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Hazard Assessment and Contaminated Sites

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Dealing with Contaminated Sites

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Abstract

Hazard Assessment is a key component of Human Health Risk Assessment and is comprised of the steps of Hazard Identification and Dose-response Assessment. Hazard Identification examines the capacity of a contaminant to cause adverse health effects in humans and other animals using data from a range of toxicological and epidemiological sources. Dose-response Assessment considers both qualitative and quantitative toxicological and epidemiological information to estimate the incidence of adverse effects occurring in human populations at different exposure levels. The conclusions from Hazard Assessment are assessed with those from Exposure Assessment to enable Risk Characterisation. This chapter provides an overview of the toxicological and epidemiological tools used for Hazard Assessment to enable a broader understanding of the Risk Assessment of contaminated sites and the principles underlying the development of risk-based policy and Soil Quality Standards.

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Notes

  1. 1.

    “Strength of evidence” is commonly taken to mean the degree of conviction regarding the outcome of an experiment e.g. The US National Toxicology Program’s “clear evidence”, “some evidence”, “equivocal evidence” and “no evidence” of carcinogenicity. “Weight of evidence” involves integration of all available data, not just one study.

  2. 2.

    The NHMRC document is oriented towards clinical interventions and clinical practice guideline development. More recently, advice to guide assessment of epidemiological evidence for environmental health practice has been provided in NHMRC (2006). Ambient Air Quality Standards Setting: An Approach to Health-Based Hazard Assessment.

Abbreviations

ADI:

Acceptable Daily Intake (WHO)

BMD:

Benchmark Dose

DOH:

Department of Health (United Kingdom)

DNA:

Deoxyribonucleic acid

IARC:

International Agency for Research on Cancer

IPCS:

International Programme on Chemical Safety

LOAEL:

Lowest Observed Adverse Effect Level

Mg/kgbw/d:

mg/kgbodyweight/day

MTD:

Maximum Tolerated Dose

NHMRC:

National Health and Medical Research Council (Australia)

NOAEL:

No Observed Adverse Effect Level

NOEL:

No Observed Effect Level

OECD:

Organisation for Economic Co-operation and Development

PCB:

Polychlorinated biphenyl

PM10 :

Particulate Matter 10 μ

PTWI:

Provisional Tolerable Weekly Intake (WHO)

Q1 * :

The 95% upper confidence limit of the slope estimate used for the linear multi-stage model

Rf D:

Reference Dose (US EPA)

TDI:

Tolerable Daily Intake (WHO)

US EPA:

United States Environmental Protection Agency

WHO:

World Health Organization

References

  • Advisory Committee on Dangerous Pathogens (ACDP) (1996) Microbiological Risk Assessment: an interim report. HMSO, London

    Google Scholar 

  • Agency for Toxic Substances and Disease Registry (ATSDR) (1996) Guidance for ATSDR Health Studies. Division of Health Studies, ATSDR, Washington

    Google Scholar 

  • Ames BN, Durston WE, Yamasaki E, Lee FD (1973) Carcinogens are mutagens: a simple test system combining liver homogenates for activation and bacteria for detection. Proc Natl Acad Sci USA 70:2281–2285

    Article  CAS  Google Scholar 

  • Ashby J, Tennant RW (1991) Definitive relationships among chemical structure, carcinogenicity and mutagenicity for 301 chemicals tested by the US NTP. Mutat Res 257:229–306

    CAS  Google Scholar 

  • Barnes DG, Dourson ML (1988) Reference Dose (RfD): description and use in health risk assessments. Reg Tox Pharmacol 8:471–486

    Article  CAS  Google Scholar 

  • Beaglehole R, Bonita R, Kjellstrom T (1993) Basic epidemiology. World Health Organization, Geneva

    Google Scholar 

  • Bishop JM (1991) Molecular themes in oncogenesis. Cell 64:235–248

    Article  CAS  Google Scholar 

  • Boobis AR, Samuel M, Cohen SM, Dellarco V et al (2006) IPCS framework for analyzing the relevance of a cancer mode of action for humans. Crit Rev Toxicol 36(10):781–792

    Article  Google Scholar 

  • Bonita R Beaglehole, Kjellstrom T (2006) Basic epidemiology, 2nd edn. World Health Organization, Geneva

    Google Scholar 

  • Breslow NE, Day NE (1987) Statistical methods in cancer research. Volume II – the design and analysis of cohort Studies. International Agency for Research on Cancer, Scientific Publication 82, Lyon

    Google Scholar 

  • Butterworth BE (1990) Consideration of both genotoxic and non-genotoxic mechanisms in predicting carcinogenic potential. Mutat Res 239:117–132

    CAS  Google Scholar 

  • Calabrese EJ, Baldwin LA (1994) Improved method of selection of the NOAEL. Reg Tox Pharmacol 19:48–50

    Article  CAS  Google Scholar 

  • Calabrese EJ, Gilbert RO (1993) Lack of total independence of uncertainty factors(UFs): implication for size of the total uncertainty factor. Reg Tox Pharmacol 17:44–51

    Article  CAS  Google Scholar 

  • Crump K (1984) A new method for determining allowable daily intakes. Fundam Appl Toxicol 4:854–891

    Article  CAS  Google Scholar 

  • Crump K (1985) Mechanisms leading to dose-response models. In: Ricci P (ed) Principles of health risk assessment, Prentice Hall, Englewood Cliffs, NJ

    Google Scholar 

  • Department of Health (DOH) (1991) Guidelines for the evaluation of chemicals for carcinogenicity. Committee on carcinogenicity of chemicals in food, consumer products and the environment. Department of Health, Report RHSS 42, HMSO, London

    Google Scholar 

  • Dickens A, Robinson J (1996) Statistical approaches. In: Evans GO (ed) Animal clinical chemistry: a primer for toxicologists. Taylor and Francis, London, pp 45–48

    Google Scholar 

  • Doull J (1980) Factors influencing toxicology. In: Casarett and Doull’s toxicology, 2nd edn. Macmillan, New York, pp 70–83

    Google Scholar 

  • Dourson et al (1996) Evolution of science-based uncertainty factors in noncancer risk assessment. Reg Toxicol Pharmacol 24(2):121–125

    Article  Google Scholar 

  • Dybing E (2002) Development and implementation of the IPCS conceptual framework for evaluating mode of action of chemical carcinogens. Toxicology 181–182:121–125

    Article  Google Scholar 

  • Eaton DL, Klaassen D (1996) Principles of toxicology. In: Casarett and Doull’s toxicology; The basic science of poisons, 5th edn. McGraw-Hill, New York, pp 13–33

    Google Scholar 

  • Elliott P, Cuzick, English D, Stern R (1992) Geographical and environmental epidemiology: methods for small-area studies. World Health Organization, Oxford

    Google Scholar 

  • Fitzgerald DJ (1993) Carcinogenic soil contaminants: an Australian approach. In: Langley AJ, van Alphen M (eds) The health risk assessment and management of contaminated sites – proceedings of the second national workshop on the health risk assessment and management of contaminated sites. South Australian Health Commission, Adelaide, pp 51–64

    Google Scholar 

  • Fowle JR, Alexeeff GV, Dodge D (1999) The use of benchmark dose methodology with acute inhalation lethality data. Reg Toxicol Pharmacol 29:262–278

    Article  Google Scholar 

  • Gad SC, Weil CS (1986) Statistics and experimental design for toxicologists. Telford, NJ

    Google Scholar 

  • Gad SC, Weil CS (1989) Statistics for toxicologists. In: Hayes AW (ed) Principles and methods of toxicology, 3rd edn. Raven, New York, Chapter 7, pp 221–274

    Google Scholar 

  • Gaylor DW, Gold LS (1998) Regulatory cancer risk assessment based on a quick estimate of a benchmark dose derived from the maximum tolerated dose. Erg Toxic Pharmacy 28:222–225

    CAS  Google Scholar 

  • Gaylor DW, Ryan L, Crews D, Zhu Y (1998) Procedures for calculating benchmark doses for health risk assessment. Erg Toxic Pharmacy 28:150–164

    CAS  Google Scholar 

  • Greenhalgh T (1997) Papers that summarise other papers – systematic reviews and meta-analysis. Br Med J 315:672–675

    CAS  Google Scholar 

  • Gregg MB (ed) (1996) Field epidemiology. Oxford University Press, New York

    Google Scholar 

  • Hansen H, De Rosa CT, Pohl H, Fay M, Mumtaz MM (1998) Public health challenges posed by chemical mixtures. Environ Health Perspect 106(Suppl 6):1271–1280

    CAS  Google Scholar 

  • Haseman JK, Huff J, Boorman GA (1984) Use of historical control data in carcinogenicity studies in rodents. Toxicol Pathol 12:126-135

    Article  CAS  Google Scholar 

  • Hayes WJ (1991) Dosage and other factors influencing toxicology. In: Hayes WJ, Laws ER (eds) Handbook of toxicology, vol 1, general principles. Academic, San Diego, pp 40–41

    Google Scholar 

  • Health Council of Netherlands (1994) Risk assessment of carcinogenic chemicals in the netherlands. Regul Toxicol Pharmacol 19:14–30

    Article  Google Scholar 

  • Hellard M (1999) The water quality study approaches a conclusion. Water Quality News, Issue 10:2

    Google Scholar 

  • Heywood R (1981) Target organ toxicity. Toxicol Lett 8: 349-358

    Article  CAS  Google Scholar 

  • Hill AB (1965) The environment and disease: association or causation? Proc Royal Soc Med 58:295–300

    CAS  Google Scholar 

  • International Agency for Research on Cancer (IARC) (1978) Some N-nitroso compounds vol 17. IARC monographs on the evaluation of the carcinogenic risk of chemicals to humans. IARC, Lyon

    Google Scholar 

  • IARC (1983) Miscellaneous pesticides vol 30. IARC monographs on the evaluation of the carcinogenic risk of chemicals to humans. IARC, Lyon

    Google Scholar 

  • IARC (1987) Overall evaluations of carcinogenicity: an updating of IARC monographs volumes 1 to 42 – suppl. 7. IARC monographs on the evaluation of carcinogenic risks to humans. IARC, Lyon

    Google Scholar 

  • IARC (1999) The use of short- and medium-term tests for carcinogens and data on genetic effects in carcinogenic hazard evaluation no. 146. International Agency for Research on Cancer Scientific, IARC, Lyon

    Google Scholar 

  • Imray P, Langley A (1996/1998). Health-based soil investigation levels. National environmental health forum monographs. Soil series no. 1. South Australian Health Commission, Adelaide, 1996

    Google Scholar 

  • IEH (1999) Risk assessment approaches used by UK government for evaluating human health effects of chemicals. Institute for Environment and Health, Leicester

    Google Scholar 

  • IRIS (1996) Integrated risk information system. US Environmental Protection Agency, Washington, DC

    Google Scholar 

  • Johannsen FR (1990) Risk Assessment of carcinogenic and noncarcinogenic chemicals. Crit Rev Toxicol 20(5):341–367

    Article  CAS  Google Scholar 

  • Klaassen CD (ed) (1996) Casarett and Doull’s toxicology; The basic science of poisons, 5th edn. McGraw-Hill, New York, p 4

    Google Scholar 

  • Korach KS (ed) (1998) Reproductive and developmental toxicology. Marcel Dekker, New York

    Google Scholar 

  • Last JM (1988) A dictionary of epidemiology, 2nd edn. Oxford University, Oxford

    Google Scholar 

  • Lee PN (1993) Statistics. In: Anderson D, Conning DM (eds) Experimental toxicology: the basic issues. Royal Society of Chemistry, Cambridge, UK

    Google Scholar 

  • Lewis SC, Lynch JR, Nikiforov AI (1990) A new approach to deriving community exposure guidelines for ‘no observed adverse effect levels’. Reg Tox Pharm 3:17–34

    Google Scholar 

  • Lilienfield AM, Lilienfield DE (1980) Foundations of epidemiology, 2nd edn. Oxford University Press, New York

    Google Scholar 

  • Lovell DP, Thomas G (1996) Quantitative risk assessment and the limitations of the linearised multistage model. Human Exp Toxicol 15:87–104

    Article  CAS  Google Scholar 

  • Lu FC (1995) A review of the acceptable daily intakes of pesticides assessed by WHO. Regul Toxicol Pharmacol 21:352–364

    Article  CAS  Google Scholar 

  • Lu FC, Sielken RL Jr (1991) Assessment of safety/risk of chemicals: inception and evolution of the ADI and dose-response modelling procedures. Toxicol Lett 59:5–40

    Article  CAS  Google Scholar 

  • McClellan RO, Henderson RF (eds) (1989) Concepts in inhalation toxicology. Hemisphere Publishing, New York, NY

    Google Scholar 

  • McMichael AJ (1991) Setting environmental exposure standards: current concepts and controversies. Int J Environ Health Res 1:2–13

    Article  Google Scholar 

  • Moolgavkar SH, Moller H, Woodward A (1999) Principles of the epidemiological approach to QEP. In: Moolgavkar SH, Krewski L, Zeise L et al (eds) Quantitative estimation and prediction of human cancer risks. International Agency for Research on Cancer, Scientific Publication 131, Lyon

    Google Scholar 

  • Mundt KA, Tritschler JP, Dell LD (1998) Validity of epidemiological data in risk assessment applications. Human Ecol Risk Assess 4:675–683

    Article  Google Scholar 

  • NHMRC (1999) Toxicity assessment for carcinogenic soil contaminants Canberra: national health & medical research council. Previously titled Draft cancer risk assessment for environmental contaminants. Commonwealth of Australia, Canberra

    Google Scholar 

  • NHMRC (2000) How to review the evidence: systematic identification and review of the scientific literature. Commonwealth of Australia, Canberra

    Google Scholar 

  • NHMRC (2004) Environmental health risk assessment guidelines for assessing human health risks from environmental hazards. Commonwealth of Australia, Canberra. Available at: http://www.health.gov.au/internet/main/Publishing.nsf/Content/ohp-ehra-2004.htm

  • NHMRC (2006) Ambient air quality standards setting: an approach to health-based hazard assessment. Commonwealth of Australia, Canberra

    Google Scholar 

  • National Committee on Radiation Programs (NCRP) (1996) NRCP commentary no. 14. A guide for uncertainty analysis in dose and risk assessments related to scientific contamination. National Committee on Radiation Programs, Washington

    Google Scholar 

  • Nurminen M (1995) Linkage failures in ecological studies. World Health Stat Quart 48:78–84

    CAS  Google Scholar 

  • Organisation for Economic Cooperation and Development (OECD) (1982) Good laboratory practice in the testing of chemicals. Organisation for Economic Cooperation and Development, Paris, 62 pp

    Google Scholar 

  • OECD (1998) OECD guidelines for the testing of chemicals. Section 4: health effects. vol 2, 10th addendum, October 1998. Organisation for economic cooperation and development, Paris

    Google Scholar 

  • OECD (Various Dates) OECD guidelines for the testing of chemicals. Section 4: health effects. Organisation for economic cooperation and development, Paris

    Google Scholar 

  • Paustenbach DJ (1995) The practice of health risk assessment in the United States (1975-1995): how the US and other countries can benefit from that experience. Human Ecol Risk Assess 1:29-79

    Google Scholar 

  • Paynter OE (1984) Oncogenic potential: guidance for analysis and evaluation of long term rodent studies. Evaluation procedure #1000.1 office of pesticide and toxic substances, EPA, Washington, DC

    Google Scholar 

  • Pershagen G (1999) Research priorities in environmental health. BMJ 318:1636–1637

    CAS  Google Scholar 

  • Pollak JK (1996) Free radical biochemistry of contaminants. In: Langley A, Imray P, Lock W, Hill H (eds) The health risk assessment and management of contaminated sites, Proceedings of the fourth national workshop on the health risk assessment and management of contaminated sites. Contaminated sites monograph series number 7. South Australian Health Commission, Adelaide, pp 323–338

    Google Scholar 

  • Porta M (2008) A dictionary of epidemiology, 5th edn. Oxford University, New York

    Google Scholar 

  • Purchase IFH, Auton TR (1995) Thresholds in chemical carcinogenesis. Regulat Toxicol Pharmacol 22:199–205

    Article  CAS  Google Scholar 

  • Renwick AG, Walker R (1993) An analysis of the risk of exceeding acceptable or tolerable daily intake. Regulat Toxicol Pharmacol 18:463–480

    Article  CAS  Google Scholar 

  • Roseman JM (1998) What can be done to ensure the usefulness of epidemiological data for risk assessment purposes? Human Ecol Risk Assess 4:737–746

    Article  Google Scholar 

  • Rothman KJ, Greenland S (1997) Causation and causal inference. In: Detels et al (eds) Oxford textbook of pubic health, 3rd edn. Oxford Medical, New York

    Google Scholar 

  • Roubicek CB, Pahnish OF, Taylor RL (1964) Growth of rats at two temperatures. Growth 28: 157–164

    CAS  Google Scholar 

  • Samet JM, Schnatter R, Gibb H (1998) Invited commentary: epidemiology and risk assessment. Am J Epidemiol 148:929–936

    Google Scholar 

  • Saunders LD, Chen W, Hrudey SE (1997) Studies of hazardous waste sites and human health: evaluation of internal validity. Environ Rev 5:167–180

    Article  CAS  Google Scholar 

  • Seefeld MD, Peterson RE (1984) Digestible energy and efficiency of feed utilisation in rats treated with 2,3,7,8,-tetrachlorodibenzo-p-dioxin. Tox Appl Pharmacol 74:214-222

    Article  CAS  Google Scholar 

  • Swaim LD, Taylor HW, Jersey GC (1985) The effect of handling techniques on serum ALT activity in mice. J Appl Toxicol 5:160–162

    Article  CAS  Google Scholar 

  • Task Force of Past Presidents (1982) Animal data in hazard evaluation: paths and pitfalls. Toxicol Sci 2:101–107

    Google Scholar 

  • Tallarida RJ, Murray RB (1987) Manual of pharmacologic calculations with computer programs, 2nd edn. Springer, New York

    Google Scholar 

  • Thomas SP, Hrudey SE (1997) Risk of death in Canada: what we know and how we know it. University of Alberta, Edmonton

    Google Scholar 

  • Thompson GE, Scheel LD, Lowe D (1982) Seasonal alteration in response to stress or physiological change. Drug Chem Toxicol 5:189–199

    Article  CAS  Google Scholar 

  • Tucker MJ (1979) The effect of long-term food restriction on tumours in rodents. Int J Cancer 23:803–807

    Article  CAS  Google Scholar 

  • Tyl RW, Marr MC (1997) In: Hood RD (ed) Handbook of developmental toxicology. CRC, Boca Raton

    Google Scholar 

  • US Environmental Protection Agency (US EPA) (1983) Good laboratory practice standards: toxicology testing. Fed Reg 48: page 53922, and: pesticide programs: good laboratory practice standards. final rule. Fed Reg 46 (No. 230): 53946–53969, Tuesday 11/29/83

    Google Scholar 

  • US EPA (1986) The risk assessment guidelines of 1986. Office of Health and Environmental Assessment, EPA/600/8 87/045. United States Environmental Protection Agency, Washington DC

    Google Scholar 

  • US EPA (1989) Risk assessment guidance for Superfund, volume 1. Human health evaluation manual, (Part A). Interim final. EPA/540/1–89/002. US Environmental Protection Agency, Office of Emergency and Remedial Response, Washington DC

    Google Scholar 

  • US EPA (1992) Guidelines for exposure assessment; notice. Part VI. federal register 29 May 1992 57(104):22888–22938

    Google Scholar 

  • US EPA (1995) Guidance for risk characterization. US Environmental Protection Agency Science Policy Council. Washington, DC

    Google Scholar 

  • US EPA (1996) Draft Revision to the guidelines for carcinogen risk assessment. Office of Health and Environmental Assessment, Office of Research and Development, United States Environmental Protection Agency, Washington, DC

    Google Scholar 

  • US EPA (2005) Guidelines for carcinogen risk assessment. Office of Health and Environmental Assessment, Office of Research and Development, United States Environmental Protection Agency, Washington, DC

    Google Scholar 

  • Vainio H, Wilbourn J (1992) Identification of carcinogens within the IARC Monograph program. Scand. J Work Environ Health 18(Suppl 1):64–73

    CAS  Google Scholar 

  • Vainio H, Heseltine E, McGregor D, Tomatis L, Wilbourn J (1992) Working group on mechanisms of carcinogenesis and the evaluation of carcinogenic risks. Cancer Res 52:2357–2361

    CAS  Google Scholar 

  • Van den Berg et al (2006) The WHO re-evaluation of human and mammalian toxic equivalency factors (TEFs) of dioxins and dioxin-like compounds. 93(2):223–41. Epub 2006 Jul 7. Available at http://www.who.int/ipcs/assessment/tef_update/en. Accessed on 25 August 2010

    Google Scholar 

  • Waner T (1992) Current statistical approaches to clinical pathology data from toxicological studies. Toxicol Pathol 20(3):Part 2

    Google Scholar 

  • Weil SC, McCollister DD (1963) Relationship between short-and-long term feeding studies in designing an effective toxicity test. Agr Food Chem 11:486–491

    Article  CAS  Google Scholar 

  • Whysner J, Williams GM (1992) International cancer risk assessment: the impact of biologic mechanisms. Regul Toxicol Pharmacol 15:41–50

    Article  CAS  Google Scholar 

  • World Health Organization (1946) Preamble to the constitution of the world health organization as adopted by the international health conference, New York, pp 19–22 June, 1946; signed on 22 July 1946 by the representatives of 61 States (Official Records of the World Health Organization, no. 2, p. 100) and entered into force on 7 April 1948

    Google Scholar 

  • World Health Organization (WHO) (1972) Evaluation of certain food additives and the contaminants mercury, lead, and cadmium. Sixteenth report of the Joint FAO/WHO Expert Committee on Food Additives (JECFA). World Health Organization Technical Report Series 505. World Health Organization, Geneva

    Google Scholar 

  • WHO (1978) Principles and methods for evaluating the toxicity of chemicals. Environmental health criteria 6. International Programme on Chemical Safety/World Health Organization. Geneva

    Google Scholar 

  • WHO (1987) Principles for the safety assessment of food additives and contaminants in food. Environmental Health Criteria 70, IPCS/WHO, Geneva

    Google Scholar 

  • WHO (1989) Evaluation of certain food additives and contaminants. Thirty third report of the Joint FAO/WHO Expert Committee on Food Additives (JECFA). World Health Organization Technical Report Series 776. World Health Organisation, Geneva

    Google Scholar 

  • WHO (1990) Principles for the toxicological assessment of pesticide residues in food, Environmental Health Criteria 104, IPCS/WHO, Geneva

    Google Scholar 

  • WHO (1992) Quality management for chemical safety testing. Environmental health criteria 141. International Programme on Chemical Safety/World Health Organization. Geneva

    Google Scholar 

  • WHO (1993) Guidelines for drinking water quality. Volume 1 Recommendations, 2nd edn, WHO, Geneva

    Google Scholar 

  • WHO (1994) Assessing human health risks of chemicals: derivation of guidance values for health based exposure limits. Environmental Health Criteria 170. IPCS/WHO, Geneva

    Google Scholar 

  • WHO (1999) Chemical risk assessment. Training Module No. 3 WHO/PCS/99.2. World Health Organization, Geneva

    Google Scholar 

  • WHO (2000) Evaluation and use of epidemiological evidence for environmental health risk assessment. World Health Organization Regional Office for Europe, Copenhagen

    Google Scholar 

  • WHO (2009) Principles for modelling dose-response for the risk assessment of chemicals, Environmental Health Criteria 239, IPCS/WHO, Geneva

    Google Scholar 

  • Yassi A, Kjellstrom T, de Kok T, Guidotti T (2001) Basic environmental health. Oxford University, New York

    Book  Google Scholar 

  • Zbinden G (1979) The role of pathology in toxicity testing. In: Progress in toxicology, vol 2. Springer, New York, pp 8-18

    Google Scholar 

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Acknowledgement

The material in this chapter is derived from Environmental Health Risk Assessment Guidelines for Assessing Human Health Risks from Environmental Hazards (NHMRC 2004) and is used with permission. The material has been summarised by Andrew Langley for this book chapter. The principal author and editor of the original publication was Andrew Langley. Jack Dempsey and Les Davies co-wrote the Hazard Identification – Toxicology section and Roscoe Taylor and Andrew Langley co-wrote the Hazard Identification – Epidemiology section.

Qualifier As the book is about contamination, the word “contaminant” is used in this chapter and generally refers to chemical agents that are not naturally occurring but the term may also refer to physical or microbiological agents in some circumstances.

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  1. Population Health Queensland, Maroochydore, QLD, Australia

    Andrew Langley

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  1. Andrew Langley
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  1. National Institute of Public Health and, Bilthoven, 3720 BA, Netherlands

    Frank A. Swartjes

Adapted from NHMRC (1999)

 

ADI

Acceptable Daily Intake. The daily intake of a chemical which, during a lifetime, appears to be without appreciable risk, on the basis of all the facts known at the time. It is expressed in milligrams per kilogram of body weight per day (mg/kgbw/day) (WHO 1989). For this purpose, “without appreciable risk” is taken to mean that adverse effects will not result even after a lifetime of exposure. Furthermore, for a pesticide residue, the acceptable daily intake is intended to give a guide to the maximum amount that can be taken daily in the food without appreciable risk to the consumer. Accordingly, the figure is derived as far as possible from feeding studies in animals.

GlossarySeeAlsoSee also “Guidance values”, “RfD” and “TDI”.
Adverse Effect

The change in morphology, physiology, growth, development or life span of an organism which results in impairment of functional capacity or impairment of capacity to compensate for additional stress or increase in susceptibility to the harmful effects of other environmental influences. Some adaptive changes are not generally considered to be adverse e.g., some changes in enzyme levels.

Agent

Any chemical, physical, biological or social substance or factor being assessed, unless otherwise noted.

Applied Dose

Amount of an agent presented to an absorption barrier and available for absorption. The amount may be the same or more than the absorbed dose.

Bias

A process resulting in a tendency to produce results that differ in a systematic value from the true values. Also known as systematic error (Beaglehole et al. 1993).

BMD

Benchmark Dose. The dose associated with a given incidence (e.g., 1%, 5% or 10% incidence) of effect, the Benchmark Risk, based on the best-fitting dose-response curve.

Bioavailability

The ratio of the systemic dose to the applied dose.

Carcinogen

Chemical, biological or physical cancer-causing agent.

Carcinogenesis

The origin, causation and development of tumours. The term applies to all forms of tumours (e.g., Benign and malignant).

Carcinogenicity

The ability to produce tumours, which may be benign or malignant (IEH 1999).

Chronic toxicity

The ability to produce an adverse effect which persists over a long period of time, whether or not it occurs immediately upon exposure to a contaminant or is delayed, or an effect which is only induced by prolonged exposure to a contaminant (IEH 1999).

Confidence

Weight assigned by the evaluator to the quality of the information available (high, medium or low confidence) to indicate that a contaminant possesses certain toxicological properties.

Confidence Limits

A range of values determined by the degree of presumed random variability in a set of data, within which the value of a parameter, e.g., The mean, lies, with a specified level of confidence or probability (e.g. 95%). The confidence limit refers to the upper or lower value of the range (DOH 1991).

Confounding Factor

A factor that distorts the apparent effect or magnitude of the effect of a study factor or risk. Such factors must be controlled for in order to obtain an undistorted estimate of a given effect (DOH 1991).

Critical Effect(s)

The adverse effect judged to be the most important for setting an acceptable human intake or exposure. It is usually the most sensitive adverse effect, i.e., that with the lowest effect level, or sometimes a more severe effect, not necessarily having the lowest effect level (IEH 1999).

Dermal

Of the skin, through or by the skin.

Dose

A stated quantity or concentration of a contaminant to which an organism is exposed over a continuous or intermittent duration of exposure. It is most commonly expressed as the amount of test contaminant per unit weight of test animal (e.g., mg/kgbw).

The applied dose is the amount of contaminant in contact with the primary absorption boundaries (e.g., skin, lungs, and gastrointestinal tract) and available for absorption The absorbed dose is the amount crossing a specific absorption barrier (e.g., the exchange boundaries of skin, lung, and digestive tract) through uptake processes. The amount of the contaminant available for interaction by any particular organ or cell is termed the delivered dose of that organ or cell (EPA 1992, p. 22933). The systemic dose is the dose to which the whole, or extensive parts, of the body is exposed. The absorbed dose may not be the systemic dose as contaminants absorbed in the digestive tract may be removed by the liver and not enter the systemic circulation.

Dosage

A general term comprising the dose, its frequency and the duration of dosing. Dosage is properly applied to any rate or ratio involving a dose. Dosages often involve the dimension of time (e.g., mg/kgbw/day), but the meaning is not restricted to this relationship (Hayes 1991).

Dose-response Assessment

Determination of the relationship between the magnitude of the dose or level of exposure to a contaminant and the incidence or severity of the associated adverse effect (IEH 1999).

Dose-response relationship

The correlative association existing between the dose administered and the response (effect) or spectrum of responses that is obtained. The concept expressed by this term is indispensable to the identification, evaluation, and interpretation of most pharmacological and toxicological responses to contaminants. The basic assumptions which underlie and support the concept are: (a) the observed response is a function of the concentration at a site, (b) the concentration at a site is a function of the dose, and (c) response and dose are causally related (Eaton and Klaassen 1996). The existence of a dose-response relationship for a particular biological or toxicological response (effect) provides a defensible conclusion that the response is a result of exposure to a known contaminant.

Endpoint

An observable or measurable biological event used as an indicator of the effect of a contaminant on a biological system (cell, organism, organ etc.).

Environmental health

Those aspects of human health determined by physical, chemical, biological and social factors in the environment. Environmental health practice covers the assessment, correction, control and prevention of environmental factors that can adversely affect health, as well as the enhancement of those aspects of the environment that can improve human health.

Environmental monitoring

The monitoring of the concentration of contaminants in the physical environment of air, water, soil and food.

Epidemiology

The study of the distribution and determinants of health related states or events in specified populations, and the application of the study to the control of health problems (Last 1988)

Expert

An expert has (1) training and experience in the subject area resulting in superior knowledge in the field (2) access to relevant information, (3) an ability to process and effectively use the information, and (4) is recognised by his or her peers or those conducting the study as qualified to provide judgements about assumptions, models, and model parameters at the level of detail required (NCRP 1996).

Exposure

Contact of a contaminant, physical or biological agent with the outer boundary of an organism, e.g., Inhalation, ingestion or dermal contact.

Exposure Assessment

The estimation (qualitative or quantitative) of the magnitude, frequency, duration, route and extent (for example, number of organisms) of exposure to one or more contaminated media for the general population, for different subgroups of the population, or for individuals.

Exposure Route

The way a contaminant enters an organism after contact e.g., By ingestion, inhalation, or dermal absorption (EPA 1992, p. 22933).

Extrapolation

For dose-response curves, an estimate of the response at a point outside the range of the experimental data. Also refers to the estimation of a response in different species or by different routes than that used in the experimental study of interest.

Factor

A single factor or product of several single factors used to derive an acceptable intake. These factors account for adequacy of the study, interspecies extrapolation, inter-individual variability in humans, adequacy of the overall data base, nature and extent of toxicity, public health regulatory concern and scientific uncertainty.

Gene

The DNA molecule of inheritance of characteristics including susceptibility to disease.

Genotoxic

Agents for which a direct activity is the alteration of the information encoded in genetic material (Butterworth 1990)

Genotoxic carcinogen

A contaminant which induces tumours via a mechanism involving direct damage to DNA (IEH 1999).

Genotoxicity

A broad term describing the ability to produce damage to the genetic material (DNA) of cells or organisms.

Guidance Values

“Values such as concentrations in air or water, which are derived after appropriate allocation of Tolerable Intake (TI) among the possible different media of exposure. Combined exposure from all media at the guidance values over a lifetime would be expected to be without appreciable health risk. The aim of a guidance value is to provide quantitative information from Risk Assessment for risk managers to enable them to make decisions concerning the protection of human health.” (WHO 1994, p. 16)

Hazard

The capacity of an contaminant to produce a particular type of adverse health or environmental effect, e.g., One hazard associated with benzene is that it can cause acute myeloid leukemia; or

The disposition of a thing, a condition or a situation to produce an adverse health or environmental effect; or an event, sequence of events or combination of circumstances that could potentially have adverse consequences (adapted from ACDP 1996).

Hazard identification

The identification, from animal and human studies, in vitro studies and structure-activity relationships, of adverse health effects associated with exposure to a contaminant (IEH 1999).

Health

Health is a state of complete physical, mental and social well being and not merely the absence of disease or infirmity (WHO 1946).

Health Risk Assessment

The process of estimating the potential impact of a chemical, biological, physical or social agent on a specified human population system under a specific set of conditions and for a certain timeframe.

Health Risk Management

The process of evaluating alternative actions, selecting options and implementing them in response to Human Health Risk Assessment. The decision making will incorporate scientific, technological, social, economic and political information. The process requires value judgements, e.g., on the tolerability and reasonableness of costs.

Immunotoxicity

The ability to produce an adverse effect on the functioning of organs and cells involved in immune competence (IEH 1999).

LD50

The quantity of a contaminant that, when applied directly to test organisms, via inhalation, oral or dermal exposure is estimated to be fatal to 50% of those organisms under the stated conditions of the test.

Number of microorganisms of a particular species that are fatal in 50% of the host organisms.

LED10

Lowest Effective Dose. The lower 95% confidence limit on a dose associated with an estimated 10% increased tumour or relevant non-tumour response (US EPA 1996).

LOEL

Lowest Observed Effect Level. The lowest concentration or amount of a contaminant, found by experiment or observation, that causes alterations of morphology, functional capacity, growth, development or life span of target organisms.

WHO (1990) define it as the lowest dose of a contaminant which causes changes distinguishable from those observed in normal (control) animals.

LOAEL

Lowest Observed Adverse Effect Level. The lowest concentration or amount of a contaminant, found by experiment or observation, that causes adverse alterations of morphology, functional capacity, growth, development or life span of target organisms.

Life-time

Covering the average life span of an organism (e.g., 70 years for humans).

Metabolite

A contaminant that is the product of biochemical alteration of the parent contaminant in an organism.

Model

A mathematical representation of a biological system intended to mimic the behaviour of the real system, allowing descriptions from empirical data and predictions about untested states of the system.

NOAEL

The No-Observed-Adverse-Effect Level is the highest dose of a contaminant at which no toxic (i.e., adverse) effects are observed (WHO 1990). It may also be worded in more detail thus: The NOAEL is defined as the highest exposure at which there is no statistically- or biologically-significant increase in the frequency of an adverse effect when compared to a control group (National Academy of Sciences/National Research Council 1994). The definition of NOEL is equivalent, but with the removal of the term, “adverse”. Often, the difficult issue in the use of the terms NOEL or NOAEL is in deciding whether a contaminant-related effect noted in a particular study is necessarily an “adverse” effect. Alterations of morphology, functional capacity, growth, development or life span of the target organism may be detected which are judged not to be adverse.

Nongenotoxic carcinogen

A contaminant which induces tumours via a mechanism which does not involve direct damage to DNA (IEH 1999).

Physiologically-based pharmacokinetics (PBPK)

Modelling the dose or degree of exposure to a contaminant at a target tissue, cell or receptor, by integration of pharmacokinetic data with anatomical, physiological and biochemical data (IEH 1999).

NOEL

The “No-Observed-Effect Level” or “No-Observable-Effect Level” (NOEL) is the highest dose of a contaminant administered to a group of experimental animals at which there is an absence of observable effects on morphology, functional capacity, growth, development or life span, which are observed or measured at higher dose levels used in the study. Thus, dosing animals at the NOEL should not produce any biologically significant differences between the group of chemically exposed animals and an unexposed control group of animals maintained under identical conditions. The NOEL is expressed in milligrams of contaminant per kilogram of body weight per day (mg/kgbw/day) or, in a feeding study, in ppm in food (converted to mg/kgbw of contaminant intake by measured or estimated food intake over the period of the study)

The NOEL has been simply defined as the highest dose of a contaminant which causes no changes distinguishable from those observed in normal (control) animals (WHO 1990).

PTWI

Provisional Tolerable Weekly Intake. The tolerable intake of a contaminant expressed as a weekly amount. The term was established by WHO (1972) for several heavy metals which “are able to accumulate within the body at a rate and to an extent determined by the level of intake and by the contaminant form of the heavy metal present in food.” (WHO 1989)

Public Health

The science and art of preventing disease, prolonging life and promoting health through organised efforts of society.

Reproductive toxicity

The ability to produce an adverse effect on any aspect of reproductive capacity, function or outcome. It includes effects on the embryo, fetus, neonate and prepubertal organism and on adult reproductive and neuroendocrine systems (IEH 1999).

RfD

Reference Dose (RfD). An estimate (with uncertainty factors spanning perhaps an order of magnitude) of the daily exposure (mg/kgbw/day) to the general human population (including sensitive sub-groups) that is likely to be without an appreciable risk of deleterious effects during a life time of exposure. It is derived from the NOAEL or the LOAEL by application of uncertainty factors that reflect various types of data used to estimate RfD and an additional modifying factor, which is based on professional judgement of the entire data base of the contaminant (IRIS 1996). Usually doses less than the RfD are not likely to be assoicated with adverse health risks, and are therefore less likely to be of regulatory concern. As the frequency and/or magnitude of the exposures exceeding the RfD increase, the probability of adverse effects in a human population increases. However, all doses below the RfD are not assumed to be “acceptable” (or risk-free) and nor are all doses that exceed the RfD necessarily “unacceptable” (i.e., Result in adverse effects)

Risk

The probability that, in a certain timeframe, an adverse outcome will occur in a person, group of people, plants, animals and/or the ecology of a specified area that is exposed to a particular dose or concentration of a contaminant, i.e., it depends on both the level of toxicity of the contaminant and the level of exposure.

Risk Assessment

The process of estimating the potential impact of a chemical, physical, microbiological or psychosocial hazard on a specified human population or ecological system under a specific set of conditions and for a certain timeframe

Risk management

The process of evaluating alternative actions, selecting options and implementing them in response to Risk Assessments. The decision making will incorporate scientific, technological, social, economic and political information. The process requires value judgements, e.g. on the tolerability and reasonableness of costs.

Safety factor

 

GlossarySeeAlsoSee factor. Safety factor usually refers to health-related concerns.
Stochastic

A random probabilistic phenomenon

Teratogenicity

The ability to produce a structural malformation or defect in an embryo or fetus (IEH 1999)

Threshold

The lowest dose or exposure level which will produce a toxic effect and below which no toxicity is observed (IEH 1999).

Threshold Dose

The lowest dose which produces an effect and below which no biological effect occurs. The acceptability and usefulness of the concept of the experimental NOEL/NOAEL depends on the scientific rationale supporting the existence and demonstrability of a threshold for responses produced by biologically active contaminant. As used here, the term “threshold” designates that level of a stimulus which comes just within the limits of perception, and below which level a recognisable response is not elicited.

TDI

Tolerable Daily Intake. An estimate of the intake of a contaminant which can occur over a lifetime without appreciable health risk. It may have different units depending on the route of administration (WHO 1994). (Imray and Langley 1996, p. 18). The term, “acceptable” daily intake is used for contaminants such as pesticides (herbicides, insecticides, antifungals etc.) which are deliberately used on food crops or food-producing animals and for which some level of residues may be expected to occur in food. The term “tolerable” daily intake is used when the contaminant is a potential food or environmental contaminant. Whilst exposure should not occur, a TDI is an established health limit below which lifetime exposure should not have any adverse health effects.

GlossarySeeAlso“Acceptable Daily Intake” and “Reference Dose”.
TWI

Tolerable Weekly Intake. The TI expressed as a weekly amount

Tolerable Intake

“an estimate of the intake of a contaminant that over a lifetime is without appreciable health risk.” (WHO 1994). Examples are the ADI, TDI and Reference Dose.

Toxicity

The quality or degree of being poisonous or harmful to plant, animal or human life.

Tumour

A mass of abnormal, disorganised cells, arising from pre-existing tissue, which is characterised by excessive and uncoordinated cell proliferation or growth and by abnormal differentiation (specialisation). There are two types of tumours, benign and malignant. Benign tumours morphologically resemble their tissue of origin, grow slowly (may also stop growing) and form encapsulated masses; they do not infiltrate other tissues, they do not metastasise and are rarely fatal. Malignant tumours resemble their parent tissue less closely and are composed of increasingly abnormal cells genetically, morphologically and functionally. Most grow rapidly, spread progressively through adjacent tissues and metastasise to distant tissues.

Uncertainty

The lack of knowledge about the correct value, e.g. a specific exposure measure or estimate

Uncertainty factor

A numerical factor applied to the no-effect level to derive an exposure level considered to be without appreciable risk to health (the NEL is divided by the uncertainty factor). The magnitude of the uncertainty factor depends on the nature of the toxicity observed, the quality of the toxicological data available, and whether the effects were observed in humans or animals (IEH 1999).

Variability

Measurable factors that differ e.g. height is variable across populations. The major types of variability are temporal, spatial and interindividual. They may be discrete (e.g. albinism) or continuous (e.g., body weight). It may be readily identifiable (e.g., presence of albinism) or difficult to identify (e.g., ability to detoxify a particular contaminant metabolite)

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Langley, A. (2011). Hazard Assessment and Contaminated Sites. In: Swartjes, F. (eds) Dealing with Contaminated Sites. Springer, Dordrecht. https://doi.org/10.1007/978-90-481-9757-6_12

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