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Laws, Regulations, and Risk Assessment Relevant to Site Assessment and Remediation
Published in Cristiane Q. Surbeck, Jeff Kuo, Site Assessment and Remediation for Environmental Engineers, 2021
Cristiane Q. Surbeck, Jeff Kuo
In general, the measured response would increase with an increase in dose. However, there may be no (or no observable) response at low doses for some stressors. The dose at which a response begins to appear is referred to as the “threshold” dose. The dose-response relationship between a human and a chemical should ideally be derived from actual data involving human subjects. However, this type of data is frequently unavailable or covers only a portion of the dose range. Often extrapolation needs to be done to estimate the dose levels that are lower than those available from scientific studies. In addition, animal studies are frequently conducted to augment the available data from human objects. These doses are usually high. Extrapolation of dose-response relationship results from animal studies to humans introduces uncertainty.
Health Risk Assessment
Published in Mary K. Theodore, Louis Theodore, Introduction to Environmental Management, 2021
Dangers are not necessarily defined by the presence of a particular chemical, but rather by the amount of that substance one is exposed to, also known as the dose. A dose is usually expressed in milligrams of chemical received per kilogram of body weight per day. For toxic substances other than carcinogens, a threshold dose must be exceeded before a health effect will occur, and for many substances, there is a dosage below which there is no harm. A health effect will occur or at least be detected at the threshold. For carcinogens, it is assumed that there is no threshold, and, therefore, any substance that produces cancer is assumed to produce cancer at any concentration. It is vital to establish the link to cancer and to determine if that risk is acceptable. Obviously, analyses of cancer risks are much more complicated than noncancer risks [3].
Environmental Epidemiology
Published in Lorris G. Cockerham, Barbara S. Shane, Basic Environmental Toxicology, 2019
The risk assessment approach depends in part on the assumptions that are made about a chemical and how it initiates or promotes disease. Some chemicals produce toxic effects only after a threshold dose is achieved. Many exposure guidelines are based on results of human and animal studies that show no adverse health effects when exposure levels do not exceed certain levels. The classic approach toward establishing acceptable exposure guidelines in these instances is to first identify the human dosage from the knee of the dose response curve at which effects start to occur if dosages increase. With that dosage level, extrapolations may need to be made from the study conditions to a broader situation such as converting 8-hour exposures in a work place setting to 24-hour exposures possibly occurring in a home. The threshold dose derived from a study may be further modified by imposing a margin of safety to account for interindividual variability and uncertainty in the scientific data. The ambient air quality standards for sulfur oxide and particulates were derived using this approach.
No clear concerns related to health risks in the European population with low inorganic arsenic exposure (overview)
Published in Human and Ecological Risk Assessment: An International Journal, 2023
Zdenka Šlejkovec, Tine Bizjak, Milena Horvat, Ingrid Falnoga
Several uncertainties related to low As exposures are mostly disregarded in daily food intake calculations, HBM studies, and risk assessments as has been already warned in several publications. One of the most recent is a review “Essential Concepts for Interpreting the Dose-Response of Low-Level Arsenic Exposure in Epidemiological Studies” published in a special issue of “Toxicity and Carcinogenicity of Arsenic” of the journal Toxicology (Tsuji et al 2021). Uncertainties are related to potential errors with all analytical techniques; unknown bioavailability of iAs from different food items; unreliable information of self-reported data related to food intake or other personal data influencing As metabolism (past exposures, nutritional status, smoking, chronic diseases), and consequently risk assessment; representativeness of populations and applicability of epidemiological data; urine DMA levels as an unreliable biomarker of iAs exposure due to its wide spread presence in food; lacking mechanistic (mode of action) explanation or evidence of a causal association between iAs exposure and specific endpoints at low doses; ignorance of adaptation mechanisms at low-level exposure; linear versus nonlinear dose-response relationship or threshold versus non-threshold dose-response approach; and susceptibility to As at population and/or individual level. Considering all of them, consistent and trustworthy risk assessments at low exposure levels seem to be hardly achievable.
Critical review on PFOA, kidney cancer, and testicular cancer
Published in Journal of the Air & Waste Management Association, 2021
Scott M. Bartell, Verónica M. Vieira
This criterion refers to evidence of increasing risk of disease with increasing exposure. Although the absence of such evidence is not a refutation of causality, and might be a consequence of a causal relationship with a non-monotonic or threshold dose-response pattern (Hill 1965; Rothman and Greenland 2005), or simply random variation with an underlying monotonic dose-response relationship (Kim, Bartell, and Gillen 2015), an average trend of increasing risk across several increasing levels of exposure is consistent with causation.