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Biomedical subjects

L R Goldman

Publications and source records attributed to L R Goldman.

At least 19 recordsLinked to original sources
PubMed2001

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.

Adenylyl Cyclases↗
PubMed2000

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.

Adolescent↗
PubMed2000

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.

Child↗
PubMed1998

Lead regulation.

Explore the source record for details and available documents.

Child↗
PubMed1998

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.

Child↗
PubMed1998

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.

Age Factors↗
PubMed1996

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.

Adult↗
PubMed1995

Lead levels in the household environment of children in three high-risk communities in California.

To assess environmental lead contamination in the household environment of children in high-risk areas of California, three urban locations were surveyed by the California Department of Health Services. Plant, soil, and dust lead levels were measured and a questionnaire was administered. This survey estimates that 3 million homes in California (27%) may have exterior paint lead levels > or = 5000 ppm, and 1.3 million homes (12%) may have interior paint lead levels > or = 5000 ppm. The highest concentrations of lead in paint were found on exterior surfaces and, for homes built between 1920 and 1959, on trim. Age of housing was the best predictor of lead in soil and dust; homes built before 1920 were 10 times more likely to have soil lead levels > or = 500 ppm compared to post-1950 homes. Most of the variability in dust lead levels could not be explained by factors measured in this survey. Sources of lead in the home were more highly correlated with lead dust concentration levels than they were with lead dust loading levels. Households with members reporting a lead job were twice as likely to have high dust lead levels compared to households with no one reporting a lead job. The significant differences in dust lead concentration levels between communities were not reflected in differences in dust lead loading levels. Measuring dust lead loading levels does not appear to be a meaningful sampling method for risk assessment in the context of prioritizing abatement.

California↗
PubMed1995

Banking of human tissue for biomonitoring and exposure assessment: utility for environmental epidemiology and surveillance.

Human tissue banking could provide a tool to address a number of public health concerns. We can potentially use it to monitor trends in human exposures, serve as an early warning system for new environmental exposures, assess low-level exposures around hazardous waste and other point sources of pollutants, evaluate the effectiveness of regulatory programs, and study etiologies of diseases (e.g., childhood cancer and birth defects) that are likely to be related to the environment. This article discusses opportunities to establish human tissue banks in connection with pre-existing public health surveillance programs for cancer and adverse reproductive outcomes. This is a cost-effective way to conduct surveillance and enhances the ability to carry out epidemiologic studies. The article also discusses ethical issues that are particularly important for public health practice. One is the issue of risk communication and the need to explain risks in a way that provides people with the information they need to determine appropriate action on the individual and community levels. Second is the issue of environmental justice. We recommend early involvement of communities that are likely to be involved in tissue-banking projects and full explanation of individual and group social risks from their participation.

Cluster Analysis↗
PubMed1995

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.

Adult↗
PubMed1993

Reduced severity of eosinophilia-myalgia syndrome associated with the consumption of vitamin-containing supplements before illness.

OBJECTIVE: To determine if the severity of subacute symptoms in eosinophilia-myalgia syndrome (EMS) was affected by medical history or use of nutritional supplements other than tryptophan before illness. DESIGN AND STUDY POPULATION: A case-control study was conducted of EMS cases systematically sampled from all those reported to a statewide surveillance system in California in 1989. Excluding two previous EMS-related deaths, interviews were completed in 73% (57/78) of the eligible case patients sampled. MAIN OUTCOME MEASURES: The severity of any myalgia(s), dyspnea, or walking impairment during each of the first 3 months of EMS was quantified by means of self-reported integer scores ranging from 0 (asymptomatic) to 10 (severe symptoms). Case patients in the top tercile of combined, unweighted monthly scores were defined as having severe symptoms. RESULTS: All interviewees (57 of 57) had consumed supplemental tryptophan before illness; 89% (51/57) were female. The odds of severe symptoms were not significantly associated with gender, age, previous antidepressant use, or cumulative amounts of supplemental tryptophan consumed before or after EMS onset (P > .1). Previous consumption of any multivitamin(s), however, was associated with significantly lower odds of severe symptoms (adjusted odds ratio, 0.05; 95% confidence limits, 0.007, 0.4; P = .006). CONCLUSIONS: The consumption of multivitamin-containing supplements before EMS appears to have modified the severity of subacute symptoms in this sample of cases from California.

Adult↗
PubMed1993

Lead screening.

Explore the source record for details and available documents.

Child↗