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 145 records · Page 8Linked to original sources
PubMed1983

Hygienic and toxicological aspects of occupational and environmental exposure to beryllium.

As the production of missile, nuclear devices and electronics grew and modern industrial technologies emerged the risk of the occupational exposure to beryllium has become increasingly common and widespread. The environmental burden of beryllium is also on the increase, not only as a result of emissions from plants producing and processing beryllium, or its alloys and compounds, but also from burning coal of higher beryllium content in some localities. This article discusses primarily the hygienic and toxicologic aspects of beryllium and its threat to human health. The following topics are included in this review: occurrence, production and uses of beryllium; its metabolism and experimental toxicology; clinical toxicology and pathogenesis of berylliosis; hygienic and epidemiologic aspects of berylliosis; berylliosis treatment and prevention. Berylliosis is here characterized as a disease combining clinical manifestations of pneumosclerosis, allergy to beryllium and, in its granulomatous form, autoimmune reactions. Importantly, the available technical means and measures can ensure that the both occupational and environmental exposure to beryllium can be kept below the established MAC values. If occasionally impossible, special preventive measures should be adopted. It is essential that all persons with allergy be prophylactically excluded from work at risk of exposure to beryllium.

Animals↗
PubMed2006

Tail hair as an indicator of environmental exposure of cows to lead and cadmium in different industrial areas.

This study examines the use of tail hair from cows as a possible biomarker of environmental exposure to lead and cadmium around different industrial areas. Respective blood and tail hair samples were collected from a total of 317 apparently healthy cows above 3 years of age. This includes 287 cows reared in industrial and urban areas and 30 cows from areas free from polluting sources. Significantly (P<0.05) higher lead and cadmium residues were recorded in hair from cows reared around lead-zinc smelter and closed lead cum operational zinc smelter. However, cows from those areas had significantly (P<0.05) higher blood lead but not cadmium concentration as compared to respective control value. Although mean blood lead concentration in cows around aluminum processing plant and urban cum small industrial areas and that of cadmium around steel processing plant were significantly (P<0.05) higher than respective control, the mean hair lead and cadmium content remained statistically (P>0.05) comparable to that of respective control values. The blood lead was significantly correlated with hair lead (r = 0.672, P<0.01) and cadmium (r = 0.309, P<0.05). There was a significant correlation between lead and cadmium concentration (r = 0.610, P<0.01) in hair and a nonsignificant correlation between blood and hair cadmium suggesting that cadmium accumulation in hair was influenced by blood and hair lead concentrations in cows environmentally exposed to lead.

Animals↗
PubMed1993

Race and gender differences in respiratory illness prevalence and their relationship to environmental exposures in children 7 to 14 years of age.

Race and gender differences in respiratory illness prevalence rates were assessed in a cohort of 8,322 white children and 1,056 black children 7 to 14 yr of age from four U.S. cities. Boys had higher rates of wheeze, asthma, cough, phlegm, and bronchitis than girls. Black children had higher rates of persistent wheeze, shortness of breath with wheeze, asthma, chronic cough, and chronic phlegm than white children. We examined whether the racial disparity in respiratory illness prevalence could be accounted for by environmental exposures and socioeconomic factors. The proportion of families without a parent who had graduated from high school was higher for blacks than for whites, as was the proportion of single-parent households. Black children took up smoking less frequently; their mothers smoked fewer cigarettes. Personal and maternal smoking predicted higher rates of persistent wheeze, chronic cough, chronic phlegm, and chest illness. The relative odds for persistent wheeze were 1.34 (1.07, 1.69) for smoking children compared with nonsmoking children. The relative odds for persistent wheeze were 1.35 (1.13, 1.60) for children whose mother smoked > 30 cigarettes per day versus children with no maternal smoke exposure. Other predictors of respiratory illnesses included parental respiratory illness, parental education, only-child status, single-parent household, air conditioner use, and body mass index. Nevertheless, adjustment for socioeconomic factors, environmental exposures, and body habitus did not significantly reduce the excess respiratory illness prevalence observed among black children. The adjusted relative odds were 1.47 (1.25, 1.74) for persistent wheeze and 1.57 (1.17, 2.10) for asthma for black children versus white children.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

Genetically based N-acetyltransferase metabolic polymorphism and low-level environmental exposure to carcinogens.

The metabolic activation or inactivation of carcinogens varies considerably in human populations, and is partly genetically determined. Inter-individual variability in the susceptibility to carcinogens may be particularly important at low degrees of environmental exposure. Examples of probable human carcinogens that present widespread low-dose exposures are environmental tobacco smoke and diesel exhaust. We have determined levels of DNA adducts in bladder cells and of 4-aminobiphenyl-haemoglobin adducts in 97 volunteers, together with the N-acetylation non-inducible phenotype, the corresponding genotype, and the levels of nicotine-cotinine in the urine. We find that among the slow acetylators, 4-aminobiphenyl adducts were higher than in rapid acetylators at low or null nicotine-cotinine levels, whereas the difference between slow and rapid acetylators was less evident at increasing nicotine-cotinine levels. The N-acetyltransferase genotype is highly predictive of the acetylation phenotype. Our results indicate that the clearance of low-dose carcinogens is decreased in the genetically based slow-acetylator phenotype. Such genetic modulation of low-dose environmental risks is relevant to 'risk assessment' procedures.

Acetylation↗
PubMed2005

Environmental exposures, toxicologic mechanisms, and adverse pregnancy outcomes.

Environmental risk factors (defined as those agents and stresses that are generally the responsibility of environmental agencies) are often tangible indicators of economic and social disparity in the United States. Many site-specific analyses have reported that communities of color and poverty are exposed more often and more intensively to such environmental hazards as lead, air pollution, agrochemicals, incinerator emissions, and releases from hazardous waste sites. Thus, exposures to these toxicants may explain part of the socioeconomic disparity that is observed in terms of risks of adverse pregnancy outcomes. The purpose of this study was to describe the associations between certain environmental exposures and reproductive outcomes through a discussion of both epidemiologic and animal model studies. In addition, we list potential sources of exposure data and describe physiologic changes in pregnancy that may increase the likelihood of both external exposures and increased internal dose. Several models for further study of environmental risk factors are suggested to increase our understanding of gene-environment interactions toward the goal of indentifying preventable risk factors to improve reproductive outcomes of particular concern to disadvantaged populations.

Environmental Exposure↗
PubMed2005

Meta-analysis for deriving age- and gender-specific dose-response relationships between urinary cadmium concentration and beta2-microglobulinuria under environmental exposure.

A meta-analysis was conducted to derive age- and gender-specific dose-response relationships between urinary cadmium (Cd) concentration and beta2-microglobulinuria (beta2MG-uria) under environmental exposure. beta2MG-uria was defined by a cutoff point of 1000 microg beta2-microglobulin/g creatinine. We proposed a model for describing the relationships among the interindividual variabilities in urinary Cd concentration, the ratio of Cd concentrations in the target organ and in urine, and the threshold Cd concentration in the target organ. The parameters in the model were determined so that good agreement might be achieved between the prevalence rates of beta2MG-uria reported in the literature and those estimated by the model. In this analysis, only the data from the literature on populations environmentally exposed to Cd were used. Using the model and estimated parameters, the prevalence rate of beta2MG-uria can be estimated for an age- and gender-specific subpopulation for which the distribution of urinary Cd concentrations is known. The maximum permissible level of urinary Cd concentration was defined as the maximum geometric mean of the urinary Cd concentration in an age- and gender-specific subpopulation that would not result in a statistically significant increase in the prevalence rate of beta2MG-uria. This was estimated to be approximately 3 microg/g creatinine for a population in a small geographical area and approximately 2 microg/g creatinine for a nationwide population.

Age Factors↗
PubMed1997

Environmental exposure, social class, and cancer risk.

Exposure to a variety of environmental factors associated with cancer occurrence varies by social class. These factors include air pollutants (SO2, NO2, total suspended particulates, etc.), toxic waste hazards, and ionizing and other radiation. Heavy environmental pollution has been associated with an increased risk of some cancers and in particular lung cancer. There is limited evidence suggesting that individuals from lower social classes are exposed to higher levels of environmental pollutants than are individuals from higher social classes. This may be due to the placement of new sources of pollution or of toxic processes in disadvantaged areas, or to the selective migration of the poorer sectors of society to these areas. The available data do not allow any conclusion on the possible contribution of exposure to environmental pollution to social class differences in cancer occurrence. Exposure to ultraviolet (UV) radiation, principally from sunlight, is modified strongly by personal behaviours such as choice of recreation and use of protective clothing. Those in outdoor occupations are likely to receive the highest cumulative exposure to UV radiation. There is no clear evidence from recent survey research in Australia and North America that socioeconomic factors are strongly related to non-occupational exposure to UV radiation. Information is lacking on the influence of socioeconomic status on sun exposure in other parts of the world. There is little information on the social distribution of exposure to ionizing radiation.

Adolescent↗
PubMed1991

Mineral fiber content of lung tissue in patients with environmental exposures: household contacts vs. building occupants.

Analysis of tissue mineral fiber content in patients with environmental exposures has seldom been reported in the past. Our studies of six household contacts of asbestos workers indicate that these individuals often have pulmonary asbestos concentrations similar to some occupationally exposed individuals. In contrast, our studies of four occupants of buildings with asbestos-containing materials indicate that these individuals often have pulmonary asbestos burdens indistinguishable from the general nonoccupationally exposed population. However, one such building occupant exposed for many years and who later developed pleural mesothelioma was studied in detail, and it was concluded that her exposure as a teacher's aide in a school building containing acoustical plaster was the likely cause of her mesothelioma.

Adult↗
PubMedDate not supplied

The Total Human Environmental Exposure Study (THEES) to benzo(a)pyrene: comparison of the inhalation and food pathways.

The assessment of human exposure to an environmental contaminant requires the measurement of levels present in each pathway of possible contact. In this paper, the design considerations and Phase I results of a human exposure study focused on Benzo(a)pyrene (BaP) are discussed. This study site, located in Phillipsburg, New Jersey, is a city that contains a metal pipe foundry, which is a suspected major source of BaP. Three outdoor PM-10 samplers (used to collect BaP-containing particles with an aerodynamic size of less than or equal to 10 micron) were located in residential areas surrounding the foundry. Ten homes were sampled indoors for PM-10. Some homes have indoor combustion sources, e.g., cigarette smoke or a coal burning stove. The indoor and outdoor samples were 24 hr in duration. The mean outdoor concentration of BaP was 0.9 ng/m3, and the indoor concentrations ranged from 0.1-8.1 ng/m3. Food samples were acquired from family meals each day. They represented a one-third portion of each meal eaten at home. The range of BaP per gram of wet weight of food was between 0.004 and 1.2 ng/g. Of the 20 wk of exposure (10 x 2 wk), 10 had higher food exposures and the other 10 had higher inhalation exposures. Of the two groups, the higher food exposures usually had a greater number of ng of BaP/wk. The dominance of one or the other pathway appeared to depend upon personal eating habits and indoor combustion source use. In some instances, outdoor air pollution led to a major portion of indoor air BaP exposures. Water appears to be a minor source of BaP exposures in the study area.

Air Pollutants↗
PubMed2003

Indoor and outdoor environmental exposures, parental atopy, and physician-diagnosed asthma in Taiwanese schoolchildren.

OBJECTIVE: Parental atopy and environmental exposures are recognized risk factors for childhood asthma. However, the relative contributions of specific risk factors and the overall contributions of indoor and outdoor exposures remain unexplored. This study was undertaken to identify risk factors, estimate the population attributable risk of each exposure, and compare the data for boys versus girls for physician-diagnosed asthma in Taiwanese schoolchildren. METHODS: During a February to June 2001 cross-sectional national survey, 35 036 6- to 15-year-old schoolchildren were chosen from 22 elementary and 22 middle schools located within 1-km catchment areas of 22 air-monitoring stations in Taiwan. The main outcome measure was physician-diagnosed asthma, as reported by the parents. We investigated hereditary and indoor and outdoor environmental factors for childhood asthma by questionnaire. The adjusted prevalences of questionnaire-determined outdoor indicators were also compared with air-monitoring data. RESULTS: Outdoor air pollutants were associated with parent-reported perceived ambient air pollution. Physician-diagnosed asthma was reported for 8.1% of the boys (1330 of 16 441) and 5.6% of the girls (894 of 16 056). The risk of physician-diagnosed asthma was significantly associated with parental atopy and perceived ambient air pollution in both sexes. The presence of visible cockroaches (odds ratio [OR]: 1.30; 95% confidence interval [CI]: 1.07-1.59), mold on walls at home (OR: 1.20; 95% CI: 1.01-1.41), and water damage (OR: 1.33; 95% CI: 1.02-1.70) were also associated with asthma in girls; however, only visible mold on walls at home was related to asthma in boys. Mutually adjusted analytical models produced statistically significant associations between any indoor factor and asthma in girls (OR: 1.24; 95% CI: 1.00-1.56) but not in boys (OR: 1.04; 95% CI: 0.87-1.25). For all hereditary and environmental factors, the total population attributable risk was 44.31% in boys and 60.61% in girls. CONCLUSIONS: Parental atopy contributed more to childhood asthma than indoor or outdoor environmental factors. Girls may be more susceptible to indoor factors than boys.

Adolescent↗
PubMed2001

Environmental exposure and cancer in children. A conceptual framework for the pediatrician.

Ultimately, after gathering and assessing all available evidence, pediatricians and health care policymakers must make informed decisions on whether exposure to a specific agent has the potential to cause cancer in children. In the case of DES, for which the results were clear, there was no question that the drug should be taken off the market; however, most cases of suspected carcinogens lack such clear evidence documenting cause and effect. An example of a murky topic is the suspected relationship between residential electromagnetic fields (EMFs) and childhood cancer. Epidemiologic and biologic researchers have tried for more than 2 decades to determine whether exposure to relatively high levels of EMFs poses health hazards, especially cancer in children. Although the preponderance of evidence favors a judgment that this ubiquitous environmental exposure is harmless, concerns remain in many public circles and some scientific ones. Any proposed intervention to remove a potentially carcinogenic agent must be weighed against the cost and inconvenience to the affected community. Pediatricians are placed in a vulnerable position when faced with questions of a carcinogenic potential because of the frequency of claims in the popular literature stating that exposure to a certain product or food is associated with an increased risk for cancer in adults and possibly children. When such studies are published or, more often, released to the press, the strength of the evidence for a causal association with cancer, coupled with the context of the study, should be considered as a reasonable starting point. Better communication models of disseminating cancer-risk information are needed so that the public understands the difference between a weak study that appeared on the local news with little evidence to support a cause-and-effect relationship versus a well-designed study that was published in a peer-reviewed journal and indicates a likely cause-and-effect association.

Carcinogens, Environmental↗
PubMed1994

Occupational and environmental exposure of garage workers and taxi drivers to airborne manganese arising from the use of methylcyclopentadienyl manganese tricarbonyl in unleaded gasoline.

Occupational and environmental exposure to airborne manganese has been measured for two groups of workers in Montreal, taxi drivers and garage mechanics. In Canada methylcyclopentadienyl manganese tricarbonyl (MMT) has replaced lead as an anti-knock agent in gasoline and represents a potentially important source of manganese contamination for the population in general and for the two chosen groups of workers in particular. Twenty workers (10 taxi drivers and 10 garage mechanics) wore a personal air sampler for five consecutive working days and two off-work periods. The amount of total Mn on each filter was determined by neutron activation analysis and then converted to atmospheric Mn concentrations. The values obtained varied from 0.004 microgram m-3 to 2.067 micrograms m-3. At work the garage mechanics were exposed to an average of 0.250 microgram m-3 and the taxi drivers to 0.024 microgram m-3. Off-work, the two groups were exposed respectively to an average of 0.007 microgram m-3 and 0.011 microgram m-3. In the garages there was twice as much Mn in the air on days when the doors were closed compared to days when they were left opened (0.314 micrograms m-3/0.152 microgram m-3). The levels found in this study remain well below the established limits for occupational and environmental airborne exposure. These results will lead to further studies to positively identify the source of Mn as MMT and to explore other pathways leading to the contamination of the general population.

Air Pollutants↗
PubMed2000

Pulmonary mineral fibers after occupational and environmental exposure to asbestos in the Russian chrysotile industry.

BACKGROUND: As an indicator of occupational, domestic, and environmental exposure, the level and type of asbestos fibers were determined from lung tissue samples of workers and residents who resided in the area of the world's largest asbestos mine at Asbest, Russia. METHODS: Electron microscopy was used to analyze and measure the concentration of asbestos fibers in a series of 47 autopsies at the Asbest Town Hospital. Work histories were obtained from pathology reports and employment records. RESULTS: In 24 chrysotile miners, millers, and product manufacturers, the pulmonary concentrations of retained fibers (over 1 microm in length) were 0. 8-50.6 million f/g for chrysotile, and < 0.1-1.9 million f/g for amphiboles (tremolite and anthophyllite). The concentrations were lower in 23 persons without any known occupational contact with asbestos; 0.1-14.6 million f/g for chrysotile, and < 0.1-0.7 million f/g for amphiboles. On average, 90% of all inorganic fibers were chrysotile, and 5% tremolite/anthophyllite. No amosite or crocidolite fibers were detected in any of the samples. CONCLUSIONS: The mean and range of pulmonary chrysotile concentrations were about the same as reported previously from the Canadian mining and milling industry. In the Russian samples, the mean concentration of tremolite fibers were less by at least one order of magnitude. Occupational contact was the most important source of asbestos exposure.

Adolescent↗
PubMed1998

Flow cytometric determination of metallothionein levels in human peripheral blood lymphocytes: utility in environmental exposure assessment.

Metallothioneins (MT) are ubiquitous, low-molecular-weight proteins that exhibit high binding affinities for heavy metal ions. The expression of these cysteine-rich proteins is induced in response to various types of chemical and physical stresses and therefore can be used to assess human exposure to cytotoxic environmental agents. In the current study, MT levels of human peripheral blood lymphocytes were determined using an MT-specific antibody and flow cytometry. Treatment of human whole blood ex vivo with CdCl2 was found to induce a concentration- and time-dependent increase in lymphocyte MT levels at concentrations as low as 0.3 microM and within a 12-h period. Interestingly, differences were observed in the magnitude of cadmium-induced MT levels in the lymphocytes of six human test subjects. Two members of the study population exhibited CdCl2-induced cellular MT levels that were up to twofold greater than the lymphocytes of other human subjects. While the lymphocytes of most test subjects exhibited a symmetric (unimodal) distribution of cadmium-induced MT-specific fluorescence, the cells of two individuals displayed a heterogeneous (nonuniform) distribution of MT levels. Dual-parameter flow cytometric analysis using phenotype-specific antibodies indicated that variations in the responsiveness of subpopulations of lymphocytes to CdCl2 were responsible for the heterogeneous distribution of MT-specific cellular fluorescence. T-helper (CD4-positive) and T-suppressor/cytotoxic (CD8-positive) lymphocytes expressed higher cellular levels of MT than other lymphocyte subpopulations (i.e., B lymphocytes, natural killer cells). Our results suggest that MT protein levels of peripheral blood lymphocytes, as determined by this flow cytometric method, may be used to assess human exposure to toxic metals and to characterize various quantitative/qualitative aspects of the response of individuals to cadmium and possibly to other types of environmental stresses.

Adult↗
PubMed1995

An assessment of a urinary biomarker for total human environmental exposure to benzo[a]pyrene.

Urinary banzo[a]pyrene (BaP) metabolite levels were compared to human environmental exposure to BaP through inhalation and dietary ingestion to assess the predictive validity of the exposure biomarker. These measurements were made for 14 adult volunteers over 14 consecutive days, once during summer/fall, again during winter periods. Based on personal air monitoring, median potential inhalation doses of 11.0 and 2.3 ng/day were estimated for the winter and summer/fall studies, respectively. A median potential ingested dose of 176 ng/day, estimated from "duplicate plate" sampling, exceeded inhalation by 6- and 122-fold for the winter and summer/fall studies, respectively. "Total" urinary BaP metabolites were measured using a published "reverse metabolism" (BaP) method of analysis. Median rates of urinary BaP metabolite elimination for the winter and summer/fall studies were 121 and 129 ng/day, respectively. The changes in inhaled and ingested potential doses were regressed on the change in urinary metabolite elimination from week 1 to week 2 to test the predictive validity of the biomarker measurement. The regression was statistically significant (r = 0.620, p = 0.015, n = 25) when body weight was included and two extreme values were removed. Consistent with the exposure measurements showing diet as the dominant route of exposure, most of the variation in urinary metabolite elimination was explained by the ingested dose. It is concluded that the measurement of urinary BaP by "reverse metabolism" is qualitative and of marginal predictive validity as an exposure biomarker due to the method's low recoveries and the large unexplained variance.

Adult↗
PubMed2003

Environmental exposure to polychlorinated biphenyls (PCBs) and breast cancer: a systematic review of the epidemiological evidence.

Some PCB congeners have shown oestrogenic effects, and this has raised concern that they may increase the risk of breast cancer. In this article we provide a quantitative review of the epidemiologic evidence on environmental exposure to PCBs and breast cancer risk. The vast majority of prospective and retrospective studies did not find any association between total PCB concentrations and breast cancer risk. No association was found for congeners in groups I (potentially oestrogenic) and III (biologically persistent phenobarbital-type cytochrome P450 inducers), according to the classification proposed by Wolff and Toniolo, while less consistent results were reported for group II (potentially anti-oestrogenic and immunotoxic, dioxin-like). Two studies found a threefold risk of postmenopausal breast cancer for women with an A2455G base change in exon 7 of the polymorphic CYP1A1 gene (a member of the cytochrome P450 family) and high PCB levels, compared with women with two wild-type alleles and low PCB, based however on very few cases. Thus, the epidemiological evidence does not support the hypothesis of an association of environmental exposure to PCBs in adulthood in the general population and risk of breast cancer, although uncertainties remain for selected subgroups of women or individual PCB congeners.

Adult↗