Association of selenium and copper with lipids in umbilical cord blood.

Altered levels of selenium and copper have been linked with altered cardiovascular disease risk factors including changes in blood triglyceride and cholesterol levels. However, it is unclear whether this can be observed prenatally. This cross-sectional study includes 274 singleton births from 2004 to 2005 in Baltimore, Maryland. We measured umbilical cord serum selenium and copper using inductively coupled plasma mass spectrometry. We evaluated exposure levels vis-à-vis umbilical cord serum triglyceride and total cholesterol concentrations in multivariable regression models adjusted for gestational age, birth weight, maternal age, race, parity, smoking, prepregnancy body mass index, n-3 fatty acids and methyl mercury. The percent difference in triglycerides comparing those in the highest v. lowest quartile of selenium was 22.3% (95% confidence interval (CI): 7.1, 39.7). For copper this was 43.8% (95% CI: 25.9, 64.3). In multivariable models including both copper and selenium as covariates, copper, but not selenium, maintained a statistically significant association with increased triglycerides (percent difference: 40.7%, 95% CI: 22.1, 62.1). There was limited evidence of a relationship of increasing selenium with increasing total cholesterol. Our findings provide evidence that higher serum copper levels are associated with higher serum triglycerides in newborns, but should be confirmed in larger studies.

The clinical presentation of environmental health problems and the role of the pediatric provider. What do I do when I see children who might have an environmentally related illness?

The practice of environmental health is concerned with the protection of the community. There are a number of tools used for assessment of environmental hazards, but environmental health is most reliant on the use of risk assessment. Risk assessment is a set of tools used to assess hazards on a community level, based on human studies, ecological studies, or toxicity testing of animals.

Iron deficiency associated with higher blood lead in children living in contaminated environments.

The evidence that iron deficiency increases lead child exposure is based primarily on animal data and limited human studies, and some of this evidence is contradictory. No studies of iron status and blood lead levels in children have accounted for environmental lead contamination and, therefore, the source of their exposure. Thus, no studies have directly determined whether iron deficiency modifies the relationship of environmental lead and blood lead. In this study, we compared blood lead levels of iron-deficient and iron-replete children living in low, medium, or highly contaminated environments. Measurements of lead in paint, soil, dust, and blood, age of housing, and iron status were collected from 319 children ages 1-5. We developed two lead exposure factors to summarize the correlated exposure variables: Factor 1 summarized all environmental measures, and Factor 2 was weighted for lead loading of house dust. The geometric mean blood lead level was 4.9 microg/dL; 14% exceeded 10 microg/dL. Many of the children were iron deficient (24% with ferritin < 12 ng/dL). Seventeen percent of soil leads exceeded 500 microg/g, and 23% and 63% of interior and exterior paint samples exceeded 5,000 microg/g. The unadjusted geometric mean blood lead level for iron-deficient children was higher by 1 microg/dL; this difference was greater (1.8 microg/dL) after excluding Asians. Blood lead levels were higher for iron-deficient children for each tertile of exposure as estimated by Factors 1 and 2 for non-Asian children. Elevated blood lead among iron-deficient children persisted after adjusting for potential confounders by multivariate regression; the largest difference in blood lead levels between iron-deficient and -replete children, approximately 3 microg/dL, was among those living in the most contaminated environments. Asian children had a paradoxical association of sufficient iron status and higher blood lead level, which warrants further investigation. Improving iron status, along with reducing exposures, may help reduce blood lead levels among most children, especially those living in the most contaminated environments.

Technical report: mercury in the environment: implications for pediatricians.

Mercury is a ubiquitous environmental toxin that causes a wide range of adverse health effects in humans. Three forms of mercury (elemental, inorganic, and organic) exist, and each has its own profile of toxicity. Exposure to mercury typically occurs by inhalation or ingestion. Readily absorbed after its inhalation, mercury can be an indoor air pollutant, for example, after spills of elemental mercury in the home; however, industry emissions with resulting ambient air pollution remain the most important source of inhaled mercury. Because fresh-water and ocean fish may contain large amounts of mercury, children and pregnant women can have significant exposure if they consume excessive amounts of fish. The developing fetus and young children are thought to be disproportionately affected by mercury exposure, because many aspects of development, particularly brain maturation, can be disturbed by the presence of mercury. Minimizing mercury exposure is, therefore, essential to optimal child health. This review provides pediatricians with current information on mercury, including environmental sources, toxicity, and treatment and prevention of mercury exposure.

GH mRNA levels are elevated by forskolin but not GH releasing hormone in GHRH receptor-expressing MtT/S somatotroph cell line.

The MtT/S somatotroph cell line should be a growth hormone-releasing hormone (GHRH)-responsive model system for the study of physiological control of growth hormone (GH) transcription because GH secretion from these cells is stimulated by GHRH. To examine the GH transcriptional activity of these cells, endogenous GH mRNA levels were measured using a ribonuclease protection assay following treatment under a variety of hormonal conditions. While omission of serum led to reduction of GH mRNA to 22% of control levels by 2 days and to 8% by 5 days (P<0.05 for both), GH mRNA levels were maintained at control values in serum-free medium containing 5 nM dexamethasone and 30 pM triiodothyronine (TDM). However, the addition of 10 nM GHRH under any treatment condition did not significantly alter GH mRNA levels. Characterization of the MtT/S cells showed that GHRH-receptor (GHRH-R) mRNA was detectable by reverse transcription-polymerase chain reaction (RT-PCR) amplification. Measurement of extracellular cAMP showed that the MtT/S cells have basal levels of > or =20 nmol/10(6) cells per h in both serum-containing and serum-free media, and that GHRH had no effect on cAMP levels, suggesting constitutive activation. To rule out the possibility of autocrine stimulation by GHRH produced endogenously, GHRH mRNA was not detectable in MtT/S cells using RT-PCR amplification. The stimulatory G-protein alpha subunit, mutations of which are known to activate adenylate cyclase constitutively in acromegaly, was sequenced but found not to differ from normal pituitary in the regions most commonly mutated. Finally, treatment with 10 microM forskolin, to directly activate adenylate cyclase, increased GH mRNA to 140% of controls in TDM, and to 163% in serum-free medium after 2 days, and to 166% in TDM-treated cells and 174% in serum-free culture after 5 days (all P<0.05). Taken together, these data indicate that although MtT/S cells express the GHRH-R, GHRH cannot stimulate adenylate cyclase to increase GH transcription due to constitutive elevation of cAMP levels, by a means that may be similar to that in cases of acromegaly not caused by oncogenic gsp mutations.

Chemicals in the environment and developmental toxicity to children: a public health and policy perspective.

There are numerous pesticides and toxic chemicals in the environment that have yet to be evaluated for potential to cause developmental neurotoxicity. Recent legislation and testing initiatives provide an impetus to generating more information about potential hazards to children. In the United States, the 1996 Food Quality Protection Act (FQPA) required the U.S. Environmental Protection Agency (U.S. EPA) to make a finding that a pesticide food use is safe for children. In addition, the law requires U.S. EPA to incorporate an additional 10-fold factor in risk assessments for pesticide residue tolerances to take into account the special sensitivities of infants and children as well as incomplete data with respect to toxicity and exposures. The potential of chemicals in food and drinking water to cause endocrine disruption will also be examined via the Endocrine Disruptor Screening and Testing Program required by the FQPA and the 1996 Safe Drinking Water Act. In addition, a new voluntary chemical information program will provide screening-level information for the some 2,800 high-volume chemicals in commerce in the United States. These initiatives will need to be accompanied by research focused on developmental toxicity for children, including developmental disabilities. Developmental disabilities exact a large toll on children's health in the United States. Three major developmental disabilities--autism, cerebral palsy, and severe mental retardation--each affect substantial numbers of children. We know very little about the etiology of these conditions. A number of priority areas for research are suggested, including a large environmental prospective study of developmental neurotoxicity.

Serum polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans among people eating contaminated home-produced eggs and beef.

We compared serum polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) among residents of two homes to levels among age- and sex-matched comparison subjects. The residents of the two homes consumed contaminated eggs and beef from animals raised at the homes. The animals had greater soil contact than those raised with conventional commercial husbandry practices. The comparison subjects were from a similar rural area, but did not consume home-produced beef and eggs. Serum levels of 2,3,7, 8-substituted tetra-, penta-, and hexaCDDs and penta-, hexa-, and heptaCDFs were increased between 2- and 6-fold in residents from one home; contaminated eggs and beef were consumed by residents for 2-15 years. Elevations were less for those in the other index home, where only home-produced eggs were consumed for 2 years; a 3-fold elevation of 1,2,3,7,8,9-hexaCDD as compared to controls was most apparent. Very strong bivariate correlations among all of the 2,3,7, 8 penta- and hexaCDDs/CDFs were observed. The elevations observed verify that PCDD/PCDF-contaminated food contributed to the body burden of these compounds. The blood levels among the highest exposed participants are generally higher than those observed in other studies of U.S. contaminated-fish consumers and higher than average adipose tissue levels observed in U.S. urban populations. There are sufficient animal toxicologic and human epidemiologic data to recommend that exposures be reduced. In the study area, pentachlorophenol and pentachlorophenol incineration sources have been identified, and the animal contamination and blood elevations probably reflect these sources. Soil reference values and site-specific risk assessments should include estimates of exposures to contamination in home-produced animal products. Such estimates can be verified with limited PCDD/PCDF sampling of animals and humans.

Linking research and policy to ensure children's environmental health.

The U.S. Environmental Protection Agency (U.S. EPA) has made protecting children's environmental health its highest priority. Data on how and when children may be at risk are vital for accomplishing this goal. Recent examples of the link between research and policy include U.S. EPA actions to carry out the recommendations of the National Academy of Sciences on pesticides in children's food, reduce and prevent childhood lead poisoning, and revise national ambient air quality standards for ozone and particulate matter. Today, the Food Quality Protection Act (FQPA), which makes protecting children from pesticide residues in food a national priority, is contributing to the growing need for data for decision making. Further impetus comes from provisions in the FQPA and 1996 Safe Drinking Water Act Amendments for establishing a screening and testing program for potential risks from endocrine disruptors. Another factor is the analysis that will be required under President William J. Clinton's executive order directing all federal agencies, for the first time, to reduce environmental health and safety risks to children. Success of the U.S. international commitment to protect children is directly tied to the strength and availability of environmental data. To meet such challenges, the U.S. EPA is revising key science policies, expanding research opportunities, and adding to the public's right-to-know tools. In this dynamic climate, there are growing opportunities for the research community to play a greater role in helping ensure the well-being of children living today and in generations to come.

Chemicals and children's environment: what we don't know about risks.

Although we know that certain types of childhood cancers are increasing, we do not know why. With few exceptions, we know little about the role of environmental carcinogens in childhood cancer. Generally, we have adequate information to screen chemicals for potential hazard for only certain categories of chemicals--drugs, food additives, and pesticides. The U.S. Environmental Protection Agency (U.S. EPA) is implementing the 1996 Food Quality Protection Act, which provides added protections against pesticide risks, especially for children. But the situation is quite different for many industrial chemicals. We lack even basic toxicity data for a majority of the U.S. EPA's list of approximately 3000 nonpolymeric high-production-volume industrial chemicals being produced in the United States each year that are found in consumer products and the workplace. We know even less about the remaining 70,000 chemicals on the U.S. EPA inventory. The U.S. EPA has initiatives underway to address the risks posed by some of these commercial chemicals, including efforts to reduce risks posed by indoor air pollutants and household products. These initiatives specifically address children's risks. We are supporting toxicity screening of high-volume industrial chemicals on a cooperative international basis through the Organisation for Economic Co-operation and Development. Until more information is available, it is difficult to assess the possible role of these chemicals in childhood cancer and to take steps to reduce exposure to children.

New approaches for assessing the etiology and risks of developmental abnormalities from chemical exposure.

Developmental toxicants, insidious in modes of action and effects, strike the very origin of our lives: the developing embryo, fetus, neonate, and child; they cause spontaneous abortions, stillbirths, malformations, early postnatal mortality, reduced birth weight, mental retardation, sensory loss as well as other functional or physical changes, including subclinical effects having far reaching social and economic impacts. The large majority of developmental defects have unknown etiologies. With this uncertainty, EPA and the scientific community world-wide give high priority to finding new approaches for assessing etiology and risks of developmental effects. The United Nations Conference on Environment and Development (UNCED) and Agenda 21 mobilized the international community to focus on risks posed by chemicals in the environment, including developmental risks. The international harmonization of test and risk assessment guidelines for developmental effects are priorities. Lead, persistent organic pollutants (POPs), endocrine disruptors, and the improvement of quantitative risk assessment methodologies, particularly for children, are priorities. EPA reinvented its research agenda of assure wide involvement of the National Science Foundation, other federal agencies, and national experts in research to address the U.S.'s public health and environmental priorities.

Elevated symptom prevalence associated with ventilation type in office buildings.

The California Healthy Building Study was designed to assess relations between ventilation system type and office worker symptoms in a set of U.S. buildings selected without regard to worker complaints. Twelve public office buildings in northern California meeting specific eligibility criteria were studied in the summer of 1990: three naturally ventilated, three mechanically ventilated (without air conditioning), and six air-conditioned buildings. Questionnaire data were collected from 880 workers in selected spaces within the study buildings. We adjusted effect estimates for various ventilation types for personal, job, and work place factors using logistic regression, and alternatively, using a mixed effects model (SAS/GLIMMIX) to adjust for correlated responses within study spaces. Higher adjusted prevalences of most symptom outcomes were associated with both mechanical and air-conditioned ventilation, relative to natural. With a conservative adjustment for problem building status, the highest adjusted prevalence odds ratios from logistic regression models were for dry or itchy skin [mechanical: odds ratio (OR) = 6.0, 95% confidence interval (CI) = 1.6-22; air-conditioned: OR = 6.0, 95% CI = 1.7-21] and lower respiratory symptoms (mechanical: OR = 2.9, 95% CI = 0.7-11; air-conditioned: OR = 4.0, 95% CI = 1.1-15). GLIMMIX estimates were similar, with slightly wider confidence intervals. Reporting bias was small. These findings of symptom increases within mechanically ventilated and air-conditioned U.S. buildings support previous findings available only from European buildings.

The four county study of childhood cancer: clusters in context.

Observations of childhood 'cancer clusters' in small communities in central California prompted us to examine the distribution of childhood cancer in communities throughout the region to see if the overall cancer rate or the distribution of 'cancer clusters' was unusual for agricultural towns where pesticide exposure might be elevated. The distribution of rates was evaluated using a variety of methods: comparison of rates to the regional average, evaluation of the empirical observed versus expected Poisson distribution of events, and multivariate modelling using Poisson regression. These analyses suggest that there were no previously undiscovered communities with excess rates, although the index community which prompted the initial investigation does stand out as unusual. We discuss the impact of a range of forces of morbidity on the likelihood of 'cancer clusters' and the distributions of observed and expected numbers of cancers in a population of locales.

Children--unique and vulnerable. Environmental risks facing children and recommendations for response.

Children may be more susceptible to exposures to environmental toxins than adults and may be more vulnerable to their effects. Because of this, the health care community and those responsible for children need to be alert to possible environmental factors in identifying and responding to the health problems of children. Their focus should be on the causes of the health problem, emphasizing environmental sources, and not on simply treating the symptoms.