Childhood Lymphohematopoietic Cancer Incidence and Hazardous Air Pollutants in Southeast Texas, 1995–2004

BACKGROUND: Cancer is the second leading cause of death among U.S. children with few known risk factors. There is increasing interest in the role of air pollutants, including benzene and 1,3-butadiene, in the etiology of childhood cancers. OBJECTIVE: Our goal was to assess whether census tracts with the highest benzene or 1,3-butadiene ambient air levels have increased childhood lymphohematopoietic cancer incidence. METHODS: Our ecologic analysis included 977 cases of childhood lymphohematopoietic cancer diagnosed from 1995–2004. We obtained the U.S. Environmental Protection Agency’s 1999 modeled estimates of benzene and 1,3-butadiene for 886 census tracts surrounding Houston, Texas. We ran Poisson regression models by pollutant to explore the associations between pollutant levels and census-tract cancer rates. We adjusted models for age, sex, race/ethnicity, and community-level socioeconomic status (cSES). RESULTS: Census tracts with the highest benzene levels had elevated rates of all leukemia [rate ratio (RR) = 1.37; 95% confidence interval (CI), 1.05, 1.78]. This association was higher for acute myeloid leukemia (AML) (RR = 2.02; 95% CI, 1.03–3.96) than for acute lymphocytic leukemia (ALL) (RR = 1.24; 95% CI, 0.92–1.66). Among census tracts with the highest 1,3-butadiene levels, we observed RRs of 1.40 (95% CI, 1.07–1.81), 1.68 (95% CI, 0.84–3.35), and 1.32 (95% CI, 0.98–1.77) for all leukemia, AML, and ALL, respectively. We detected no associations between benzene or 1,3-butadiene levels and lymphoma incidence. Results that examined joint exposure to benzene and 1,3-butadiene were similar to those that examined each pollutant separately. CONCLUSIONS: Our ecologic analysis suggests an association between childhood leukemia and hazardous air pollution; further research using more sophisticated methodology is warranted

The Independent Effects of Cigarette Smoking, Alcohol Consumption, and Serum Aspartate Aminotransferase on the Alanine Aminotransferase Ratio in Korean Men for the Risk for Esophageal Cancer

∙The authors have no financial conflicts of interest. Purpose: The goal of this study is to assess the interactions among alcohol consumption, cigarette smoking, and aspartate aminotransferase (AST) / alanine aminotransferase (ALT) ratios on esophageal cancer. Materials and Methods: Alcohol and the risk of incidence and death from esophageal cancer were examined in a 14-year prospective cohort study of 782,632 Korean men, 30 to 93 years of age, who received health insurance from the National Health Insurance Corporation and had a medical evaluation from 1992 to 1995. Results: Smoking, alcohol intake, and AST/ALT ratios were associated with the increased risk of esophageal cancer in a dose-dependent manner independent of each other. Smoking was associated with an increased risk of incidence [Hazard ratio (HR) = 2.2, 95 % CI = 1.8 to 2.5] and mortality (HR = 2.5, 2.0 to 3.1). Combined HR of incidence for alcohol consumption (> 25 g/day) and smoking was 4.5 (3.8-5.5); for alcohol (> 25 g/day) and the AST/ALT ratio ( ≥ 2.0), it was 5.8 (4.6-7.2); fo

The Combined Influence of Oral Contraceptives and Human Papillomavirus Virus on Cutaneous Squamous Cell Carcinoma

The vast majority of cutaneous squamous cell carcinoma (CSCC) will occur in those with fair complexion, tendency to burn, and high ultraviolet radiation (UVR) exposure. Organ transplant recipients also are an important population at great risk for CSCC. An association has been reported between oral contraceptive (OC) use, human papillomavirus virus (HPV) and cervical cancer, and there could be a similar association for CSCC. The cutaneous HPV β-E6 protein, a close cousin of the transformative E6 protein underlying anogenital cancers, has been shown to inhibit apoptosis in response to UVR damage and stimulate morphologic transformation in rodent fibroblast cell lines. Furthermore, OC use has been shown to enhance HPV transcription and may contribute to CSCC risk through this pathway

Respiratory Cancer and Inhaled Inorganic Arsenic in Copper Smelters Workers: A Linear Relationship with Cumulative Exposure that Increases with Concentration

BACKGROUND: Inhalation of high levels of airborne inorganic arsenic is a recognized cause of respiratory cancer. Although multiple epidemiologic studies have demonstrated this association, there have been few analyses of the mathematical relationship between cumulative arsenic exposure and risk of respiratory cancer, and no assessment as to whether and how arsenic concentration may modify this association. OBJECTIVES: The objective is an evaluation of the shape of the relationship between respiratory cancer mortality and cumulative inhaled arsenic exposure among copper smelter workers, and the modification of that relationship by arsenic concentration. METHODS: We used Poisson regression methods to analyze data from a cohort of arsenic-exposed copper smelter workers under a linear-exponential model for the excess relative risk. RESULTS: Within categories of arsenic concentration, the association between respiratory cancer and cumulative arsenic exposure was consistent with linearity. The slope of the linear relationship with cumulative exposure increased with increasing arsenic concentration category. CONCLUSIONS: Our results suggested a direct concentration effect from inhaled inorganic arsenic, whereby the excess relative risk for a fixed cumulative exposure was greater when delivered at a higher concentration and shorter duration than when delivered at a lower concentration and longer duration. KEY WORDS: arsenic, dose–response relationship, lung neoplasms, occupational diseases. Environ Health Perspect 116:1661–1665 (2008). doi:10.1289/ehp.11515 available vi

Impact of Smoking and Chewing Tobacco on Arsenic-Induced Skin Lesions

BACKGROUND: We recently reported that the main reason for the documented higher prevalence of arsenic-related skin lesions among men than among women is the result of less efficient arsenic metabolism. OBJECTIVE: Because smoking has been associated with less efficient arsenic methylation, we aimed to elucidate interactions between tobacco use and arsenic metabolism for the risk of developing skin lesions. METHODS: We used a population-based case-referent study that showed increased risk for skin lesions in relation to chronic arsenic exposure via drinking water in Bangladesh and randomly selected 526 of the referents (random sample of inhabitants > 4 years old; 47% male) and all 504 cases (54% male) with arsenic-related skin lesions to measure arsenic metabolites [methylarsonic acid (MA) and dimethylarsinic acid (DMA)] in urine using high-performance liquid chromatography (HPLC) and inductively coupled plasma mass spectrometry (ICPMS). RESULTS: The odds ratio for skin lesions was almost three times higher in the highest tertile of urinary %MA than in the lowest tertile. Men who smoked cigarettes and bidis (locally produced cigarettes; 33% of referents, 58% of cases) had a significantly higher risk for skin lesions than did nonsmoking men; this association decreased slightly after accounting for arsenic metabolism. Only two women smoked, but women who chewed tobacco (21% of referents, 43% of cases) had a considerably higher risk of skin lesions than did women who did not use tobacco. The odds ratio (OR) for women who chewed tobacco and who had < or = 7.9%MA was 3.8 [95% confidence interval (CI), 1.4-10] compared with women in the same MA tertile who did not use tobacco. In the highest tertile of %MA or %inorganic arsenic (iAs), women who chewed tobacco had ORs of 7.3 and 7.5, respectively, compared with women in the lowest tertiles who did not use tobacco. CONCLUSION: The increased risk of arsenic-related skin lesions in male smokers compared with nonsmokers appears to be partly explained by impaired arsenic methylation, while there seemed to be an excess risk due to interaction between chewing tobacco and arsenic metabolism in women

Epigenetic Changes Induced by Air Toxics: Formaldehyde Exposure Alters miRNA Expression Profiles in Human Lung Cells

Bac k g r o u n d: Exposure to formaldehyde, a known air toxic, is associated with cancer and lung disease. Despite the adverse health effects of formaldehyde, the mechanisms underlying formaldehydeinduced disease remain largely unknown. Research has uncovered microRNAs (miRNAs) as key posttranscriptional regulators of gene expression that may influence cellular disease state. Although studies have compared different miRNA expression patterns between diseased and healthy tissue, this is the first study to examine perturbations in global miRNA levels resulting from formaldehyde exposure. Objectives: We investigated whether cellular miRNA expression profiles are modified by formaldehyde exposure to test the hypothesis that formaldehyde exposure disrupts miRNA expression levels within lung cells, representing a novel epigenetic mechanism through which formaldehyde may induce disease. Me t h o d s: Human lung epithelial cells were grown at air–liquid interface and exposed to gaseous formaldehyde at 1 ppm for 4 hr. Small RNAs and protein were collected and analyzed for miRNA expression using microarray analysis and for interleukin (IL-8) protein levels by enzyme-linked immunosorbent assay (ELISA). Res u l t s: Gaseous formaldehyde exposure altered the miRNA expression profiles in human lun

Estimate of the incidence of bladder cancer in Africa: A systematic review and Bayesian meta‐analysis

Objectives To quantify the epidemiology of bladder cancer in Africa to guide a targeted public health response and support research initiatives. Methods We systematically searched publicly available sources for population‐based registry studies reporting the incidence of bladder cancer in Africa between January 1980 and June 2017. Crude incidence rates of bladder cancer were extracted. A Bayesian network meta‐analysis model was used to estimate incidence rates. Results The search returned 1328 studies. A total of 22 studies carried out across 15 African countries met our pre‐defined selection criteria. Heterogeneity across studies was high (I2 = 98.9%, P < 0.001). The pooled incidence of bladder cancer in Africa was 7.0 (95% credible interval 5.8–8.3) per 100 000 population in men and 1.8 (95% credible interval 1.2–2.6) per 100 000 in women. The incidence of bladder cancer was consistently higher in North Africa in both sexes. Among men, we estimated a pooled incidence of 10.1 (95% credible interval 7.9–11.9) per 100 000 in North Africa and 5.0 (95% credible interval 3.8–6.6) per 100 000 in sub‐Saharan Africa. In women, the pooled incidence was 2.0 (95% credible interval 1.0–3.0) per 100 000 and 1.5 (95% credible interval 0.9–2.0) per 100 000 in North Africa and sub‐Saharan Africa, respectively. Incidence rates increased significantly among men from 5.6 (95% credible interval 4.2–7.2) in the 1990s to 8.5 (95% credible interval 6.9–10.1) per 100 000 in 2010. Conclusions The present study suggests a growing incidence of bladder cancer in Africa in recent years, particularly among men and in North Africa. This study also highlights the lack of quality data sources and collection of essential clinical and epidemiological data in several African countries, and this hinders public health planning