori with environmental exposure: the control group largely consumed olive oil, fresh fruits, and vegetables and histories of never or formerly smoking and the case group (those positive for H. pylori and metaplasia) largely consumed eggs, meat and butter and had histories of smoking cigarettes. CONCLUSIONS: These findings suggested that H. pylori infection is not influenced by a genetic compound and confirmed the relevance of environmental exposure.

Adult↗

Social inequality in perceived environmental exposures in relation to housing conditions in Germany.

In Germany the impact of socioeconomic factors on environmental exposures and adverse housing conditions has been rarely studied up to now. The aim of our study was to assess whether and, if yes, how perceived exposure to noise and air pollution is influenced by socioeconomic status in Germany. We used data from a large-scale population-based survey. In this survey, data on perceived exposure to noise and air pollution and on socioeconomic status and housing conditions were collected on an individual basis. The study population consisted of 7,275 adults aged 17-98 years (40% women), each representing the head of one household. For the association between perceived environmental exposure and social factors confounder-adjusted odds ratios (OR) with 95% confidence intervals were calculated by binary or ordinal logistic regression. In bivariate analyses subjects with non-German nationality, East Germans, respondents with low income, those with lower educational and occupational status, and subjects living in adverse housing conditions were more likely to report being highly exposed. In multivariate analyses high perceived exposure to noise was associated with low household income (OR 1.52 [95% CI 1.13-2.05] lowest versus highest income group). Perceived air pollution exposure was also related to household income (1.67 [1.14-2.44] lower middle versus highest income group). Further associated variables were need for renovation of the house, type of house, and type of neighborhood. This study shows that in Germany, as in other industrial countries, environmental exposures are distributed unequally and that especially economic differences play important roles.

Adolescent↗