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INTRODUCTION

Humans are exposed to chemicals from their environment on a daily basis. Fortunately, mammals have evolved mechanisms to protect themselves from toxic effects of many exogenous chemicals, including the xenobiotic transport and metabolic mechanisms described in Chapters 4 to 7. While the human body is relatively well adapted to deal with xenobiotics, there are situations in which such environmental agents may cause significant toxicity. The Industrial Revolution and the development of chemical industries have increased human exposures to chemicals that were previously infrequent or absent. Concern about environmental toxicants has stimulated interest and research in environmental toxicology, the study of how chemicals in our environment adversely affect human health; and in occupational toxicology, the study of how chemicals in the workplace affect human health. Many authoritative textbooks are available in these areas. This chapter does not attempt a thorough coverage; rather, it sets forth a few basic principles, discusses carcinogens and chemoprevention and heavy metal intoxication and chelation therapy, and provides an overview of endocrine disruptors and immunotoxicants. The chapter concludes with emerging data on how microbiome-mediated metabolism contributes to xenobiotic biotransformation and toxicity.

ABBREVIATIONS

Abbreviations

AhR: aryl hydrocarbon receptor

AR: androgen receptor

ARE: antioxidant response element

ATSDR: Agency for Toxic Substances Disease Registry

BAL: British anti-Lewisite (dimercaprol)

BLL: blood lead level

BPA: bisphenol A

CaNa2EDTA: calcium disodium ethylenediaminetetraacetic acid

CDC: U.S. Centers for Disease Control and Prevention

COX-2: cyclooxygenase 2

DDE: dichlorodiphenyldichloroethylene

DDT: dichlorodiphenyltrichloroethane

DEHP: di-2-ethylhexyl phthalate

DMPS: sodium 2,3-dimercatopropane sulfonate, dimercaprol

EDC: endocrine-disrupting chemical

EDTA: ethylenediaminetetraacetic acid

EPA: U.S. Environmental Protection Agency

ER: estrogen receptor

FSHR: follicle-stimulating hormone receptor

GI: gastrointestinal

GSH: reduced glutathione

Hg0: elemental mercury

IARC: International Agency for Research on Cancer

LHR: luteinizing hormone receptor

LOAEL: lowest adverse effect level

MCL: maximum contaminant level

MeHg+: methyl mercury

MMA: monomethylarsenic

NF-κB: nuclear factor-κB

NO: nitric oxide

NOAEL: no adverse effect level

NR: nuclear receptor

PAH: polycyclic aromatic hydrocarbon

PCB: polychlorinated biphenyls

PFAS: per- and poly-fluoroalkyl substances

PFOA: perfluorooctanoic acid

PFOS: perfluorooctane sulfonate

PKC: protein kinase C

PM: particulate matter

PPAR: peroxisome proliferator-activated receptor

RfD: reference dose

ROS: reactive oxygen species

TCDD: 2,3,7,8-tetrachlorodibenzo-p-dioxin

ASSESSMENT AND MANAGEMENT OF ENVIRONMENTAL RISK

People are exposed to many environmental xenobiotics at low doses over long periods of time, which poses challenges for assessing the risks from those exposures. Thus, the focus of environmental risk assessment is on the low end of the dose-response curve, using experiments based on chronic exposures. Unlike drugs, which are given to treat a specific disease and should have benefits that outweigh the risks, environmental toxicants are usually only harmful. In addition, exposures to environmental toxicants usually are involuntary, there is uncertainty about the severity of their effects, and people are much less willing to accept their associated risks.

Epidemiology and toxicology provide complimentary approaches to predict the toxic effects of environmental ...

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