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Arsenic is a ubiquitous, naturally occurring metalloid that poses a significant risk for human cancer and non-cancer diseases. It is now evident that arsenic contamination in food, especially rice and grains, presents a significant exposure to hundreds of millions of individuals worldwide. However, the disease risk from chronic exposure to the low amounts of arsenic found in food remains to be established. Thus, this research estimates the global burdens of disease expressed as Disability-Adjusted Life Years (DALYs) for lung, skin and bladder cancers, as well as coronary heart disease (CHD) attributable to inorganic arsenic in food. To determine foodborne inorganic arsenic exposures worldwide, we used the World Health Organization (WHO) estimates of food consumption in 17 country clusters, in conjunction with the reported measurements of total and inorganic arsenic in different foods. We estimated cancer potency factors for arsenic related bladder and lung cancers, and from US Environmental Protection Agency risk estimates for skin cancer to calculate the cancer incidence in males and females within each of the WHO member states. Summary relative risk estimates and population attributable fractions were developed to estimate the YLD, YLL, and DALYs for arsenic-induced CHD. The findings indicate that, globally, each year the combined DALYs for all cancers attributable to inorganic arsenic in food are approximately 1.4 million with variation in global distribution based on population and food consumption patterns. The global burden of CHD attributable to foodborne inorganic arsenic also varied with WHO region and may contribute as much as 49 million DALYs. However, in contrast to cancer burden, there is a threshold effect for arsenic-associated CHD with no increased risk of heart disease at the expected lower bound of arsenic consumption in food. These estimates indicate that foodborne arsenic exposure causes a significant yet avoidable global burden of human disease., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Objective: The purpose of this review is to evaluate the impact of recent epidemiologic literature on the National Research Council (NRC) assessment of the lung and bladder cancer risks from ingesting low concentrations (< 100 µg/L) of arsenic-contaminated water., Data Sources, Extraction, and Synthesis: PubMed was searched for epidemiologic studies pertinent to the lung and bladder cancer risk estimates from low-dose arsenic exposure. Articles published from 2001, the date of the NRC assessment, through September 2010 were included. Fourteen epidemiologic studies on lung and bladder cancer risk were identified as potentially useful for the analysis., Conclusions: Recent epidemiologic studies that have investigated the risk of lung and bladder cancer from low arsenic exposure are limited in their ability to detect the NRC estimates of excess risk because of sample size and less than lifetime exposure. Although the ecologic nature of the Taiwanese studies on which the NRC estimates are based present certain limitations, the data from these studies have particular strengths in that they describe lung and bladder cancer risks resulting from lifetime exposure in a large population and remain the best data on which to conduct quantitative risk assessment. Continued follow-up of a population in northeastern Taiwan, however, offers the best opportunity to improve the cancer risk assessment for arsenic in drinking water. Future studies of arsenic < 100 µg/L in drinking water and lung and bladder cancer should consider adequacy of the sample size, the synergistic relationship of arsenic and smoking, duration of arsenic exposure, age when exposure began and ended, and histologic subtype.

Environmental regulations aimed at reducing cancer risks usually have the effect of reducing exposure to a carcinogen at the time the regulation is implemented. The reduction of cancer risk may occur shortly after the reduced exposure or after a considerable period of time. The time of risk reduction associated with exposure reduction will vary by compound. Some recommended measures of the economic benefits associated with environmental regulations are sensitive to the timing of the risk reductions and cannot be effectively addressed by the conventional dose-response procedures. This paper introduces the concept and methodologies for calculating cessation lag effects, with the specific goal of answering the following questions: (1) How many cancer cases are avoided at age t after cessation (or reduction) of exposure concentration? and (2) How long does the effect of an exposure last after exposure has terminated (or been reduced)? The proposed procedures do not require more information than what is required by the conventional dose-response procedures for which cumulative or an averaged lifetime exposure is used.

Background: Arsenic exposures from drinking water increase the risk of various cancers and noncancer health endpoints. Limited evidence suggests that arsenic may have adverse human reproductive effects. We investigated the association between drinking water arsenic exposure and fetal growth, as manifest in birth weight., Methods: We conducted a prospective cohort study in two Chilean cities with contrasting drinking water arsenic levels: Antofagasta (40 micro g/L) and Valparaíso (<1 micro g/L). Study subjects completed in-depth interviews and provided urine samples for exposure analysis. We obtained pregnancy and birth information from medical records. The birth weight analysis was restricted to liveborn, singleton infants born between December 1998 and February 2000., Results: The final study group consisted of 424 infants from Antofagasta and 420 from Valparaíso. After controlling for confounders, results of the multivariable analysis indicated that Antofagasta infants had lower mean birth weight (-57 g; 95% confidence interval = -123 to 9)., Conclusion: This study suggests that moderate arsenic exposures from drinking water (<50 micro g/L) during pregnancy are associated with reduction in birth weight, similar in magnitude to that resulting from other environmental exposures such as environmental tobacco smoke and benzene.

Millions now suffer the effects of chronic arseniasis related to environmental arsenic exposure. The biological mechanisms responsible for arsenic-induced toxicity and especially chronic effects, including cancer, are not well known. The U.S. Armed Forces Institute of Pathology (AFIP) is participating in an international research effort to improve this understanding by the development of the International Tissue and Tumor Repository for Chronic Arsenosis (ITTRCA). The ITTRCA obtains, archives, and makes available for research purposes, tissues from subjects exposed to arsenic. We provide here a short overview of arsenic-induced pathology, briefly describe arsenic-induced lesions in the skin and liver, and present five case reports from the ITTRCA. Arsenic-induced skin pathology includes hyperkeratosis, pigmentation changes, Bowen disease, squamous cell carcinoma, and basal cell carcinomas. A unique spectrum of skin lesions, known as arsenical keratosis, is rather characteristic of chronic arseniasis. Bowen disease, or squamous cell carcinoma in situ of the skin, has been well documented as a consequence of arsenical exposure. A spectrum of liver lesions has also been attributed to chronic arseniasis. Of these, hepatocellular carcinoma, angiosarcoma, cirrhosis, and hepatoportal sclerosis have been associated with arsenic exposure. We present case reports that relate to these health conditions, namely, squamous cell carcinoma, basal cell carcinoma, and Bowen disease of the skin and hepatocellular carcinoma and angiosarcoma of the liver. Four patients had been treated with arsenical medications for such conditions as asthma, psoriasis, and syphilis, and one case occurred in a boy chronically exposed to arsenic in drinking water.

The impact of foodborne metals on the burden of disease has been largely overlooked, in comparison to the attention on acute diseases associated with infectious foodborne agents. Four articles in this special section describe in detail the burden of disease from foodborne lead, methylmercury, arsenic, and cadmium. Ingested lead and methylmercury are causally associated with lifelong intellectual disability. Long term ingestion of arsenic is causally associated with an increased risk of cancer. Long term ingestion of cadmium is causally associated with an increased risk of late stage chronic kidney disease. This article presents an overview of the burden of disease from these four foodborne metals and discusses them in the context of the World Health Organization's initiative to estimate the global burden of foodborne disease. The results indicate that in 2015, ingestion of arsenic, methylmercury, lead, and cadmium resulted in more than 1 million illnesses, over 56,000 deaths, and more than 9 million disability-adjusted life years (DALYs) worldwide. The greatest impact on DALYs was in the Western Pacific B subregion. All of the metals were found to have high DALYs per case in comparison with other foodborne disease agents, including infectious and parasitic agents. In addition, lead, arsenic, and methylmercury were found to have high DALYs per 100,000 population in comparison to other foodborne disease agents. • Study of burden of disease from foodborne methylmercury, lead, arsenic and cadmium. • These foodborne metals account for 9 million Disability Adjusted Life Years (DALYs). • Lead is estimated to account for the most illnesses and DALYs globally. • All four metals have > 1 DALY per case; three have > 10 DALYs per 100,000. [ABSTRACT FROM AUTHOR]