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Results for “environmental exposures”

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At least 19 recordsLinked to original sources

PubMed2002

Parent-reported environmental exposures and environmental control measures for children with asthma.

BACKGROUND: Mounting evidence suggests that indoor allergens and irritants contribute to childhood asthma. National asthma guidelines highlight the importance of their reduction as part of comprehensive asthma treatment. OBJECTIVES: To assess the prevalence of potential environmental triggers, to identify risk factors for such exposures, and to determine whether prior parental education about trigger avoidance is associated with fewer such exposures. SETTING AND PATIENTS: Children with asthma in practices affiliated with 3 managed care organizations. INTERVENTIONS: Parents of 638 children, aged 3 to 15 years, were interviewed on enrollment in a randomized trial of asthma care improvement strategies. Parents reported recent asthma symptoms and exposures to potential environmental triggers. Multivariate models were used to identify specific demographic risk factors for environmental exposures and to determine if prior education was associated with fewer such exposures. RESULTS: Exposures to environmental triggers were frequent: 30% of households had a smoker, 18% had household pests, and 59% had furry pets. Other exposures included bedroom carpeting (78%) and forced-air heat (58%). Most children did not have mattress (65%) or pillow (84%) covers. Of the parents, 45% reported ever receiving written instructions regarding trigger avoidance and 11% reported them given in the past year. However, 42% reported discussing triggers in the home environment with a clinician in the past 6 months. In multivariate models, predictors of smoking at home included low annual family income and lower parental educational attainment. Dog ownership was associated with low educational attainment, and dog and cat ownership were less likely with black race. Reports of pests were increased for black children compared with white children. Black race was associated with lower rates of other exposures, including bedroom carpeting. After controlling for potential confounders, there was no association of reduced exposures with prior receipt of environmental control instructions. CONCLUSIONS: Exposure to potential environmental triggers is common, and recommended trigger avoidance measures are infrequently adopted. While specific exposures may vary with demographic and socioeconomic variables, all children are at risk. New methods for educating parents to reduce such exposures should be tested.

Adolescent↗

PubMed2001

Environmental exposure of the pediatric age groups in Cairo City and its suburbs to cadmium pollution.

In a trial to assess the exposure of subjects in the pediatric age group to cadmium (Cd) pollution, serum Cd was estimated by atomic absorption spectrometry in 405 subjects, birth-18 years old, from Cairo City and its suburbs. Serum Cd mean concentrations were: 0.92 microg/l in 32 neonates (birth-4 weeks); 1.33 microg/l in 70 infants (4 weeks-2 years); 1.11 microg/l in 100 children in the preschool period (2-6 years); 1.34 microg/l in 103 primary school children (6-12 years); and 1.24 microg/l in 100 adolescents (12-18 years). In neonates, serum Cd was higher in babies with weights and heights that remained below the 5th percentile for age. Breast-fed infants had a serum Cd geometric mean level (1.25 microg/l) that was not in accordance to that of their mothers' milk (0.52 microg/l, P < 0.001), suggesting alternative routes of exposure. Environmental tobacco-smoke exposure was the most important determinant of Cd status in the school-aged children, the geometric mean being 1.42 microg/l in passive smokers vs. 1.2 microg/l in non-exposed children (P < 0.05). Moreover, adolescents who were active smokers had a significantly higher serum Cd level (1.7 microg/l) as compared to non-smokers (1.2 microg/l). Gender did influence the Cd status in adolescents, being higher among males, probably related to smoking, or to the difference in lifestyle of adolescents according to gender in the community. Alpha-1-microglobulinuria was accompanied by a higher serum Cd concentration in the group of adolescents only, suggesting a subclinical renal effect after several years of cumulative exposure. The residential classification, whether urban or suburban, did not influence the serum Cd status; neither did the present or past history of bronchial asthma. These findings certainly justify further evaluation of the problem of Cd pollution among Cairene individuals, knowing the long-term consequences of exposure to it. Systematic efforts for the proper disposal of Cd wastes and prevention of smoking in public places are recommended.

Adolescent↗

PubMed1999

Environmental exposure to cadmium, forearm bone density, and risk of fractures: prospective population study. Public Health and Environmental Exposure to Cadmium (PheeCad) Study Group.

BACKGROUND: Chronic low-level exposure to cadmium may promote calcium loss via urinary excretion. We undertook a prospective population study to investigate whether environmental exposure to cadmium lowers bone density and increases risk of fractures. METHODS: We measured urinary cadmium excretion, a biomarker of lifetime exposure, in people from ten districts of Belgium, of which six districts bordered on three zinc smelters. We also measured cadmium in soil and in vegetables from the districts, and collected data on incidence of fractures and height loss. Bone density was measured at the forearm just above the wrist by single photon absorptiometry, and calculated as the mean of six proximal and four distal scans. FINDINGS: Mean cadmium excretion at baseline was 8.7 nmol daily. Across the ten districts, mean cadmium concentration in soil ranged from 0.8 to 14.7 mg/kg, and from 0.1 to 4.0 mg/kg dry weight in vegetables. Median follow-up was 6.6 years. Mean forearm bone density in proximal and distal scans was 0.54 g/cm2 and 0.43 g/cm2 in men, and 0.44 g/cm2 and 0.34 g/cm2 in women. In postmenopausal women, a twofold increase in urinary cadmium correlated with 0.01 g/cm2 decrease in bone density (p<0.02). The relative risks associated with doubled urinary cadmium were 1.73 (95% CI 1.16-2.57; p=0.007) for fractures in women and 1.60 (0.94-2.72, p=0.08) for height loss in men. Cadmium excretion in districts near smelters was 22.8% higher (p=0.001) than in other districts, with fracture rates of 16.0 and 10.3 cases per 1000 person-years, respectively, and a population-attributable risk of 35.0%. INTERPRETATION: Even at a low degree of environmental exposure, cadmium may promote skeletal demineralisation, which may lead to increased bone fragility and raised risk of fractures.

Absorptiometry, Photon↗

PubMed1997

Breast cancer risk and environmental exposures.

Although environmental contaminants have potential to affect breast cancer risk, explicit environmental links to this disease are limited. The most well-defined environmental risk factors are radiation exposure and alcohol ingestion. Diet is clearly related to the increased incidence of breast cancer in developed countries, but its precise role is not yet established. Recent studies have implicated exposure to organochlorines including DDT as a risk factor for breast cancer in the United States, Finland, Mexico, and Canada. Other investigations have discovered associations between breast cancer risk and exposures to chemical emissions and some occupational exposures. Several points must be considered in evaluating the relationship of environmental exposure to breast cancer. Among these considerations are the mechanism of tumorigenesis, timing of environmental exposure, and genetic modulation of exposure. Epidemiologic and ecologic investigations must take into account the very complex etiology of breast cancer and the knowledge that tumorigenesis can arise from different mechanisms. Thus crucial exposures as well as reproductive events related to breast cancer may occur years before a tumor is evident. Moreover, environmental contaminants may alter reproductive development, directly or indirectly, and thereby effect the course of tumorigenesis. Such alterations include change in gender, change in onset of puberty, and inhibition or promotion of tumor formation. Timing of exposure is therefore important with respect to mechanism and susceptibility. Finally, genetic polymorphisms exist in genes that govern capacity to metabolize environmental contaminants. Higher risk may occur among persons whose enzymes either are more active in the production of procarcinogens or fail to detoxify carcinogenic intermediates formed from chemicals in the environment.

Breast Neoplasms↗

PubMed2003

Presence of asthma risk factors and environmental exposures related to upper respiratory infection-triggered wheezing in middle school-age children.

Viral respiratory infections and exposure to environmental constituents such as tobacco smoke are known or suspected to trigger wheezing/asthma exacerbations in children. However, few population-based data exist that examine the relationship between wheezing triggered by viral respiratory infections and environmental exposures. In this investigation we used population-based data to evaluate differences in exposures between symptomatic middle school-age children who did and did not report wheezing triggered by viral respiratory infections. As part of the North Carolina School Asthma Survey (NCSAS), a 66-question data instrument was used to collect information from children enrolled in North Carolina public middle schools during the 1999-2000 school year. Associations between exposures and upper respiratory infection-triggered wheezing (URI-TW) among symptomatic children were examined using adjusted prevalence odds ratios (PORs). Video methods developed for the International Study of Asthma and Allergies in Childhood were used to assess wheezing. Among the 33,534 NCSAS symptomatic participants, positive associations were observed between most exposures and URI-TW. Reported presence of all allergy variables (PORs ranging from 2.11 to 2.45) was more strongly associated with URI-TW than either smoking or other exposures. Presence of URI-TW was higher at increasing levels of tobacco smoke exposure, but no apparent dose-response effect was observed for other indoor air pollutants. URI-TW in middle school children is most associated with reported allergen sensitivity, relative to other asthma risk factors and environmental exposures. Data from this investigation may be useful in developing assessment, screening, and targeting strategies to improve asthma and wheezing management in children.

Adolescent↗

PubMed2001

Epidemiologic associations between occupational and environmental exposures and autoimmune disease: report of a meeting to explore current evidence and identify research needs.

To advance understanding of autoimmunity associated with exposure to environmental factors, an "Exploratory Meeting Epidemiology on Occupational and Environmental Factors Associated with Autoimmunity" was organized in Bilthoven, the Netherlands, from May 10-12, 2000. Even if no firm conclusions can be drawn on a role of certain chemicals in the environment and in the work place in causing or exacerbating autoimmune responses and illnesses, many indications of this to occur exist. The aim of the meeting was to determine the optimal methodology for assessment of autoimmunity associated with occupational or environmental exposures in the human population, and to set up interdisciplinary and collaborative epidemiological studies to investigate the association of exposure to silica, hexachlorobenzene, ultraviolet radiation, and other agents with autoimmunity and autoimmune diseases in the human population. These agents were selected as carrying particular suspicion at present. It was concluded that there is a need for experimental studies in laboratory animals and for clinical investigations to improve scientific knowledge about the causes and mechanisms of environmentally-induced autoimmune disorders and their treatment; in addition there is a need for an interdisciplinary approach to epidemiological studies of the environmental and other causes of these disorders in human populations. Specific designs for epidemiological studies in this context, as well as laboratory assays for health outcomes, were reviewed. Several recommendations for the epidemiological approach to evaluating effects of environmental or occupational agents on autoimmunity were made. The prime recommendations are the following: 1) systematic descriptive epidemiological data on autoimmunity and autoimmune disorders are required; 2) the establishment of disease-reporting registries should be encouraged; 3) the development of internationally accepted standard diagnostic criteria for all autoimmune diseases should be encouraged; 4) the social impact of these disorders should be evaluated and estimations of direct and indirect economic costs should also be made; 5) the methods of exposure assessment used in epidemiological studies should be standardized; 6) laboratory methods for measurement of biological responses should be standardized; and 7) the inclusion of indicators of autoimmunity and autoimmune diseases and of relevant environmental exposures in ongoing epidemiological studies should be encouraged. The importance of studying environmental causes of autoimmune diseases and autoimmunity lies in the identification and prevention of risks to the public health, and in improving our knowledge of basic mechanisms of health and disease.

Animals↗

PubMed1995

[Principles of evaluation of public health risk for environmental exposures].

Assessing environmental health risk is fraught with difficulties: often, the agents under study are weak pathogens, and exposures are poorly characterised. Direct studies in man are frequently inconclusive (or inconsistent) because of the limited sensitivity of epidemiological studies. Experimental studies raise questions about the validity of animal to man extrapolation. However, taking steps to protect public health is needed and impose the use of all available data. Remaining uncertainties lead the health risk assessor to make assumptions. Such a process implies as much transparency as possible, both for ethical reasons and to allow the public to be involved in the debate. A formalized approach has been proposed by various US agencies in charge of public health. One important matter is a strict separation between risk assessment and risk management. The procedure is divided into four portions: hazard assessment, exposure assessment, dose-response assessment which includes the study of risk at low doses--sometimes through the use of mathematical high to low dose extrapolation modelling--and risk characterisation.

Animals↗

PubMed2003

Workshop report: environmental exposures and cancer prevention.

The Workshop on Environmental Exposures and Cancer was held by Cancer Care Ontario (CCO) 25-26 April 2001. An expert panel convened to achieve consensus on a list of important environmental exposures, priority environmental exposures in Ontario, and recommendations for CCO in the areas of surveillance, research, and prevention activities to address these environmental exposures. Panel members developed a working definition of environmental exposure and criteria to prioritize the identified exposures. The process followed in the workshop provided CCO with important direction for its surveillance, research, and prevention activities to address environmental exposures and cancer. It is hoped that the environmental exposures and the opportunities identified through this workshop process will guide policy makers, program personnel, and researchers interested in and struggling with the challenges associated with surveillance, research, and prevention of environmental exposures.

Environmental Exposure↗

PubMed2005

National exposure measurements for decisions to protect public health from environmental exposures.

Protecting public health from environmental exposures requires four steps: detection of exposures known or expected to cause disease, assessment of health risk from exposure, implementation of an exposure intervention, and assurance that the exposure intervention is effective. To prioritize efforts in these four areas one must consider the size of the population affected, the seriousness of health effects, and the availability of cost-effective exposure interventions. Population exposure data is critical to each of these steps for protecting health. Biomonitoring data for the US population is now available to assist public health scientists and physicians in preventing disease from environmental exposures, and it complements that available for levels of chemicals in environmental media. The Second National Report on Human Exposure to Environmental Chemicals provides for the US population serum, blood and urine levels for 116 environmental chemicals over the years 1999 and 2000, with separate analyses by age, sex, and race/ethnicity. This national exposure information identifies which chemicals get into Americans in measurable quantities; determines whether exposure levels are higher among population subgroups; determines how many Americans have levels of chemicals above recognized health threshold levels (for chemicals with such threshold levels); establishes reference ranges that define general population exposure so unusual exposures can be recognized; assesses the effectiveness of public health efforts to reduce population exposure to selected chemicals; and tracks over time trends in US population exposure. Blood lead measurements in the population were important in identifying lead in gasoline as a significant source of human lead exposure and documenting the reduction in blood lead levels in the population as a result of removing lead from gasoline and other products in the United States. Serum cotinine levels in the early 1990s found more widespread exposure to environmental tobacco smoke (ETS) in the United States than previously thought and additional measurements in 1999 and 2000 documented major declines in exposure to ETS as a result of public health actions in the 1990s. A new biomonitoring assessment of the exposure of the US population will be released every 2 years as the "National Report on Human Exposure to Environmental Chemicals." These reports will include the current 116 chemicals and new chemicals added to monitor priority exposures of the population.

Adolescent↗

PubMed1985

Drug and environmental exposure histories in selective patient populations.

Drug histories and environmental exposures are an important part of all medical histories and are particularly significant in specific at-risk primary care patient populations such as obstetrical patients, primary care genetic referrals, and pediatric patients being evaluated in developmental centers. A review of genetic referrals made by primary care physicians to a satellite genetics clinic over a one-year period showed that 29 percent of all referrals had a significant history of single drug exposure, single environmental exposure, or multiple environmental and drug exposures. Drug and environmental exposures must be an important consideration in all at-risk groups.

Drug Prescriptions↗

PubMed2005

Influence of environmental exposure to PAHs on the susceptibility of lymphocytes to DNA-damage induction and on their repair capacity.

The influence of occupational exposure to environmental carcinogenic polycyclic aromatic hydrocarbons (c-PAHs) on DNA damage detected in lymphocytes of exposed people (city policemen) was studied. The cellular susceptibility to the induction of the DNA damage and the repair capacity of exposed donors are presented in comparison with matched controls. Monitoring was performed and blood samples (164 donors) were collected in Prague, Czech Republic, during the winter and summer seasons. The single-cell gel electrophoresis (SCGE) assay with an internal standard was applied to evaluate the DNA damage. A challenging dose of 2Gy of X-rays was used to study cellular capacities. In the results of studies of the DNA damage induced in vivo or as an immediate response to the challenging treatment no significant difference was found between exposed and unexposed subgroups. The percentage of non-repaired X-ray-induced DNA damage (residual damage, RD) overall in both seasons was significantly higher in lymphocytes of policemen exposed to c-PAHs than in matched controls (RD(T-DNA), %DNA in the comet tail: winter 36.4+/-22.1 versus 22.7+/-10.8, p < 0.001; summer 47.7+/-22.9 versus 34.7+/-15.2, p < 0.001). The results suggest that occupational exposure to environmental c-PAHs significantly reduces the cellular capacity to repair the DNA damage induced by a challenging treatment. A significant decrease of repair efficiency in donors occupationally exposed to environmental c-PAHs was also observed when subgroups were stratified according to smoking history. In conclusion, our results suggest that environmental exposure to c-PAHs affects the cellular repair processes and can lead to harmful effects hazardous to human health.

Adult↗

PubMed1993

Assessment of carcinogenic risk from personal exposure to benzo(a)pyrene in the Total Human Environmental Exposure Study (THEES).

The Total Human Environmental Exposure Study (THEES) was an investigation of multimedia exposure to the ubiquitous environmental carcinogen, benzo(a)pyrene (BaP). The three-phase study was conducted in Phillipsburg, New Jersey and involved the participation of 14-15 individuals (8-10 homes) during each 14-day monitoring period. Microenvironmental sampling of air, food, water and soil indicated that environmental exposure to BaP was primarily through air and food. Exposure and risk estimates were, therefore, based on the results of personal monitoring of breathing zone air and prepared food samples. Based on a comparison of the range and magnitude of inhalation and dietary BaP exposures, food ingestion was clearly the predominant exposure to pathway. The relative contributions of other potential sources of community exposure to BaP (e.g., soil and drinking water ingestion) were also assessed. The excess cancer risk estimates for food ingestion were consistently greater than those for personal air, reflecting both the predominantly higher BaP exposures through the diet and the higher carcinogenic potency value for oral exposure. Overall, the total lifetime risk from personal exposure to BaP for nonsmokers in the community was estimated at 10(-5). In identifying risk reduction options, it is important to account for the observation that personal activities, lifestyle, and diet strongly influenced individual exposures to BaP.

Air Pollutants↗

PubMed1995

Age-specific carcinogenesis: environmental exposure and susceptibility.

Environmental exposures in children may occur through many routes, including diet, air, and the ingestion of various nonfood items such as medications and household materials. This article focuses on dietary exposure, but it does highlight the importance of considering other routes of exposure when assessing exposure in children. It presents many of the findings in the two recent reports, Pesticides in the Diets of Infants and Children and Science and Judgment in Risk Assessment of the National Academy of Sciences (NAS)/National Research Council (NRC). Diet is an important source of exposure for children to potential carcinogens. The trace quantities of chemicals present on or in foodstuffs are termed residues. In addition, there are substances that children may be exposed to in air and water that should be considered in a total exposure analysis. To minimize exposure of the general population to chemical residues in food, water, and air, the U.S. government has instituted regulatory controls. These are intended to limit exposures to residues while ensuring an abundant and nutritious food supply, and safe drinking water and air. The legislative framework for these controls was established by the Congress through various local and state laws and such federal laws as the Insecticide, Fungicide, and Rodenticide Act (FIFRA), the Federal Food, Drug, and Cosmetic Act (FFDCA), the Safe Drinking Water Act (SDWA), and the Clean Air Act (CAA). This article summarizes current approaches to assessing exposure and susceptibility in children.

Air Pollution↗

PubMed1991

Analysis of human exposure to benzo(a)pyrene via inhalation and food ingestion in the Total Human Environmental Exposure Study (THEES).

The Total Human Environmental Exposure Study (THEES) focuses on benzo(a)pyrene (BaP) as an example of a combustion-generated polycyclic aromatic hydrocarbon (PAH) compound. Primary pathways for environmental exposures to BaP are inhalation and ingestion. This program of field studies was conducted in Phillipsburg, New Jersey, a small, industrial city in the Delaware River valley. The study protocols included direct monitoring of BaP exposures via inhalation and ingestion pathways during three separate periods, each lasting 14 days. BaP concentrations in air were sampled at outdoor and in-home locations, with personal air sampling added during the latter two phases. Cooked food samples from each household were acquired, using a constant portion "second plate" of each meal prepared at home. Ambient levels were 4-10 times higher during the cold months compared with the late summer study period. Space heating and regional aerosol were major contributors to community levels of BaP in the air during the wintertime. Penetration of outdoor air, cooking activities, combustion appliances, and cigarette smoke were important sources of indoor air exposures. Cooking activities, besides releasing BaP-enriched particles indoors, produced food imbued with BaP and added substantially to exposure via the ingestion route. Among the study subjects, the range and magnitude of dietary exposures (2 to 500 ng/d) were much greater than for inhalation (10 to 50 ng/d). Nevertheless, there were ample individual cases where inhalation of BaP was the predominant exposure route. Indoor air BaP levels were closely correlated with ambient levels in most of the homes. For some individuals, measured personal air BaP exposures were adequately predicted by time-weighting of microenvironmental (i.e., outdoor and in-home) concentrations. However, enormously high exposures for ingestion or inhalation were detected only by direct observation, not from microenvironmental data.

Administration, Inhalation↗

PubMed2006

A brief targeted review of susceptibility factors, environmental exposures, asthma incidence, and recommendations for future asthma incidence research.

Relative to research on effects of environmental exposures on exacerbation of existing asthma, little research on incident asthma and environmental exposures has been conducted. However, this research is needed to better devise strategies for the prevention of asthma. The U.S. Environmental Protection Agency (EPA) and National Institute of Environmental Health Sciences held a conference in October 2004 to collaboratively discuss a future research agenda in this area. The first three articles in this mini-monograph summarize the discussion on potential putative environmental exposure; they include an overview of asthma and conclusions of the workshop participants with respect to public health actions that could currently be applied to the problem and research needs to better understand and control the induction and incidence of asthma, the potential role of indoor/outdoor air pollutants in the induction of asthma), and biologics in the induction of asthma. Susceptibility is a key concept in the U.S. EPA "Asthma Research Strategy" document and is associated with the U.S. EPA framework of protecting vulnerable populations from potentially harmful environmental exposures. Genetics, age, and lifestyle (obesity, diet) are major susceptibility factors in the induction of asthma and can interact with environmental exposures either synergistically or antagonistically. Therefore, in this fourth and last article we consider a number of "susceptibility factors" that potentially influence the asthmatic response to environmental exposures and propose a framework for developing research hypotheses regarding the effects of environmental exposures on asthma incidence and induction.

Asthma↗

PubMed1999

[Difficulties of the methods for studying environmental exposure and neural tube defects].

OBJECTIVE: To discuss the attitudes in the assessment of environmental exposures as risk factors associated with neural tube defects, and to present the main risk factors studied to date. RESULTS: Environmental exposures have been suggested to have a roll in the genesis of birth defects. However, studies conducted in human populations have found difficulties in the design and conduction to show such an association for neural tube defects (anencephaly, espina bifida and encephalocele) because of problems raised from: a) the frequency measures used to compare time trends and communities, b) the classification of heterogeneous malformations, c) the inclusion of maternal, paternal and fetal factors as an integrated process and, d) the assessment of environmental exposures. CONCLUSIONS: Hypothetically both maternal and paternal environmental exposures can produce damage before and after conception by direct action on the embryo and the fetus-placenta complex. Therefore, in the assessment of environmental exposures we need to take into account: a) both paternal and maternal exposures; b) the critical exposure period, three months before conception for paternal exposures and one month around the conceptional period for maternal exposures; c) quantitatively evaluate environmental exposures when possible, avoiding a dichotomous classification; d) the use of biological markers of exposure is highly recommended as well as markers of genetic susceptibility.

Environmental Exposure↗

PubMed2005

Are separate standards for occupational and environmental exposures good public health policy?

Occupational and environmental exposures are treated as distinct entities for the purpose of public health protection. Yet workers and community members may experience the same exposures simultaneously or within a very narrow time frame. Agricultural chemicals applied by workers in the field drift into residential communities. Chemicals may be carried from a work site, with or without physical boundaries, into the home and delivered to household members. Meteorological conditions transport agricultural chemicals or stored ashes to residential communities during and after the work day. Occupational standards generally allow a higher level of exposure to workers than environmental standards allow for community exposures. For some chemicals, standards exist for only one exposure group, thus leaving the other exposed group without protection. The distinction between occupational and environmental exposures assumes the identification of specific human activities as work or non-work. However, not all human activity falls clearly into one specific category. The strict separation of occupational and environmental exposures therefore renders public health protection of all exposed people difficult to achieve. An in-depth discussion about the factors and assumptions that are used when occupational and environmental standards are separately applied to exposed populations is needed to enhance the public health of all people.

Journal Article↗

PubMedDate not supplied

Measurement of benzene in human breath associated with an environmental exposure.

The concentration of benzene in breath was measured after exposure to environmental benzene. Five volunteers were exposed to environmental tobacco smoke at different exposure levels and for different exposure durations. The breath samples were collected before, during, and postexposure for up to three hours. Benzene in breath was confirmed as a short-term biomarker of environmental benzene exposure at the sub-ppm level. Less than 10% of the inhaled benzene was expired within three hours following two-hour inhalation exposures, with a greater percentage expired following shorter exposures. An average of 64% percent of the inhaled benzene was absorbed through the lung barrier, with the percentage absorbed decreasing with continued exposure. Benzene biological half-lives of 7.6 and 68 minutes were calculated empirically using a two-compartment model based on the exponential benzene decay curve after correcting the breath concentrations for background breath concentrations. The breath concentration calculated at the end of the exposure by extrapolation of the postexposure breath samples demonstrates a discontinuity with the breath concentration collected during exposure, consistent with equilibrium exchange between blood and breath.

Adult↗