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Biomedical subjects

Steven H Lamm

Publications and source records attributed to Steven H Lamm.

16 recordsLinked to original sources
PubMed2006

Iodine supplementation for pregnancy and lactation-United States and Canada: recommendations of the American Thyroid Association.

The fetus is totally dependent in early pregnancy on maternal thyroxine for normal brain development. Adequate maternal dietary intake of iodine during pregnancy is essential for maternal thyroxine production and later for thyroid function in the fetus. If iodine insufficiency leads to inadequate production of thyroid hormones and hypothyroidism during pregnancy, then irreversible fetal brain damage can result. In the United States, the median urinary iodine (UI) was 168 microg/L in 2001-2002, well within the range of normal established by the World Health Organization (WHO), but whereas the UI of pregnant women (173 microg/L; 95% CI 75-229 microg/L) was within the range recommended by WHO (150-249 microg/L), the lower 95% CI was less than 150 microg/L. Therefore, until additional physiologic data are available to make a better judgment, the American Thyroid Association recommends that women receive 150 microg iodine supplements daily during pregnancy and lactation and that all prenatal vitamin/mineral preparations contain 150 microg of iodine.

Adolescent↗
PubMed2006

Arsenic cancer risk confounder in southwest Taiwan data set.

Quantitative analysis for the risk of human cancer from the ingestion of inorganic arsenic has been based on the reported cancer mortality experience in the blackfoot disease (BFD) -endemic area of southwest Taiwan. Linear regression analysis shows that arsenic as the sole etiologic factor accounts for only 21% of the variance in the village standardized mortality ratios for bladder and lung cancer. A previous study had reported the influence of confounders (township, BFD prevalence, and artesian well dependency) qualitatively, but they have not been introduced into a quantitative assessment. In this six-township study, only three townships (2, 4, and 6) showed a significant positive dose-response relationship with arsenic exposure. The other three townships (0, 3, and 5) demonstrated significant bladder and lung cancer risks that were independent of arsenic exposure. The data for bladder and lung cancer mortality for townships 2, 4, and 6 fit an inverse linear regression model (p < 0.001) with an estimated threshold at 151 microg/L (95% confidence interval, 42 to 229 microg/L) . Such a model is consistent with epidemiologic and toxicologic literature for bladder cancer. Exploration of the southwest Taiwan cancer mortality data set has clarified the dose-response relationship with arsenic exposure by separating out township as a confounding factor. Key words: arsenic, blackfoot disease, bladder cancer, cancer risk, confounder, dose-response relationship, southwest Taiwan, threshold model.

Arsenic↗
PubMed2004

The effect of perchlorate, thiocyanate, and nitrate on thyroid function in workers exposed to perchlorate long-term.

Perchlorate (ClO(4)(-)) and thiocyanate (SCN(-)) are potent and nitrate (NO(3)(-)) a weak competitive inhibitor of the thyroid sodium-iodide symporter. To determine the effects of long-term, high ClO(4)(-) exposure on thyroid function, we conducted a study of 29 workers employed for at least 1.7 yr (50% over 5.9 yr) in an ammonium ClO(4)(-) production plant in Utah. Serum ClO(4)(-), SCN(-), and NO(3)(-); serum T(4), free T(4) index, total T(3), thyroglobulin (Tg), and TSH; 14-h thyroid radioactive iodine uptake (RAIU); and urine iodine (I) and ClO(4)(-) were assessed after 3 d off (Pre) and during the last of three 12-h night shifts in the plant (During) and in 12 volunteers (C) not working in the plant. Serum and urine ClO(4)(-) were not detected in C; urine ClO(4)(-) was not detected in 12 of 29 and was 272 microg/liter in 17 Pre workers; serum ClO(4)(-) was not detected in 27 of 29 Pre; and serum and urine ClO(4)(-) were markedly elevated during ClO(4)(-) exposure to 868 microg/liter and 43 mg/g creatinine, respectively. Serum SCN(-) and NO(3)(-) concentrations were similar in all groups. Thyroid RAIUs were markedly decreased in During compared with Pre (13.5 vs. 21.5%; P < 0.01, paired t) and were associated with an increase in urine I excretion (230 vs. 148 microg I/g Cr; P = 0.02, paired t) but were similar to those in the C group (14.4%). Serum TSH and Tg concentrations were normal and similar in the three groups. Serum T(4) (8.3 vs. 7.7 microg/dl), free T(4) index (2.4 vs. 2.2), and total T(3) (147 vs. 134 ng/dl) were slightly but significantly increased in the During vs. Pre workers (P < 0.01, paired t). Thyroid volumes and patterns by ultrasound were similar in the 29 workers and 12 community volunteers. In conclusion, high ClO(4)(-) absorption during three nights work exposure decreased the 14-h thyroid RAIU by 38% in ClO(4)(-) production workers compared with the RAIU after 3 d off. However, serum TSH and Tg concentrations and thyroid volume by ultrasound were not affected by ClO(4)(-), suggesting that long-term, intermittent, high exposure to ClO(4)(-) does not induce hypothyroidism or goiter in adults.

Creatinine↗
PubMed2004

Arsenic in drinking water and bladder cancer mortality in the United States: an analysis based on 133 U.S. counties and 30 years of observation.

This study analyzes the relationship between arsenic exposure through drinking water and bladder cancer mortality. The county-specific white male bladder cancer mortality data (1950-1979) and county-specific groundwater arsenic concentration data were obtained for 133 U.S. counties known to be exclusively dependent on groundwater for their public drinking water supply. No arsenic-related increase in bladder cancer mortality was found over the exposure range of 3 to 60 microg/L using stratified analysis and regression analyses (both unweighted and weighted by county population and using both mean and median arsenic concentrations). These results, which provide a direct estimate of arsenic-related cancer risk for U.S. residents, exclude the National Research Council's 2001 risk estimate that was based on Southwest Taiwan data and required adjusting for differences between the body mass and water consumption rates of U.S. and Taiwanese residents.

Adult↗
PubMed2003

Bendectin and birth defects. II: Ecological analyses.

BACKGROUND: Bendectin was the primary pharmaceutical treatment of nausea and vomiting of pregnancy (NVP) in the United States until the early 1980s. Its manufacture was then discontinued after public allegations that it was causing birth defects. Subsequently, meta-analyses of the many epidemiological cohort and case/control studies used to examine that hypothesis have demonstrated the absence of a detectable teratogenic effect. This study presents an ecological analysis of the same hypothesis that examines specific malformations. METHODS: Annual birth defect prevalence data for the 1970s to the 1990s have been obtained for specific birth defects from the Center for Disease Control's nationwide Birth Defect Monitoring Program. These data for the US have been compared graphically to the annual US Bendectin sales for the treatment of NVP. Data have also been obtained for annual US rates for hospitalization for NVP. The three data sets have been temporally compared in graphic analysis. RESULTS: The temporal trends in prevalence rates for specific birth defects examined from 1970 through 1992 did not show changes that reflected the cessation of Bendectin use over the 1980-84 period. Further, the NVP hospitalization rate doubled when Bendectin use ceased. CONCLUSIONS: The population results of the ecological analyses complement the person-specific results of the epidemiological analyses in finding no evidence of a teratogenic effect from the use of Bendectin.

Abnormalities, Drug-Induced↗
PubMed2003

Lack of a relation between human neonatal thyroxine and pediatric neurobehavioral disorders.

The growth and differentiation of the central nervous system are closely related to the presence of iodine and thyroid hormones. It has been hypothesized that neurobehavioral disabilities of childhood, such as attention deficit hyperactivity disorder (ADHD), learning disorders, and autism can be attributed to fetal thyroidal endocrine disruption in utero. To determine whether there is an association between neonatal thyroid status and a subsequent diagnosis of a neurobehavioral disability, neonatal thyroxine (T(4)) levels have been used as the indicator of the presence of intrauterine thyroidal dysfunction. Neonatal T(4) levels were obtained from the neonatal hypothyroidism screening program. All cases were diagnosed at medical school diagnostic clinics, the diagnostic categories being ADHD, autism spectrum disorder, behavioral disorder, cognitive disorder, developmental delay, emotional disorder, learning disability, and speech/language disorder. Conditional logistic regression analysis was performed for each clinical condition. Odds ratios for the conditions ranged from 0.92 to 1.13 with p values ranging between 0.19 and 0.84. No significant differences were detected between neonatal T(4) values of the cases and the controls for any of the neurobehavioral conditions. All neonatal T(4) values were within normal ranges. The data provide no evidence to suggest that intrauterine thyroid status as reflected by the neonatal T(4) values had an impact on the neurologic disorders diagnosed in childhood.

Case-Control Studies↗
PubMed2003

Bladder cancer and arsenic exposure: differences in the two populations enrolled in a study in southwest Taiwan.

OBJECTIVE: Analyses of bladder cancer mortality in the Black Foot Disease (BFD) endemic area of southwest Taiwan conducted by Morales et al. showed a discontinuity in risk at 400 microg/L arsenic in the drinking water in a stratified analysis and no discontinuity in a continuous analysis. As the continuous analysis presentation had been used by both the NRC and the EPA to assess the carcinogenic risk from arsenic ingestion, an explanation of the discontinuity was sought. METHODS: Review of 40 years of published health studies of the BFD-endemic area of SW Taiwan showed that earlier publications had limited their cancer associations with arsenic levels in artesian well waters and that the reports of Morales et al., NRC, and EPA failed to do so. Underlying data for the Morales et al. study were obtained from the appendix to the NRC report. Bladder cancer mortality rates were calculated from case counts and person-years of observation for each study village. Villages were categorized by water source according to the descriptions from the underlying study. Graphic and regression analyses were conducted of the bladder cancer mortality rates using exposure as a continuous variable and simultaneously stratifying by water source. RESULTS: The median village well arsenic levels ranged from 350 to 934 microg/L for villages solely dependent on artesian well water and from 10 to 717 microg/L for villages not solely dependent on artesian well water. Bladder cancer mortality rates were found to be dependent upon the arsenic level only for those villages that were solely dependent on artesian well water for their water source. Bladder cancer mortality rates were found to be independent of arsenic level for villages with non-artesian well water sources. CONCLUSIONS: The data indicate that arsenic exposure levels do not explain the bladder cancer mortality risk in SW Taiwan among villages not dependent upon artesian well water. The association for villages dependent upon artesian well water may be explained either by arsenic acting as a high-dose carcinogen or in artesian well water as a co-carcinogen with some other aspect of artesian well water (possibly humic acid). Arsenic exposure level alone appears to be an insufficient exposure measure to describe the risk of bladder cancer mortality in the BFD-endemic area. Risk analyses that fail to take water source into account are likely to misrepresent the risk characterization, particularly at low arsenic levels.

Adolescent↗
PubMed2002

Newborn thyroxine levels and childhood ADHD.

OBJECTIVES: Normal brain development is highly dependent on adequate levels of iodine and thyroid hormone. It has been suggested that Attention Deficit Hyperactivity Disorder (ADHD) is the consequence of prenatal thyroidal endocrine disruption. The hypothesis was examined using neonatal thyroxine levels as a bio-marker of prenatal thyroid status and comparing it to subsequent development of ADHD. DESIGN AND METHODS: In a matched case-control study, cases were defined as children diagnosed with ADHD, while children born in the same hospital and tested on the same day served as matched controls. Conditional logistic regression analysis with unequal numbers of controls was performed. RESULTS: The neonatal thyroxine levels were within normal limits for each of the children who were subsequently diagnosed as having ADHD, and their distribution was no different from that of their controls. CONCLUSIONS: Children diagnosed with ADHD do not demonstrate prenatal thyroidal dysfunction as reflected in the newborn thyroxine levels, therefore neonatal thyroxine levels are not a bio-marker for the subsequent development of ADHD.

Age Factors↗
PubMedDate not supplied

Human health effects of sodium azide exposure: a literature review and analysis.

Sodium azide, used mainly as a preservative in aqueous laboratory reagents and biologic fluids and as a fuel in automobile airbag gas generants, has caused deaths for decades. Its exposure potential for the general population increases as the use of airbags increase. In order to characterize the known health effects of sodium azide in humans and the circumstances of their exposure, the authors conducted a systematic review of the literature from 1927 to 2002 on human exposure to sodium azide and its health effects. The most commonly reported health effect from azide exposure is hypotension, almost independent of route of exposure. Most industrial exposures are by inhalation. Most laboratory exposures or suicide attempts are by ingestion. Most of the reported cases involved persons working in laboratories. The time between exposure and detection of hypotension can predict outcome. Fatal doses occur with exposures of >or=700 mg (10 mg/kg). Nonlethal doses ranged from 0.3 to 150 mg (0.004 to 2 mg/kg). Onset of hypotension within minutes or in less than an hour is indicative of a pharmacological response and a benign course. Hypotension with late onset (>1 hour) constitutes an ominous sign for death. All individuals with hypotension for more than an hour died. Additional health effects included mild complaints of nausea, vomiting, diarrhea, headache, dizziness, temporary loss of vision, palpitation, dyspnea, or temporary loss of consciousness or mental status decrease. More severe symptoms and signs included marked decreased mental status, seizure, coma, arrhythmia, tachypnea, pulmonary edema, metabolic acidosis, and cardiorespiratory arrest. The signs and symptoms from lower exposures (<700 mg) are physiological responses at the vascular level and those at or above are toxicological responses at the metabolic level. There is no specific antidote for sodium azide intoxication. Recommended preventive measures for sodium azide exposure consist of education of people at high risk, such as laboratory workers, regarding its chemical properties and toxicity, better labeling of products containing sodium azide, and strict enforcement of laboratory regulations and access control.

Air Bags↗