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Results for “Environmental Exposure”

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PubMedDate not supplied

Wegener's granulomatosis: role of environmental exposures.

OBJECTIVE: The etiology of Wegener's granulomatosis (WG) remains unknown. The predominant involvement of the airways and the presence of neutrophilic alveolitis at disease onset have led us to postulate that an inhaled agent may trigger the onset of WG. This study is designed to analyze differences in self-reported environmental exposures between patients with WG and various control populations. METHODS: We conducted a standard interviewer-administered questionnaire case controlled survey of 101 patients with WG, 54 healthy controls, 24 patients with sarcoidosis or idiopathic pulmonary fibrosis, and 45 patients with various inflammatory rheumatologic diseases. We assessed environmental exposures for one year prior to the onset of symptoms or prior to the interview date for healthy controls. RESULTS: Seasonal differences in the onset of WG were not apparent. More than 75% of the patients in all groups noted remarkable environmental exposure to inhaled substances (fumes or particulate matter), within one year prior to disease onset for WG and other diseases or prior to the interview date for healthy controls. Differences between WG and control groups were apparent in several categories of exposure. Statistically significant differences occurred in regard to a vocational exposure to fumes or particulate materials (WG > healthy controls and rheumatic disease controls), residential exposure to particulate materials from construction (WG > pulmonary disease controls) and occupational exposure to pesticides (WG > healthy, pulmonary and rheumatic disease controls). CONCLUSION: This study confirms the absence of seasonal differences in the onset of WG. It also demonstrates high rates of self-reported environmental exposures to inhaled substances in WG and all control populations. It is possible that more significant differences in the quality, quantity and intensity of exposure to inhaled potential precipitants of WG had occurred between groups, but were not detected by our survey. Alternatively, the absence of substantial differences in patients with WG and controls may reflect the more important role of host susceptibility factors.

Adolescent↗

PubMed1997

Onset of action, efficacy, and safety of a single dose of fexofenadine hydrochloride for ragweed allergy using an environmental exposure unit.

BACKGROUND: Fexofenadine hydrochloride is the active acid metabolite of terfenadine. Fexofenadine's anti-allergic properties require confirmation in a clinical setting. OBJECTIVE: The purpose of this study was to characterize the time to onset of clinically important relief of symptoms of allergic rhinitis in subjects taking single doses of either 60 mg or 120 mg fexofenadine HCl, or placebo, after exposure to ragweed pollen in a controlled environment. Other objectives were to assess the efficacy and safety of single doses of fexofenadine HCl. METHODS: One hundred forty-six ragweed-sensitive subjects were primed in the off-season with ragweed pollen in the environmental exposure unit. One hundred thirty-six subjects who adequately responded to priming entered a single-dose placebo phase. Placebo-responders were disqualified from the study, leaving 99 subjects with adequate symptoms to be randomized and given a single dose of either fexofenadine HCl 120 mg (33), 60 mg (33) or placebo (33), after 60 minutes of allergen exposure. Exposure continued over five hours and subjects recorded symptoms every 20 minutes. This study was of a randomized, placebo-controlled, double-blind, parallel design. RESULTS: Median time to onset for relaxed criteria clinically important relief was 60 minutes for both fexofenadine treatment groups, and 100 minutes for placebo (P = .018). The proportion with relief was 82% at 60 mg, 85% at 120 mg, and 64% for placebo. Treated groups had reductions in symptom scores double that of placebo. CONCLUSIONS: Fexofenadine is safe and efficacious at single doses of 60 mg and 120 mg. Average time to onset was 60 minutes using controlled pollen exposure in an environmental exposure unit.

Adolescent↗

PubMed2003

Monitoring human occupational and environmental exposures to polycyclic aromatic compounds.

Many research groups have been carrying out studies to develop biomarkers of exposure to polycyclic aromatic compounds (PACs) and apply these for human biomonitoring. The main objectives of the use of biomarkers are to determine specific occupational and environmental exposures to monitor the effectiveness of exposure controls and prediction of the risk of disease. This article presents a review of the literature in the field of biomarkers of human exposure to PACs and an evaluation of the relevant biomarkers for monitoring exposure to PACs in a range of exposure situations from coke ovens to bitumen handling and environmental exposures. For this evaluation, the relationships between external PAC exposures and the corresponding biomarker levels have been studied. The literature data indicate that urinary excretion of 1-hydroxypyrene correlates well with external PAC exposure and this compound appears to be a suitable marker for internal exposure to PACs. DNA adducts, mostly measured in white blood cells, do not show satisfactory correlations with exposure to PACs in a variety of workplace and exposure situations. It is not clear which factors are mainly responsible for this poor correlation. Micronuclei and sister chromatid exchanges measured in peripheral white blood cells are also unsatisfactory as biomarkers for PAC exposure. From the relatively limited data available, chromosome aberrations appear to show considerable promise as indicators of exposure to PACs. Because of their strong association with cancer, chromosome aberrations are considered suitable indicators of increased cancer risk arising from exposure to PACs.

Animals↗

PubMedDate not supplied

[Evaluation of a questionnaire for measuring individual environmental exposure to disinfection byproducts found in drinking water].

Epidemiological studies to evaluate the association between environmental exposure to risk factors and negative health effects often use population level aggregated data to measure exposure, but do not consider personal characteristics that may affect the degree of exposure at the individual level. The aim of this study was to evaluate the validity and reproducibility of a questionnaire specifically designed to measure individual oral, inhalation and transdermal exposure to disinfection byproducts in drinking water. Reproducibility of the questionnaire was evaluated by administering the questionnaire twice, in different time periods, to the same subjects. On the other hand, validity was tested by comparing responses to the questions with information contained in diaries filled out by the subjects daily over a period of one week (gold standard). Questionnaire reproducibilty and validity were both found to be very good, as shown by high Spearman's correlaton coefficients, Intraclass correlation coefficients (ICC), kappa concordance coefficient, sensibility and specificity. The use of a questionnaire such as the one evaluated in this study may be a valuable aid when conductin epidemiological studies to assess individual environmental exposure to risk factors found in drinking water and to explain the effect of such factors on human health.

Adolescent↗

PubMed1997

Multiple sclerosis in India: a case-control study of environmental exposures.

OBJECTIVES: To compare the rate of prior environmental exposures between Indian multiple sclerosis (MS) patients and controls in order to identify potential disease triggering factors. MATERIAL AND METHODS: A standard self-administered questionnaire regarding prior exposures was presented to 56 Indian MS patients and 147 other neural disease and healthy controls at two large medical centers in India. RESULTS: The rate of prior foreign travel, surgeries, blood transfusions, clinical chicken pox and mumps infections and exposure to cats and farm animals was not significantly different between MS patients and controls. However, clinical measles infection and dog exposure occurred significantly more often in the MS patients. CONCLUSION: These findings are consistent with but do not prove an association between prior measles infection, dog exposure and MS.

Adult↗

PubMed2006

Early environmental exposure and the development of lupus.

Systemic lupus erythematosus (SLE) is a complex trait with evidence of polygenic inheritance influenced by environmental factors. However, the precise underlying causes of SLE remain unclear. A number of environmental exposures have been associated with lupus or related autoimmune phenomena. Evidence suggests that some environmental exposures need to be present many years before the onset of SLE. Both SLE and rheumatoid arthritis (RA) can occur in very young children and this supports the possibility that important environmental factors must be present during or before this time. In addition, the immune pathology, including autoantibody production, in adult lupus may begin years before clinical disease. There is also evidence that the developing immune system demonstrates developmental plasticity and can be permanently altered or 'programmed' by the early environment. We describe how early life environmental influences including infectious exposure may lead to autoantibody production in later life thus beginning the journey that leads to autoimmune diseases such as lupus in susceptible individuals.

Arthritis, Rheumatoid↗

PubMed2004

[Pleural mesothelioma and environmental exposure to mineral fibres: the case of a rural area in the Basilicata region, Italy].

The main aspects of the sites characterized by environmental exposure to mineral asbestiform fibres are described. Several adverse health effects including high incidence of pleural mesothelioma are reported. The average concentration of airborne fibres is generally low but it rises significantly in association with mechanical disturb of materials with fibres. Multiple sources of exposure have been identified, fibres can be found in the soil and in many materials locally used, mainly in buildings. Three mesothelioma cases were observed in a small rural area of the Basilicata region (Italy). Two of them had a possible occupational exposure to asbestos, the third had a proved environmental exposure to tremolite. This fibre, found in the area, is the same observed in two of the three biological samples analysed.

Asbestos↗

PubMedDate not supplied

Environmental exposure to polychlorinated biphenyls and breast cancer risk.

Breast cancer is a major public health problem in the United States and in most industrialized countries. Although epidemiologic studies have identified a number of established risk factors for this disease, these factors explain only a small proportion of breast cancer incidence. Environmental exposure has been implicated in breast cancer etiology because of the vast geographic variation in breast cancer incidence rates across countries and regions within countries. Further, the steady increase in breast cancer rates over the past decades points to a potential role of environmental exposure in its development. One suspected environmental factor is the polychlorinated biphenyls (PCBs), which were manufactured commercially for a variety of industrial applications from the 1930s until the 1970s. PCBs have been associated with estrogenic, tumor promoting, and immunosuppressive activities, all of which are relevant in the development of breast cancer. The purpose of this review is to summarize the growing body of epidemiological evidence on the association between environmental PCB exposure and breast cancer risk. Three major types of study design have been used to investigate such a relation: clinic-based case-control studies, retrospective case-control studies, and nested case-control studies. Although findings from clinic-based case-control studies tend to point to an adverse effect of high PCB body burden on risk, the results from the more methodologically sound retrospective and nested studies do not provide strong support for a role of PCBs in breast cancer development. The association between PCB exposure and risk among racially and genetically susceptible subgroups may warrant further investigation. Methodological challenges in the design and analysis of epidemiologic studies on PCBs and breast cancer risk are discussed.

Breast Neoplasms↗

PubMed1998

Environmental exposure to crocidolite and mesothelioma: exposure-response relationships.

This study aimed to estimate exposure-response relationships for mesothelioma and environmental exposure to crocidolite. All 4,659 former residents of Wittenoom, Western Australia (WA) who lived there between 1943 and 1993 for at least 1 mo and were not directly employed in the crocidolite industry, were followed-up through the WA death, cancer and mesothelioma registries, electoral rolls, and telephone books. In 1992, all subjects who should be traced were sent a questionnaire. Exposure levels were estimated from results of periodic environmental surveys and duration of residence. Incidence rates were standardized to the World Population and Cox Regression was used to estimate the effects of exposure on incidence. To the end of 1993, 27 cases of mesothelioma were diagnosed. Mesothelioma cases stayed longer at Wittenoom, had a higher average intensity of exposure, and a higher cumulative exposure to crocidolite than control subjects. The standardized incidence of mesothelioma was 260 per million person-years, and was similar for males and females. The rate increased significantly with time from first exposure, duration of exposure and cumulative exposure. At these levels of crocidolite exposure, there is a significantly increased risk of mesothelioma, which is dose-dependent.

Adult↗

PubMed2000

Mutagen sensitivity and environmental exposures as contributing causes of chromosome 3p losses in head and neck cancers.

The interaction between environmental exposures and host susceptibility may lead to specific mutational events within head and neck squamous cell carcinoma (HNSCC). Furthermore, this interplay may determine not only the probability of cancer development but also the biologic characteristics of the tumor once it occurs. To better understand the relationship of mutagen sensitivity and tobacco and/or alcohol consumption on HNSCC carcinogenesis, we examined loss of heterozygosity on chromosome 3p in 58 HNSCCs using 10 microsatellite markers. Mutagen sensitivity was determined in vitro by quantitating bleomycin-induced chromatid breaks utilizing peripheral blood lympocytes from respective patients. Forty-six of the 58 invasive cancers showed allelic loss at one or more loci. Consistent with previous investigations, three discrete regions of deletions were identified: 3p13-14.2, 3p21.1-21. 2, and 3p25.1-26.1. The frequency and types of deletions were dependent upon tobacco and alcohol exposures. The distal region of 3p but not the remaining two regions was most frequently influenced by tobacco exposure. In contrast, heavy alcohol use when combined with tobacco use was associated with whole-arm loss of 3p rather than identifiable site-specific damage. Furthermore, this combined influence of alcohol and tobacco exposures on whole-arm loss was most apparent in those patients who expressed mutagen-sensitivity; the odds ratio of whole-arm loss increasing from 2.67 (95% CI 0. 21-33.49) in those individuals who were mutagen resistant to 13.5 (95% CI 1.3-136.0; P = 0.02 by Fisher's exact test) in those who were mutagen sensitive. An assessment of clinical parameters in this population demonstrated that patients with whole-arm loss were more likely to present with cervical lymph node metastases and advanced stage disease than patients with partial losses. Results indicate that various environmental exposures as well as the expression of mutagen sensitivity will influence the types of chromosome 3p allelic losses in head and neck cancers as well as the behavior of disease once it develops.

Alleles↗

PubMed1990

Health effects of environmental exposure to cadmium: objectives, design and organization of the Cadmibel Study: a cross-sectional morbidity study carried out in Belgium from 1985 to 1989.

Cadmium is a cumulative environmental pollutant. For the general population mainly exposed by the oral route and through tobacco smoke inhalation, the kidney is the critical organ. Belgium is the principal producer of cadmium in Europe, and certain areas of the country are polluted by cadmium mainly because of past emissions from nonferrous industries. Preliminary studies carried out in one polluted area have suggested that environmental pollution might lead to an increased uptake of cadmium by the human body and possibly to health effects. Thus, a large-scale morbidity study has been initiated to assess the validity of this hypothesis. The present paper describes the protocol of this study. Its main objectives are to determine to what extent environmental exposure to cadmium resulting from industrial emissions may lead to accumulation of the metal in the human organism; to establish whether or not environmental exposure may induce renal changes and/or influence blood pressure; and to assess the acceptable internal dose of cadmium for the general population. The study design takes advantage of the fact that biological indicators of exposure, body burden, and early nephrotoxic effects of cadmium are available, which increase the likelihood of detecting a cause-effect relationship.

Adult↗

PubMed2003

Environmental exposure reduction in high-risk newborns: where do we start?

BACKGROUND: When analyzing the effect of environmental exposure reduction measures on asthma in high-risk children, one must know how far asthmatic families already have applied such measures, because this would affect the effectiveness and efficiency of interventions aimed at reducing environmental exposure. OBJECTIVE: To describe the room for improvement by asthmatic families in mite, pet, and food allergen reducing measures and in parental passive smoking and to determine the resulting levels of mite and pet allergens by the applied sanitation measures. METHODS: Data were sampled by observation, weekly diary entries, and questionnaire when the infant was 6 months old and 1 year old. Dust samples were collected by vacuuming the living room floor and the parental and infant mattresses. Multiple logistic regression analyses were applied with the use of mattress encasing, having a smooth floor covering, having pets, exclusive breast-feeding and/or hypoallergenic formula during the infant's first 6 months, and passive smoking as the dependent variables. RESULTS: Frequencies of applied measures were as follows: having a smooth floor covering, 36%; daily house cleaning, 27%; use of parental and infant antimite mattress encasings, 13% and 9%, respectively; keeping no pets, 66%; no cow's milk-based regular formula, 13%; no solid foods in the first 6 months of life, 28%; and abstinence of smoking by the mother prenatally, 89%; by the mother postnatally, 85%; and by her partner, 76%. Having a smooth floor covering and daily cleaning but not use of antimite mattress encasings resulted in significantly lower mite and pet allergen levels. CONCLUSIONS: There is (still) enough room for improvement to reduce exposure to inhalant and food allergens, especially by application of mattress encasings, exclusive breast-feeding and/or hypoallergenic formula feeding, and postponing the time until first solids are given.

Air Pollution, Indoor↗

PubMed1995

Occupational and environmental exposure of automobile mechanics and nonautomotive workers to airborne manganese arising from the combustion of methylcyclopentadienyl manganese tricarbonyl (MMT).

Inhalation exposure to manganese (Mn) was measured for a group of garage mechanics and a control group of nonautomotive workers. The airborne Mn exposure of 35 garage mechanics suspected of being relatively highly exposed to Mn from MMT was measured at the workplace over one-week period. It also was measured for 30 nonautomotive workers at the University of Montreal. The environmental exposure also was measured for the two groups, as was the exposure to three other metals, aluminum (Al), iron (Fe), and zinc (Zn). At work the mechanics were exposed to Mn concentrations varying from 0.010 to 6.673 micrograms m-3 with a mean of 0.45 microgram m-5, while the control group was exposed to concentrations varying from 0.011 to 1.862 microgram m-3 with a mean of 0.04 microgram m-3. The mean environmental exposure for the two groups was similar to the Mn concentrations gathered in Montreal in 1992. Workplace concentrations of Al, Fe, and Zn also were higher for the garage mechanics. The results suggest that less than 10% of the Mn exposure of the garage mechanics was due to MMT. The levels of the metals measured were below the established limits for industrial and even environmental exposure.

Air Pollutants, Occupational↗

PubMed2004

Effects of environmental exposures on the cardiovascular system: prenatal period through adolescence.

Exposures to drugs, chemical and biological agents, therapeutic radiation, and other factors before and after birth can lead to pediatric or adult cardiovascular anomalies. Furthermore, nutritional deficiencies in the perinatal period can cause cardiovascular anomalies. These anomalies may affect heart structure, the conduction system, the myocardium, blood pressure, or cholesterol metabolism. Developmental periods before and after birth are associated with different types of risks. The embryonic period is the critical window of vulnerability for congenital malformations. The fetal period seems to have lifelong effects on coronary heart disease and its precursors. During the weeks immediately after birth, susceptibility to myocardial damage seems to be high. Exposure to cancer chemotherapy or radiotherapy in childhood raises the risk of long-term progressive left ventricular dysfunction and other cardiovascular problems. In childhood and adolescence, use of recreational drugs such as cocaine and tobacco poses cardiovascular dangers as well. Where evidence about environmental exposures is limited, we have included models of disease and other exposures that are suggestive of the potential impact of environmental exposures.

Adolescent↗

PubMed2005

Assessing occupational and environmental exposure.

Exposure assessment is a poorly understood component of the science of epidemiology. The relationship between exposure to chemicals and ill-health outcomes is often calculated using crude exposure measures such as ever/never exposed or duration. When investigating subtle effects, exposures need to be characterized much more fully in terms of intensity, frequency, duration and route. While occupational exposures tend to be much greater than those experienced from the wider environment there is a need to remember that, for many chemicals, exposure can occur occupationally, environmentally and through consumer use of products containing the material of interest. Inhalation exposure has generally been the traditional focus for most epidemiological investigations but there is now growing awareness of the importance of the dermal and ingested routes of contact and internalization. Quantification of the exposure also needs to be related to a biological mechanism of action and exposure metrics need to be selected accordingly. Occupational exposures can generally be measured using simple well-validated techniques. Environmental exposures require much more sensitive instruments and are more difficult to assess. Exposure modelling, particularly for the environmental fate of chemicals has undergone many recent developments and Monte Carlo techniques can be used to characterize model uncertainty and variability. This approach to exposure assessment can now be used in the setting of the wider environment and will enable a far better understanding of the relationship between exposure and disease.

Environmental Exposure↗

PubMed1999

Combining environmental exposure and genetic effect measurements in health outcome assessment.

The presence of overwhelming difficulties in assessing the extent or even the presence of a causal association between modern environmental exposures and disease has promoted the use of more complex models in the design of human biomonitoring studies. The concatenation of environmental exposure, genetic effect and individual susceptibility is a key issue in the assessment of risks for populations exposed to environmental pollutants. The use of a biological event laying in the causal pathway from exposure to outcome as surrogate end-point of disease, can potentially anticipate clinical diagnosis, offering a number of possibilities for application of preventive measures. Numerous biomarkers are currently employed to study human populations exposed to environmental carcinogens, among these, the frequency of chromosomal aberration (CA) in peripheral blood lymphocytes has the most abundant literature linking a genetic effect with the occurrence of cancer. Findings from recent epidemiological studies which have followed-up a large group of healthy subjects screened for CAs have lent further support to the use of chromosomal breakage as a relevant biomarker of cancer risk. The applicability of surrogate end-points of cancer on an individual basis thus far seems to be limited to few examples. On the other hand, from a public health outlook, increases in the frequency of surrogate end-points are suggestive of an increased risk of cancer, and for validated biomarkers such as CAs intervention policies and actions in exposed populations showing increased frequency of these end-points should be always recommended.

Chromosome Aberrations↗

PubMed2006

Studies of multiple sclerosis in communities concerned about environmental exposures.

Multiple sclerosis (MS) is an autoimmune disease that differentially affects women, people 30-60 years old, and Caucasians. Evidence indicates that it is a complex disease determined by both environmental factors and genetic susceptibility. People across the United States have expressed concern about perceived clusters of MS in their communities and the role of environmental exposures in the development of the disease. The Agency for Toxic Substances and Disease Registry (ATSDR) has funded several studies to address this issue, including a cluster investigation, several prevalence studies, and a case-control study. The cluster investigation illustrated that there are few data regarding the number of individuals with MS in the United States. Prevalence studies were conducted in Ohio, Missouri, and Texas to address this deficiency. The results support a regional difference in MS prevalence, although the reason for this difference is unclear. The results also underscore the need for additional epidemiological information about the distribution of MS in other areas of the United States and information on the underlying etiology of the disease. A case-control study is currently being conducted to examine potential risk factors for MS, including the role of environmental exposures and genetic susceptibility. Future research on MS should focus on large-scale studies and include collaboration among researchers with varied fields of expertise, such as epidemiology, neurology, and genetics.

Adult↗

PubMed2001

The prevalence of environmental exposure to perceived asthma triggers in children with mild-to-moderate asthma: data from the Childhood Asthma Management Program (CAMP).

BACKGROUND: The Childhood Asthma Management Program, a 5-year randomized clinical trial of treatments for childhood asthma, has enrolled and characterized a cohort of 1041 children with mild-to-moderate asthma. OBJECTIVE: We sought to describe self-reported sensitivities and environmental exposures and investigate the relationships between self-report of these exposures as asthma triggers and their prevalence in the home. METHODS: Self-reports of sensitivities and home exposures were obtained by interview with the child or parent. Sensitivities were further assessed by using allergy skin testing (prick or puncture) against a core battery of allergens. Home exposures were further assessed by using analysis of a home dust sample. RESULTS: Environmental exposures were surprisingly common despite self-reported sensitivities to environmental factors. Of patients reporting that cigarette smoking frequently causes asthma symptoms, 26% reported having at least one parent who smokes cigarettes. Thirty-nine percent of patients reporting that exposure to animals frequently causes asthma symptoms live with a furry pet in their home. We found a smaller proportion of homes with a high level of cat allergen (P <.001) among the children who reported that animals frequently or always trigger asthma symptoms compared with those who reported that animals never or occasionally trigger asthma symptoms, suggesting modification of the home environment. No such results were seen for dog exposure. However, clinical symptoms did not reduce exposure to parental cigarette smoking (P =.15), house dust (P =.31), or damp and musty areas (P =.51). CONCLUSION: These data suggest that children with mild-to-moderate asthma are frequently symptomatic and exposed to a wide variety of environmental exposures that are perceived to trigger symptoms by means of self-report. Although environmental modification of asthmatic homes may occur, many children remain exposed to agents that are known to trigger their asthma.

Asthma↗