Contents | Environmental Health Perspectives 111, 9

No evidence of dioxin cancer threshold.

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Assessing human exposure to phthalates using monoesters and their oxidized metabolites as biomarkers.

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Phthalates are a group of industrial chemicals with many commercial uses, such as solvents, additives, and plasticizers. For example, di-(2-ethylhexyl) phthalate (DEHP) is added in varying amounts to certain plastics, such as polyvinyl chloride, to increase their flexibility. In humans, phthalates are metabolized to their respective monoesters, conjugated, and eliminated. However, despite the high production and use of DEHP, we have recently found that the urinary levels of the DEHP metabolite mono-(2-ethylhexyl) phthalate (MEHP) in 2,541 persons in the United States were lower than we anticipated, especially when compared with urinary metabolite levels of other commonly used phthalates. This finding raised questions about the sensitivity of this biomarker for assessing DEHP exposure. We explored the utility of two other DEHP metabolites, mono-(2-ethyl-5-oxohexyl) phthalate (MEOHP) and mono-(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP), as additional DEHP biomarkers. These metabolites are formed by oxidative metabolism of MEHP. In urine from 62 people, both the range and the mean urinary levels of MEOHP and MEHHP were on average 4-fold higher than those of MEHP; the mean of the individual ratios of MEHHP/MEOHP, MEHHP/MEHP, and MEOHP/MEHP were 1.4, 8.2, and 5.9, respectively. These data suggest that MEOHP and MEHHP are more sensitive biomarkers of exposure to DEHP than is MEHP. These findings also suggest a predominant human metabolic route for DEHP hydrolysis to MEHP followed by oxidation of MEHP; they also imply that a similar mechanism may be relevant for other high-molecular-weight phthalates, such as di-n-octyl, di-isononyl, and di-isodecyl phthalates.

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A climate-based model predicts the spatial distribution of the Lyme disease vector Ixodes scapularis in the United States.

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Effects of the isoflavones genistein and equol on the gonadal development of Japanese medaka Oryzias latipes.

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The relationship between environmental exposures to phthalates and DNA damage in human sperm using the neutral comet assay.

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Phthalates are industrial chemicals widely used in many commercial applications. The general population is exposed to phthalates through consumer products as well as through diet and medical treatments. To determine whether environmental levels of phthalates are associated with altered DNA integrity in human sperm, we selected a population without identified sources of exposure to phthalates. One hundred sixty-eight subjects recruited from the Massachusetts General Hospital Andrology Laboratory provided a semen and a urine sample. Eight phthalate metabolites were measured in urine by using high-performance liquid chromatography and tandem mass spectrometry; data were corrected for urine dilution by adjusting for specific gravity. The neutral single-cell microgel electrophoresis assay (comet assay) was used to measure DNA integrity in sperm. VisComet image analysis software was used to measure comet extent, a measure of total comet length (micrometers); percent DNA in tail (tail%), a measure of the proportion of total DNA present in the comet tail; and tail distributed moment (TDM), an integrated measure of length and intensity (micrometers). For an interquartile range increase in specific gravity-adjusted monoethyl phthalate (MEP) level, the comet extent increased significantly by 3.6 micro m [95% confidence interval (95% CI), 0.74-6.47]; the TDM also increased 1.2 micro m (95% CI, -0.05 to 2.38) but was of borderline significance. Monobutyl, monobenzyl, monomethyl, and mono-2-ethylhexyl phthalates were not significantly associated with comet assay parameters. In conclusion, this study represents the first human data to demonstrate that urinary MEP, at environmental levels, is associated with increased DNA damage in sperm.

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On the relationship between time-series studies, dynamic population studies, and estimating loss of life due to short-term exposure to environmental risks.

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There is a growing concern that short-term exposure to combustion-related air pollution is associated with increased risk of death. This finding is based largely on time-series studies that estimate associations between daily variations in ambient air pollution concentrations and in the number of nonaccidental deaths within a community. Because these results are not based on cohort or dynamic population designs, where individuals are followed in time, it has been suggested that estimates of effect from these time-series studies cannot be used to determine the amount of life lost because of short-term exposures. We show that results from time-series studies are equivalent to estimates obtained from a dynamic population when each individual's survival experience can be summarized as the daily number of deaths. This occurs when the following conditions are satisfied: a) the environmental covariates vary in time and not between individuals; b) on any given day, the probability of death is small; c) on any given day and after adjusting for known risk factors for mortality such age, sex, smoking habits, and environmental exposures, each subject of the at-risk population has the same probability of death; d) environmental covariates have a common effect on mortality of all members of at-risk population; and e) the averages of individual risk factors, such as smoking habits, over the at-risk population vary smoothly with time. Under these conditions, the association between temporal variation in the environmental covariates and the survival experience of members of the dynamic population can be estimated by regressing the daily number of deaths on the daily value of the environmental covariates, as is done in time-series mortality studies. Issues in extrapolating risk estimates based on time-series studies in one population to estimate the amount of life lost in another population are also discussed.

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High body burdens of 2,2',4,4'-tetrabromodiphenyl ether (BDE-47) in California women.

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Bisphenol A is released from used polycarbonate animal cages into water at room temperature.

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Bisphenol A (BPA) is a monomer with estrogenic activity that is used in the production of food packaging, dental sealants, polycarbonate plastic, and many other products. The monomer has previously been reported to hydrolyze and leach from these products under high heat and alkaline conditions, and the amount of leaching increases as a function of use. We examined whether new and used polycarbonate animal cages passively release bioactive levels of BPA into water at room temperature and neutral pH. Purified water was incubated at room temperature in new polycarbonate and polysulfone cages and used (discolored) polycarbonate cages, as well as control (glass and used polypropylene) containers. The resulting water samples were characterized with gas chromatography/mass spectrometry (GC/MS) and tested for estrogenic activity using an MCF-7 human breast cancer cell proliferation assay. Significant estrogenic activity, identifiable as BPA by GC/MS (up to 310 micro g/L), was released from used polycarbonate animal cages. Detectable levels of BPA were released from new polycarbonate cages (up to 0.3 micro g/L) as well as new polysulfone cages (1.5 micro g/L), whereas no BPA was detected in water incubated in glass and used polypropylene cages. Finally, BPA exposure as a result of being housed in used polycarbonate cages produced a 16% increase in uterine weight in prepubertal female mice relative to females housed in used polypropylene cages, although the difference was not statistically significant. Our findings suggest that laboratory animals maintained in polycarbonate and polysulfone cages are exposed to BPA via leaching, with exposure reaching the highest levels in old cages.

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The temporal pattern of respiratory and heart disease mortality in response to air pollution.

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Arsenic groundwater contamination in Middle Ganga Plain, Bihar, India: a future danger?

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The pandemic of arsenic poisoning due to contaminated groundwater in West Bengal, India, and all of Bangladesh has been thought to be limited to the Ganges Delta (the Lower Ganga Plain), despite early survey reports of arsenic contamination in groundwater in the Union Territory of Chandigarh and its surroundings in the northwestern Upper Ganga Plain and recent findings in the Terai area of Nepal. Anecdotal reports of arsenical skin lesions in villagers led us to evaluate arsenic exposure and sequelae in the Semria Ojha Patti village in the Middle Ganga Plain, Bihar, where tube wells replaced dug wells about 20 years ago. Analyses of the arsenic content of 206 tube wells (95% of the total) showed that 56.8% exceeded arsenic concentrations of 50 micro g/L, with 19.9% > 300 micro g/L, the concentration predicting overt arsenical skin lesions. On medical examination of a self-selected sample of 550 (390 adults and 160 children), 13% of the adults and 6.3% of the children had typical skin lesions, an unusually high involvement for children, except in extreme exposures combined with malnutrition. The urine, hair, and nail concentrations of arsenic correlated significantly (r = 0.72-0.77) with drinking water arsenic concentrations up to 1,654 micro g/L. On neurologic examination, arsenic-typical neuropathy was diagnosed in 63% of the adults, a prevalence previously seen only in severe, subacute exposures. We also observed an apparent increase in fetal loss and premature delivery in the women with the highest concentrations of arsenic in their drinking water. The possibility of contaminated groundwater at other sites in the Middle and Upper Ganga Plain merits investigation.

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Skin as a route of exposure and sensitization in chronic beryllium disease.

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Chronic beryllium disease is an occupational lung disease that begins as a cell-mediated immune response to beryllium. Although respiratory and engineering controls have significantly decreased occupational beryllium exposures over the last decade, the rate of beryllium sensitization has not declined. We hypothesized that skin exposure to beryllium particles would provide an alternative route for sensitization to this metal. We employed optical scanning laser confocal microscopy and size-selected fluorospheres to demonstrate that 0.5- and 1.0- micro m particles, in conjunction with motion, as at the wrist, penetrate the stratum corneum of human skin and reach the epidermis and, occasionally, the dermis. The cutaneous immune response to chemical sensitizers is initiated in the skin, matures in the local lymph node (LN), and releases hapten-specific T cells into the peripheral blood. Topical application of beryllium to C3H mice generated beryllium-specific sensitization that was documented by peripheral blood and LN beryllium lymphocyte proliferation tests (BeLPT) and by changes in LN T-cell activation markers, increased expression of CD44, and decreased CD62L. In a sensitization-challenge treatment paradigm, epicutaneous beryllium increased murine ear thickness following chemical challenge. These data are consistent with development of a hapten-specific, cell-mediated immune response following topical application of beryllium and suggest a mechanistic link between the persistent rate of beryllium worker sensitization and skin exposure to fine and ultrafine beryllium particles.

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Toxicologic and epidemiologic clues from the characterization of the 1952 London smog fine particulate matter in archival autopsy lung tissues.

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Exposure to atmospheric fine particulate matter (PM), even at low ambient concentrations, has clearly been linked to increases in mortality and morbidity. A 10- micro g m(-3) increase in PM10 (PM < 10 micro m) has been found to produce a 0.5% increase in daily mortality. The mechanism of action is a source of debate, although recent attention has focused on the cardiac effects of PM exposures. Likewise, several possible etiologic agents have been implicated, including ultrafine PM (PM <or= 100 nm), metals, and the acid components, yet the responsible constituent remains undetermined. During the catastrophic PM exposure episode in London in December 1952, some 4,000 excess deaths occurred at the height of the event. The extreme mortality during that episode and the preservation of archival autopsy tissues allow us the unique opportunity to report on the form and composition of December 1952 London PM in situ in tissues from persons known to have died from the smog exposure. Because absolute increases in mortality with current levels of PM in Western Europe and North America are low, analogous tissues are unlikely to be contemporaneously available. Taking a lung compartment (airway, airspace, interstitium, and lymph node) approach, we differentiated exposures contemporary with death from those of earlier origin. Electron microscopic analyses revealed the dominance of retained soot and a surfeit of other particle types. A variety of metal-bearing particle types were found in all compartments, but Pb, Zn, and SnZn types appeared the least biopersistent. The results support the acute toxicologic importance of ultrafine carbonaceous and metal PM.

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Inhalation exposure of rats to asphalt fumes generated at paving temperatures alters pulmonary xenobiotic metabolism pathways without lung injury.

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Asphalt fumes are complex mixtures of various organic compounds, including polycyclic aromatic hydrocarbons (PAHs). PAHs require bioactivation by the cytochrome P-450 monooxygenase system to exert toxic/carcinogenic effects. The present study was carried out to characterize the acute pulmonary inflammatory responses and the alterations of pulmonary xenobiotic pathways in rats exposed to asphalt fumes by inhalation. Rats were exposed at various doses and time periods to air or to asphalt fumes generated at paving temperatures. To assess the acute damage and inflammatory responses, differential cell counts, acellular lactate dehydrogenase (LDH) activity, and protein content of bronchoalveolar lavage fluid were determined. Alveolar macrophage (AM) function was assessed by monitoring generation of chemiluminescence and production of tumor necrosis factor-alpha and interleukin-1. Alteration of pulmonary xenobiotic pathways was determined by monitoring the protein levels and activities of P-450 isozymes (CYP1A1 and CYP2B1), glutathioneS-transferase (GST), and NADPH:quinone oxidoreductase (QR). The results show that acute asphalt fume exposure did not cause neutrophil infiltration, alter LDH activity or protein content, or affect AM function, suggesting that short-term asphalt fume exposure did not induce acute lung damage or inflammation. However, acute asphalt fume exposure significantly increased the activity and protein level of CYP1A1 whereas it markedly reduced the activity and protein level of CYP2B1 in the lung. The induction of CYP1A1 was localized in nonciliated bronchiolar epithelial (Clara) cells, alveolar septa, and endothelial cells by immunofluorescence microscopy. Cytosolic QR activity was significantly elevated after asphalt fume exposure, whereas GST activity was not affected by the exposure. This induction of CYP1A1 and QR with the concomitant down-regulation of CYP2B1 after asphalt fume exposure could alter PAH metabolism and may lead to potential toxic effects in the lung.

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Distribution of methyl sulfone metabolites of polychlorinated biphenyls and p,p'-DDE in human tissues.

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A study of urban housing demolitions as sources of lead in ambient dust: demolition practices and exterior dust fall.

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Demolition of older housing for urban redevelopment purposes benefits communities by removing housing with lead paint and dust hazards and by creating spaces for lead paint-free housing and other community resources. This study was conducted to assess changes, if any, in ambient dust lead levels associated with demolition of blocks of older lead-containing row houses in Baltimore, Maryland (USA). In this article we present results based on dust-fall samples collected from fixed locations within 10 m of three demolition sites. In subsequent reports we will describe dust lead changes on streets, sidewalks, and residential floors within 100 m of the demolition sites. Geometric mean (GM) lead dust-fall rate increased by > 40-fold during demolition to 410 micro g Pb/m2/hr (2,700 micro g Pb/m2 per typical work day) and by > 6-fold during debris removal to 61 micro g Pb/m2/hr (440 micro g Pb/m2 per typical work day). Lead concentrations in dust fall also increased during demolition (GM, 2,600 mg/kg) and debris removal (GM, 1,500 mg/kg) compared with baseline (GM, 950 mg/kg). In the absence of dust-fall standards, the results were compared with the U.S. Environmental Protection Agency's (U.S. EPA's) dust-lead surface loading standard for interior residential floors (40 micro g/ft2, equivalent to 431 micro g/m2); daily lead dust fall during demolition exceeded the U.S. EPA floor standard by 6-fold on average and as much as 81-fold on an individual sample basis. Dust fall is of public health concern because it settles on surfaces and becomes a pathway of ambient lead exposure and a potential pathway of residential exposure via tracking and blowing of exterior dust. The findings highlight the need to minimize demolition lead deposition and to educate urban planners, contractors, health agencies, and the public about lead and other community concerns so that society can maximize the benefits of future demolition activities nationwide.

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Human prenatal and postnatal exposure to polybrominated diphenyl ethers, polychlorinated biphenyls, polychlorobiphenylols, and pentachlorophenol.

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The work environment and workers' health in four large office buildings.

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We conducted a 1-year epidemiologic study in Boston, Massachusetts, beginning May 1997, to examine the associations between environmental factors and office workers' health. We recruited 98 subjects (81 females and 17 males) in 21 offices in four office buildings. We conducted environmental sampling every 6 weeks and concurrently administered detailed questionnaires to collect information on work-related symptoms, psychosocial factors, and perceptions of the office environments. In multivariate analyses, eye irritation was positively correlated with floor dust [odds ratio (OR) = 1.46; 95% confidence intervals (CI), 1.14-1.86] and reported lack of office cleanliness (OR = 1.52; 95% CI, 1.11-2.08). Nonspecific symptoms were positively associated with unidentified chair fungi (OR = 1.87; 95% CI, 1.11-3.15) and several self-reported conditions, including a history of asthma (OR = 3.15; 95% CI, 1.26-7.87), more people in offices (OR = 1.71; 95% CI, 1.16-2.51), lack of office cleanliness (OR = 2.85; 95% CI, 1.72-4.73), and low job satisfaction (OR = 1.72; 95% CI, 1.06-2.81). Upper respiratory symptoms were positively associated with total fungal concentrations recovered from chair dust (OR = 1.35; 95% CI, 1.07-1.70) and the following self-reported conditions: more people in offices (OR = 1.45; 95% CI, 1.01-2.08), lack of office cleanliness (OR = 1.62; 95% CI, 1.15-2.30), and jobs frequently requiring hard work (OR = 1.43; 95% CI, 1.05-1.95). This study emphasizes the importance of maintaining a clean, uncrowded workspace and the importance of chair fungi as a correlate for health effects.

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Polybrominated diphenyl ethers in maternal and fetal blood samples.

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Polybrominated diphenyl ethers (PBDEs) are widely used as flame retardants in consumer goods, such as plastics, electronics, textiles, and construction material. PBDEs have been found in human milk, fat, and blood samples. Rodent studies indicate that PBDEs may be detrimental to neurodevelopment, possibly by lowering thyroid hormone concentrations in blood. In the present study, we determined concentrations of PBDEs and thyroid hormones in human fetal and maternal serum. Patients presenting in labor to Indiana University and Wishard Memorial County hospitals in Indianapolis, who were older than 18 years, were recruited to participate. Twelve paired samples of maternal and cord blood were obtained and analyzed using gas chromatographic mass spectrometry; thyroid hormone concentrations were determined by radioimmunoassay. Six congeners of PBDE were measured in maternal and fetal serum samples. The concentrations of total PBDEs found in maternal sera ranged from 15 to 580 ng/g lipid, and the concentrations found in fetal samples ranged from 14 to 460 ng/g lipid. Individual fetal blood concentrations did not differ from the corresponding maternal concentrations, indicating that measurement of maternal PBDE blood levels is useful in predicting fetal exposure; similarly, other reports have shown a high correlation between PBDE in mother's milk and fetal exposure. In accord with reports on other biologic samples, the tetrabrominated PBDE congener BDE-47 accounted for 53-64% of total PBDEs in the serum. The concentrations of PBDEs found in maternal and fetal serum samples were 20-106-fold higher than the levels reported previously in a similar population of Swedish mothers and infants. In this small sample, there was no apparent correlation between serum PBDEs and thyroid hormone concentrations. Our study shows that human fetuses in the United States may be exposed to relatively high levels of PBDEs. Further investigation is required to determine if these levels are specific to central Indiana and to assess the toxic potential of these exposure levels.

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Assessment of pre- and postnatal exposure to polychlorinated biphenyls: lessons from the Inuit Cohort Study.

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Polychlorinated biphenyls (PCBs) are food-chain contaminants that have been shown to induce adverse developmental effects in humans. In the course of an epidemiologic study established to investigate neurodevelopmental deficits induced by environmental PCB exposure in the Inuit population of northern Québec (Nunavik, Canada), we compared three biomarkers of prenatal exposure and models to predict PCB plasma concentration at 6 months postpartum. Concentrations of 14 PCB congeners were measured by high-resolution gas chromatography with electron capture detection in lipids extracted from maternal plasma, cord plasma, breast milk (collected at approximately 1 month postpartum), and 6-month-old infant plasma samples. Similar congener profiles were observed in all biologic samples, and PCB-153, the most abundant and persistent PCB congener, was strongly correlated with other frequently detected PCB congeners in all biologic media. When expressed on a lipid basis, maternal plasma, cord plasma, and milk concentrations of this congener were strongly intercorrelated, indicating that PCB concentration in any of these biologic media is a good indicator of prenatal exposure to PCBs. A multivariate model that included maternal PCB-153 plasma lipid concentration, breast-feeding duration, and the sum of two skin-fold thicknesses (an index of infant body fat mass) explained 72% of PCB-153 plasma concentration variance at 6 months postpartum (p < 0.001). By contrast, based on the product of breast-feeding duration times the concentration of PCBs in plasma lipids, which was used as an index of postnatal PCB exposure in several studies, only 36% of infant plasma concentration was explained.

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Birth malformations and other adverse perinatal outcomes in four U.S. Wheat-producing states.

Dina M Schreinemachers

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Chlorophenoxy herbicides are widely used in the United States and Western Europe for broadleaf weed control in grain farming and park maintenance. Most of the spring and durum wheat produced in the United States is grown in Minnesota, Montana, North Dakota, and South Dakota, with more than 85% of the acreage treated with chlorophenoxy herbicides such as 2,4-dichlorophenoxyacetic acid (2,4-D) and 4-chloro-2-methylphenoxyacetic acid (MCPA). Rates of adverse birth outcomes in rural, agricultural counties of these states during 1995-1997 were studied by comparing counties with a high proportion of wheat acreage and those with a lower proportion. Information routinely collected and made available by federal agencies was used for this ecologic study. Significant increases in birth malformations were observed for the circulatory/respiratory category for combined sexes [odds ratio (OR) = 1.65; 95% confidence interval (CI), 1.07-2.55]. A stronger effect was observed for the subcategory, which excluded heart malformations (OR = 2.03; 95% CI, 1.14-3.59). In addition, infants conceived during April-June--the time of herbicide application--had an increased chance of being diagnosed with circulatory/respiratory (excluding heart) malformations compared with births conceived during other months of the year (OR = 1.75; 95% CI, 1.09-2.80). Musculoskeletal/integumental anomalies increased for combined sexes in the high-wheat counties (OR = 1.50; 95% CI, 1.06-2.12). Infant death from congenital anomalies significantly increased in high-wheat counties for males (OR = 2.66; 95% CI, 1.52-4.65) but not for females (OR = 0.48; 95% CI, 0.20-1.15). These results are especially of concern because of widespread use of chlorophenoxy herbicides.

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Particle concentrations in inner-city homes of children with asthma: the effect of smoking, cooking, and outdoor pollution.

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Inner-city children have high rates of asthma. Exposures to particles, including allergens, may cause or exacerbate asthma symptoms. As part of an epidemiologic study of inner-city children with asthma, continuous (10-min average) measurements of particle concentrations were made for 2-week periods in 294 homes drawn from seven cities. Measurements were made using an optical scattering device that is most sensitive to fine particles. The concentrations recorded by these devices were corrected to agree with colocated outdoor gravimetric PM2.5 monitors. Indoor concentrations in the homes averaged 27.7 (standard deviation = 35.9) micro g/m3, compared with concurrent outdoor concentrations of 13.6 (7.5) micro g/m3. A multivariate model indicated that outdoor particles penetrated indoors with an efficiency of 0.48 and were therefore responsible for only 25% of the mean indoor concentration. The major indoor source was smoking, which elevated indoor concentrations by 37 micro g/m3 in the 101 homes with smokers. Other significant sources included frying, smoky cooking events, use of incense, and apartment housing, although the increases due to these events ranged only from 3 to 6 micro g/m3. The 10-min averaging time allowed calculation of an average diurnal variation, showing large increases in the evening due to smoking and smaller increases at meal times due to cooking. Most of the observed variance in indoor concentrations was day to day, with roughly similar contributions to the variance from visit to visit and home to home within a city and only a small contribution made by variance among cities. The small variation among cities and the similarity across cities of the observed indoor air particle distributions suggest that sources of indoor concentrations do not vary considerably from one city to the next, and thus that simple models can predict indoor air concentrations in cities having only outdoor measurements.

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Environmental health in developing countries: an overview of the problems and capacities.

Hiremagalur N B Gopalan

Table of Contents

Research Article

No evidence of dioxin cancer threshold.

Abstract

Assessing human exposure to phthalates using monoesters and their oxidized metabolites as biomarkers.

Abstract

A climate-based model predicts the spatial distribution of the Lyme disease vector Ixodes scapularis in the United States.

Abstract

Effects of the isoflavones genistein and equol on the gonadal development of Japanese medaka Oryzias latipes.

Abstract

The relationship between environmental exposures to phthalates and DNA damage in human sperm using the neutral comet assay.

Abstract

On the relationship between time-series studies, dynamic population studies, and estimating loss of life due to short-term exposure to environmental risks.

Abstract

High body burdens of 2,2',4,4'-tetrabromodiphenyl ether (BDE-47) in California women.

Abstract

Bisphenol A is released from used polycarbonate animal cages into water at room temperature.

Abstract

The temporal pattern of respiratory and heart disease mortality in response to air pollution.

Abstract

Arsenic groundwater contamination in Middle Ganga Plain, Bihar, India: a future danger?

Abstract

Skin as a route of exposure and sensitization in chronic beryllium disease.

Abstract

Toxicologic and epidemiologic clues from the characterization of the 1952 London smog fine particulate matter in archival autopsy lung tissues.

Abstract

Inhalation exposure of rats to asphalt fumes generated at paving temperatures alters pulmonary xenobiotic metabolism pathways without lung injury.

Abstract

Distribution of methyl sulfone metabolites of polychlorinated biphenyls and p,p'-DDE in human tissues.

Abstract

A study of urban housing demolitions as sources of lead in ambient dust: demolition practices and exterior dust fall.

Abstract

Human prenatal and postnatal exposure to polybrominated diphenyl ethers, polychlorinated biphenyls, polychlorobiphenylols, and pentachlorophenol.

Abstract

The work environment and workers' health in four large office buildings.

Abstract

Polybrominated diphenyl ethers in maternal and fetal blood samples.

Abstract

Assessment of pre- and postnatal exposure to polychlorinated biphenyls: lessons from the Inuit Cohort Study.

Abstract

Birth malformations and other adverse perinatal outcomes in four U.S. Wheat-producing states.

Abstract

Particle concentrations in inner-city homes of children with asthma: the effect of smoking, cooking, and outdoor pollution.

Abstract

Environmental health in developing countries: an overview of the problems and capacities.

Letter

Herbicide effects on embryo implantation and litter size.

Reported seasonal dependence of herbicide developmental toxicity in mice.

Asthma and Gulf War exposures.

Correspondence

Asthma and Gulf War Exposures: Response

Communication in Emergencies: Response

Letter

Communication in emergencies.

Article

Corrections

Research Article

WHO names top 10 health risks.

New paint: no harm, no foul?

MODIS operandi for mapping haze.

Building self-reliance in environmental science: the ITREOH experience.

The capacity to change: building global environmental health expertise.

Environmental triage in Afghanistan.

Connecting to a sustainable future.

Article

Suspect inheritance: potential neurotoxicants passed to fetuses.

Research Article

Concentrating on PBDEs: chemical levels rise in women.

Heavy on the metals: parsing the particulate content of the London smog.

Article

Extramural Update July 2003

Book Review

Precaution Environmental Science and Preventive Public Policy

Article

Science Selections August 2003

Extramural Update August 2003

Fellowships Grants and Awards August 2003

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