Chronic myelogenous leukemia and benzene exposure: a systematic review and meta-analysis of the case-control literature.

Benzene exposure is well demonstrated as a cause of acute myelogenous leukemia, but not of chronic myelogenous leukemia. Previous literature reviews based on case series and cohort studies have not shown an association. We have now conducted a literature search for case-control studies that examine the association between benzene exposure and chronic myelogenous leukemia. Six case-control studies have been found. These derive from occupational groups, cancer registries, and a clinical laboratory. Their exposure ascertainments are all based on job histories, job-exposure matricies, or industrial hygiene data. The odds ratios (ORs) for individual studies range from 0.73 to 1.2. The pooled OR is 1.003 with 95% confidence interval (CI) of 0.94-1.07 (p=0.98) for both a fixed effects model and a random effects model. The case-control literature indicates that chronic myelogenous leukemia does not appear to be related to benzene exposure.

Arsenic exposure and childhood cancer--a systematic review of the literature.

The literature on environmental arsenic exposure and childhood cancer risk comprises 1) studies seeking childhood cancers among arsenic-exposed populations, 2) studies seeking arsenic exposure among childhood cancer cases, and 3) studies seeking associations in populations with both arsenic exposures and childhood cancer cases. No skin cancers were found in dermal examinations of over 25,000 children in Southwest Taiwan or West Bengal, India, with high drinking-water arsenic levels. Childhood cancer types were not different for those living near a Swedish smelter. In Montreal, Canada, children with acute lymphoblastic leukemia did not have drinking-water arsenic more frequently either prenatal or postnatal, and British children with cancer did not have early exposure to environmental sources of airborne arsenic. Neither hair arsenic levels in Woburn, Massachusetts, nor water arsenic levels in Fallon, Nevada, were elevated for children with leukemia. The literature, while limited, does not seem to support an association between arsenic exposure and childhood cancers.

Cigarette smoking and iodine as hypothyroxinemic stressors in U.S. women of childbearing age: a NHANES III analysis.

BACKGROUND: Exposure to environmental thiocyanate through smoking has been suggested to lead to hypothyroxinemia, which potentially impairs brain development in the fetuses of affected women, though studies are conflicting. It was hypothesized that iodine status might modulate the effects of thiocyanate exposure on the prevalence of hypothyroxinemia in women of childbearing age. DESIGN: The study population comprised 6967 women (age range: 15- 44 years) from the National Health and Nutrition Examination Survey (NHANES) III database. Smoking status was stratified into nonsmokers and those who smoked 1-10, 11-20, 21-30, and 31+ cigarettes a day. Iodine status was stratified based on urinary iodine excretion as <50, 50-99, 100-199, 200-299, and 300+ microug/L. Hypothyroxinemia was defined as the lower fifth percentile of total thyroxine levels among nonsmokers, adjusted for age and race/ethnicity. Univariate, multivariate, and regression analyses were conducted to evaluate the impact of smoking and urinary iodine excretion on the prevalence of hypothyroxinemia. RESULTS: Increasing levels of cigarette smoking are associated with increasing prevalence of hypothyroxinemia [chi(2)(4) = 14.15, p = 0.007]. When analyzed by urinary iodine level, the hypothyroxinemic effect of smoking was limited to the highest two urinary iodine strata [chi(2)(4) = 41.48, p < 0.001; and chi(2)(4) = 40.62, p < 0.001]. A significant interaction effect between smoking and urinary iodine was noted, underscoring the relationship between high levels of urinary iodine excretion and smoking with respect to hypothyroxinemia. CONCLUSIONS: Heavy smoking was associated with a higher prevalence of hypothyroxinemia. The impact of thiocyanate exposure from smoking on the prevalence of hypothyroxinemia is limited to those women of childbearing age with the highest urinary iodine excretion. Iodine supplementation should be cautiously considered in women of childbearing age who are smokers.

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.

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.

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.