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GWU / Engineering / PUBH 6004 / What is the slope factor?

What is the slope factor?

What is the slope factor?

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School: George Washington University
Department: Engineering
Course: Environmental and Occupational Health in a Sustainable World
Professor: Peter lapuma
Term: Fall 2016
Tags: Environmental Studies and Public Health
Cost: 50
Name: 6004 MIDTERM STUDY GUIDE
Description: MIDTERM STUDY GUIDE
Uploaded: 03/01/2018
124 Pages 100 Views 5 Unlocks
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MID TERM STUDY GUIDE  


What is the slope factor?



1.Risk Assessment and Toxicology

Ch 29 (pp. 1037-1047, 1059) Ch 2 (49-67, 73-75) 

 Ch 29 Sections: Environmental Health Risk Assessment Process,  Risk Management, Summary

 Ch 2 Sections: Intro, Toxicology and Environmental Public Health,  Toxicant Classification, Toxicants in the Body, Regulatory Toxicology,  Summary

 o Key terms & Concepts for Ch 2: 

∙ NOAEL: Value for the highest dose administered for  which no harmful effects are observed.  

o 1 of most important values generated by the evaluation of  dose-response curves yielded during animal testing, where  several values are determined & can serve as basis 4  


What is the dose-response relationship?



regulatory decisions.  

o The NOAL is 1 of the values determined in such studies as  described above.  

o Used by the Environmental Protection Agency in establishing  the reference dose (RfD). If you want to learn more check out Under the mailbox rule, acceptance is valid when?
If you want to learn more check out What does a synthesizer do?

o A selection of a specifically tested dose that is not  associated with statistically significant increases in  adverse health effects.  

o When this no-observed-adverse-effect-level (NOAEL) is  derived from experiments in laboratory animals, it is  We also discuss several other topics like What is export oriented industry mean?

typically divided by uncertainty factors,  

sometimes totaling as much as 1,000, in order to determine a reasonably safe reference dose.  

 Typically, a factor of 10 is applied to account for  


What is a monotonic dose-response curve?



potential differences in susceptibility across species (for  

example, rats versus humans)

 Another factor of 10 is applied for potential individual  

differences in human susceptibility

∙ LOAEL: the lowest observed adverse effect levelthe  lowest concentration/amount of a substance that  causes harmful effects.  

∙   LD50: Lethal dose for 50 Percent. Dose of the chemical  that kills 50% of those exposed to it in a defined time  frame.  

o Low LD50 indicates less of the compound is needed to   cause toxicity, i.e. it is more potent. Expressed in terms  of dose per kilogram of body weight.

∙ Dermal Exposure, Ingestion, Inhalation: Major routes by which humans can be exposed to chemicals. The route of  administration can have significant affect on the toxicity of certain  chemicals.  If you want to learn more check out What are the factors influencing consumer behavior?

o Chlorpyrifos=10x more toxic via oral administration than  dermal application.  

∙   **RfD: an estimate of the daily oral dose of a chemical  that is likely to be w/out appreciable risk 4 an individual when taken over a lifetime. 

o Factors 2 consider when calculating RfD: Uncertainty  factors (when factors are used quantitatively):  ∙ Interspecies uncertainty factor: The 1st 

uncertainty factor (Uf) reflects possible human

animal differences, and introduces a margin of  

safety to account for such interspecies  

differences.  

∙ Intraspecies uncertainty factor: the Second UF

there may be intraspecies differences in the  

response.

∙ Other uncertainty factors: recognition that  If you want to learn more check out What are the titles of ada?

sensitive subpopulations exist.  

o This factor originally thought 2 be addressed

by the intraspecies uncertainty factor, but it  

isn’t.  

 Recent data demonstrates the unique  

susceptibility of children have led to  

the inclusion of an additional safety  

factor for chemicals that may more  

disproportionately children.  

o ***RfD DERIVED AS FOLLOWS***  

 RfD (mg/kg/day) = NOAEL (mg/kg/day)  

UFinter x UFintra x UFother

Don't forget about the age old question of 5th generation peach and pecan grower are from where?

∙ UFs are typically set @ 10. 

∙ The NOAEL derived from animal studies would be divided by 100 to find the RfD, if no other UFs were deemed to be required/necessary to factor in.  

∙ Slope Factor: used to estimate the risk of harmful  effects (like cancer, disease, etc.) associated with  exposure to a carcinogenic or potentially carcinogenic  substance.

o A slope factor is an upper bound, approximating a 95%  confidence limit, on the increased cancer risk from a lifetime  exposure to an agent by ingestion or inhalation.  

o The estimate is usually expressed in units of proportion of a  population affected per mg of substance/kg body weight-day o Generally reserved for use in the low-dose region of the dose response relationship, that is, for exposures corresponding to  risks less than 1 in 100.

o Slope factors for cancer are also referred to as cancer  potency factors (PF).

∙ Dose response relationship: Most critical aspect of  determining the risk-benefit balance for a given chemical,  used to characterize adverse effects.  

o Must know that the response observed is due to  exposure to the compound.  

o Magnitude of the response should be a function of the  dose administered.

o Should be quantitative method for measuring the  response.  

∙ Dose Response Curve: Part of dose response relationship.  Critical/has important implications 4 risk assessment of toxicity. Critical part of risk assessment.  

 Shape of dose response curve: one can  

determine whether or not a threshold exists 4  the expression of toxicity via evaluation of the  

shape of the dose response curve.  

∙ Threshold concept: built on observation that

4 many chemicals there is a dose below  

which no toxicity is observed.  

o Presence of threshold is well established 4  

many compounds, but GENOTOXIC  

CARCINOGENS (those that directly  

damage DNA) are considered to exhibit a

no-threshold phenomenon: there is no  

dose without risk.  

 Monotonic dose-response curve: typically  

considered in risk assessment. May not be correct for all chemicals.  

∙ For example, vitamins exhibit a U-shaped dose

response curve. Hormesis is often attributed to a  

pattern of low-dose stimulation and high-dose  

inhibition, which produces the characteristic U- or  

J-shaped dose-response curve.  

o At very low levels of consumption, vitamin D

deficiency causes toxic effects such as  

rickets. Once intake rises above the  

deficiency level, a region of homeostasis is  

achieved. However, vitamin D in excess of  

that level can result in kidney damage.  

 Hormesis: Although this U-shaped curve was initially  described 4 radiation effects & nutrients, there is  

emerging evidence that environmental toxicants  

may also exhibit similar dose-response  

relationships. Hormesis is often attributed to a

pattern of low-dose stimulation and high-dose  

inhibition, which produces the characteristic U- or J-shaped dose-response curve

o Biological mechanisms behind hermetic effects  

aren’t currently well established, which brings the  

concept of applying hormesis to the risk  

assessment into question.  

∙ Toxicant Classifications: Chemical class, source of  exposure, & specific organ systems/effects on human  health.

o Examples:  

 Chemical Class: Alcohols, solvents, heavy metals,  oxidants, acids.

∙ May also address physical state whether a  

toxicant exists as a liquid, solid, gas, vapor,  

dust, or fume.  

 Source of Exposure: Industrial wastes, agricultural  chemicals, waterborne toxicants, air pollutants, food  additives.  

∙ This system ignores the biological  

mechanisms that underlie toxicity.

 Organ system affected: Kidney (nephrotoxins),  Liver (hepatotoxins), Heart (cardiotoxins), Nervous  system (neurotoxins), DNA (mutagens,  

carcinogens).  

∙ Looks @ the organ system in which toxic  

effects are most pronounced, I.E. the target  

organ.

∙ FAVORED by most toxicologists when  

working to protect human health one needs  

to consider how a chemical will affect a  

particular physiological function (whether  

blood pressure, respiration, memory, urine  

production, etc) b/c each of these fxns is  

controlled by an organ system Therefore,

organ system classification provides logical  

framework for toxicologists.  

o Example: mercury is known to damage S3

segments of the proximal tubule, S3 brush  

border fxns may slough off into the urine,  

providing a marker for this injury. A  

toxicologist is interested in identifying how  

mercury alters renal fxn might isolate  

proximal tubules in the lab & perform

toxicity tests on these isolated cellular  

sections.  

∙ Endocrine Disruptors: exogenous substances or  mixtures that alter the function of an endocrine system  and cause adverse health effects.  

o Thyroid system, androgenic pathway.

o Six suspected endocrine disrupting chemicals:

Isoflavone, Vinclozolin, Estradiol, DDE, PCB, and PBDE

∙ Toxicology:  

• IDENTIFICATION & CHARACTERIZATION OF TOXIC AGENTS  determined by the following values/tests:  

o Lethal Dose for 50% (LD50) value.  

o Involves exposing laboratory animals 2 compounds &  

determining the dose that killed half the animals. Serves as an  index that allows comparisons among several unrelated  

compounds.  

∙ Weakness:  

o It is a crude method of identification &  

characterization.  

∙ Strengths:  

o The exposure is well defined (unlike the  

exposure in most human situations)

 o the outcome is unambiguous 

 o the measure can be applied across  

different compounds

o Can lead 2 the useful & practical  

 conclusion: if a compound is lethal at very low

doses then human exposures should be  

prevented or strictly controlled. If compound is  

not lethal at very low doses, exposures may be  

less strictly regulated/prevented/controlled.  

o Animal Testing 

o Animals are exposed to a suspected carcinogen at several dose levels. There is also a placebo group. Animals are  observed for defined period of time then sacrificed 2  check 4 evidence of neoplasm.

∙ Example: if a compound causes excess liver cancer in  rats at a relatively low dose, it is prudent to restrict  human exposures. If rodent studies show no adverse  effects at doses orders of magnitude higher than  

humans experience, then a chemical may be approved  to proceed through development.

o Desktop analysis:

o Relies on quantitative structure-activity relationships   ( QSARs); Frequently used by pharma companies in  screening libraries of compounds 4 potential therapeutic  use.

∙ if toxicologist notes that a particular chemical structure  has a particular toxicity, then other chemicals with  

related structures are assessed for the potential to cause similar effects.

∙ Weaknesses:  

o Less definitive: Need 2 extrapolate results to  

human responses, making it Less Definitive  

than animal testing & epidemiological studies.

∙ Strengths:  

o Less expensive  

o More rapid than animal testing  

o In Vitro Testing: 

∙ I nvolves exposure of cell systems (like bacteria   or cultured human cells) 2 a potential toxin. 

Cellular responses such as mutation are observed  & help predict human responses.  

∙ Frequently used by pharma companies in screening  libraries of compounds 4 potential therapeutic use.  ∙ Weaknesses:

o Less definitive: Need 2 extrapolate results to  

human responses, making it Less Definitive  

than animal testing & epidemiological studies.

∙ Strengths:  

o Less expensive  

o More rapid than animal testing  

o QSARs 

 ∙     Used extensively in toxicology 2 ascertain molecular  

mechanisms of action & to identify compounds most  

likely 2 cause potential health effects in living organisms. 

∙ Key function/relied upon function for Desktop  

Analysis.

o Omic Technologies: Genomic, proteomic, & metabolomics tests that provide opportunity 2 examine genes, proteins, &  metabolites on a global scale.  

o DIAGRAM OF test relationships: 

∙ Acute toxicity: exposure 2 high levels of toxicants in  short amount of time/after single dose of a  

substance/multiple doses in a 24-hours, or inhalation  exposure of 4 hours.  

o Example: herbicide paraquat specifically targets the lung via  selective uptake by the diamine/ polyamine transporter. Once in

lung, paraquat readily undergoes oxidation-reduction reactions,  generating free radicals, which can result in lung fibrosis &  ultimately in death b/c of reduced respiratory capacity. Exposure  of humans 2 less than 3 grams of paraquat has been  

demonstrated 2 be lethal.  

∙ Acute Toxicity Test: LD50 test, a multiconcentration or  definitive test(s) consisting of 5 effluent concentrations  designed 2 provide dose-response information expressed as  the percent effluent concentration that is lethal to 50% of test  organisms in a prescribed period of time.

o Tests may be Static OR Flow Through. 

o Static renewal tests: organisms are exposed to a fresh solution of the same concentration of sample every 24 h or other prescribed  interval, either by transferring the test organisms from one test  chamber to another, or by replacing all or a portion of solution in  the test chambers.

 Strengths: Reduced possibility of dissolved oxygen (DO)  depletion from high chemical oxygen demand (COD) and/or  

biological oxygen demand (BOD), or ill effects from metabolic wastes from organisms in the test solutions, Reduced  

possibility of loss of toxicants through volatilization and/or  

adsorption to the exposure vessels, Test organisms that  

rapidly deplete energy reserves are fed when the test  

solutions are renewed, and are maintained in a healthier  

state.

 Weaknesses: Require greater volume of effluent that non renewal tests, generally less sensitive than flow-through  

tests, because the toxic substances may degrade or be  

adsorbed, thereby reducing the apparent toxicity. Also, there  is less chance of detecting slugs of toxic wastes, or other  

temporal variations in waste properties.

o Non renewal tests: organisms are exposed to the same test  solution for the duration of the test.

 Strengths: cheap, cost effective in determining compliance  w/ permit conditions, limited resources required (space,  

manpower, equipment), would permit staff 2 perform many  

more tests in same amount of time, smaller volume of  

effluent required.

 Weaknesses: Dissolved oxygen (DO) depletion may result  from high chemical oxygen demand (COD), biological oxygen  demand (BOD), or metabolic wastes, Possible loss of  

toxicants through volatilization and/or adsorption to the  

exposure vessels, Generally less sensitive than static renewal or flow-through tests, because the toxic substances may  

degrade or be adsorbed, thereby reducing the apparent  

toxicity, Lesser chance of detecting slugs of toxic wastes, or  

other temporal variations in waste properties.

o Flow-through :(1) sample is pumped continuously from the  sampling point directly to the dilutor system; and (2) grab or  

composite samples are collected periodically, placed in a tank  

adjacent to the test laboratory, and pumped continuously from the  tank to the dilutor system. The flow-through method employing  continuous sampling is the preferred method for on-site tests.  

Because of the large volume (often 400 L/day) of effluent normally  required for flow-through tests, it is generally considered too costly  and impractical to conduct these tests off-site at a central  

laboratory.  

 Strengths: Provide a more representative evaluation of the  acute toxicity of the source, especially if sample is pumped  

continuously directly from the source and its toxicity varies  

with time, DO concentrations are more easily maintained in  

the test chambers, A higher loading factor (biomass) may be  

used, The possibility of loss of toxicant due to volatilization,  

adsorption, degradation, and uptake is reduced.

 Weaknesses: Large volumes of sample and dilution water  

are required,Test equipment is more complex and expensive,  

and requires more maintenance and attention, More space is  

required to conduct tests, b/c of the resources required, it  

would be very difficult to perform multiple or overlapping  

sequential tests.

∙ Chronic toxicity: exposure to low levels of toxicants for  long periods of time.

o Example: development of emphysema or developing lung  cancer following years of cigarette smoking.  

 In this situation, the compounds contained in cigarette  smoke don’t cause an immediate acute toxic outcome, but  years of exposure 2 compounds in cig smoke may  

overwhelm the protective defenses of the body & result in  damage 2 the lung.  

∙ Chronic Toxicity Test: Animal Testing. 

• Chemical absorption, distribution, metabolism and  excretion: the sequence of steps that determine a bodily response after  exposure 2 a XENOBIOTIC (a chemical foreign to the body).  ∙ ABSORPTION: 

o Once someone has come in contact w/ toxic compound, the  compound may gain access 2 the body.  

o Compound must actually traverse a biological barrier (not  enough 4 compound 2 just come in contact w/ skin, be inhaled  into the lungs or enter intestinal track).

o Each of these pathways/entrance ways exhibit  

characteristics that affect absorption:  

o GI track: designed for nutrient absorption. Large  

surface area w/ numerous transport mechanism. Many

toxicants can take advantage of this system to enter the  body.  

o Lungs: toxicants can be absorbed thru pulmonary  

alveolithe alveoli are fxnal units of the lung & are sites  of gas exchange b/t air & the blood supply. Allow  

diffusion of most water-soluble compounds. Water

soluable compounds dissolve mucous lining of the  

airways & may be absorbed from there. Lipid-soluable  (fat soluable) gases can also cross into bloodstream via  alveoli. Large particles & aerosol droplets of a toxicant  can be deposited in the upper part of the lungs where  cilia attempt 2 excrete them. Smaller particles &  

aerosols penetrate more deeply, reaching alveoli, where  absorption is very efficient.  

o Skin: Many occupational exposures occur via this route.  Intact skin offers an effective barrier against water

soluble toxicants, but fat-soluble toxicants can readily  penetrate the skin & enter bloodstream.  

∙ DISTRIBUTION: 

o Once in bloodstream, toxicant can be distributed  

throughout body.

o If toxicant=Lipid soluble, it’s often carried thru the aqueous  environment of the bloodstream in association w/ blood proteins  such as albumin.  

 Toxicants generally follow the laws of diffusionthey  move from areas of high concentration 2 areas of low  

concentration.  

o Chemicals absorbed thru intestines are shunted 2 the liver thru  portal vein in the First Pass Process & may undergo  

metabolism promptly. Limited # of chemicals may be excreted  unchanged into bile or by the kidneys into urine.  

∙ METABOLISM:  

o Once in the body, most toxicants undergo Metabolic  Conversion, aka BIOTRANSFORMATION 

 A process mediated by enzymes. Majority of  

biotransformation rxns occur in liver, which is rich in  

metabolic enzymes.  

 Nearly all cells in body have some capacity for  

metabolizing xenobiotics.

 Generally, metabolic transformations lead 2 produx  that are more polar & less fat soluble.

 B.T.’s sometimes yield increasingly toxic products ∙ Example: oxidation of methanol to formaldehyde  

and formic acid (Methanol is a a relatively nontoxic

compound in its native form, formaldehyde & formic  

acid are compounds that are quite toxic 2 the optic  

nerve & can cause blindness).  

o The METABOLIC PRODUCT yielded is thus more soluble in  urine which facilitates excretion.  

 Example: benzene is oxidized to phenol & glutathione  combines w/ halogenated aromatics 2 form nontoxic &  

more polar mercapturic acid metabolites.

 o Key terms & Concepts for Ch 29: ∙ Risk assessment: Process of identifying & evaluating  adverse events that could occur in defined scenarios.  o Attempts 2 answer 3 questions: What Can Happen? How  likely is it to happen? What are the consequences if it does  happen?  

o Consists of hazard identification, dose-response  assessment, exposure assessment, and risk  

characterization.

o It is a rapidly evolving, interdisciplinary endeavor that  encompasses many philosophies and techniques.  

o Is the synthesis of existing scientific information often  aimed at addressing specific regulatory or policy issues. A mixture of science and judgement. Not a “science”, relies heavily on science based info but does not generate new empirical  evidence on health effects like toxicology of epi do.  

∙ Environmental health setting Risk Assessment: A  Quantitative framework for evaluating & combining evidence  from toxicology, epidemiology, & other disciplines, w/ the goal of  providing a basis 4 decision making.  

o Formally defined by the Red Book in 1983. It is common  practice.

∙ USES DATA from human and animal studies are combined with  assumptions and mathematical models to quantify the risk of  various exposures & 2 guide decision making about those  exposures. 

o It’s a process that involves hazard identification, hazard  characterization or dose-response assessment,  exposure assessment, and risk characterization. 

o Focuses on health impacts that might result from  exposure 2 a particular agent or from working in, living in, or  visiting a particular environment.  

o Used 2 help determine acceptable limits 4  

concentrations of pollutants in air, water, soil, & biota  & in emissions from vehicles & industry.

o Susceptible 2 criticism b/ c it is an attempt either 2 estimate  an unmeasured past or present, OR 2 predict an unknown future, or both.

 When used as basis 4 environmental health regulations or  other important decisions, even small changes in risk  

estimates can have large econ consequences.

 Example of risk assessors in this context: looks  

@/analyzes the health risks of…

o drinking water w/ chemical & microbial  

contaminants.

o eating fish contaminated with mercury or  

polychlorinated biphenyls (PCBs).

o breathing particulate matter and other airborne  

contaminants.

o being exposed to natural and man-made sources of  

ionizing radiation.

∙ **4 STEPS OF RISK ASSESSMENT:** A conceptual  framework 4 enviro health risk assessment. Formalized in  NRC report. Divides risk assessment into 4 elements: Outlined  in the The Red Book.

o Hazard Identification: 

 The process of identifying & selecting environmental  agent(s) & health effect(s) 4 assessment.

 Process includes causal inference for particular health  outcomes based on the strength of the toxicological  and epidemiological evidence for causation.

∙ Sometimes the scope of inquiry is limited to a single  agent and single health effect from the outset, leading to a  fairly straightforward hazard identification process. Other times  

∙ Sometimes the scope of inquiry is very broad typically  leading to the selection of key agents and their most important  health effects for risk assessment purposes.

o Dose Response Assessment 

 Attempts 2 describe the quantitative relationship  b/t exposure & disease.  

∙ In some cases direct evidence of the level of response @ the  dose of interest is available, & a mathematical dose-response  model is unnecessary. This is RARE.  

 Most Dose Response Assessments frequently rely on  mathematical models in order 2 estimate responses 4  exposure that fall b/t experimental dose groups or 4  

observational data 4 which doses are typically continuous w/  few or no repetitions.

o Mathematical models may also be used to adjust  effect estimates 4 differences in species, gender,  race & other factors that may confound the  

observed dose-response relationship, or may be used  2 directly incorporate toxicological mechanisms that affect the shape of the dose response curve.  

 ***Linearized Multistage Model:*** Example of  well known dose-response model for cancer. o Assumes every molecule of exposure adds more  risk of cancer. 

o At low risks, this model predicts a nearly linear  

relationship between the dose (d) and the  

probability of response (πd): 

πd ≍ π0 + β1d 

(π0 is the estimated probability of response 

without any exposure & β1 is the effect of the dose.) 

 Threshold Models : example of another well-known  dose response model.

o Assumes nobody exposed @ a level below a  

critical threshold dose will develop cancer as a  

result of exposure.  

 Maximum Likelihood Estimation: Method used in risk  assessments that assumes equivalence on a mg/ kg/  day basis.  

o Although other methods are sometimes used to  

extrapolate results from one species to another, many  risk assessments use this method.  

o Used 2 determine that β1 = 0.00011 (mg/ kg/  day)-1 

 This provides the best fit to the rat data for the  

multistage model.

o This multistage model predicts that every mg/  kg/ day of chloroform exposure contributes an additional lifetime cancer risk of  

approximately 0.011 percent.  

o Exposure Assessment 

 Includes the estimation or measurement of the  magnitude, duration, and timing of human  

exposures to the agent of concern.

∙ Requires explicit definition of the exposed population  and the routes by which it might be exposed to the  agent.  

∙ Often quite difficult to conduct due 2 inherent difficulties in  measuring complex, time-varying behavior (such as the  frequency and amounts of water consumed by an individual or  the amounts & origins of soil and dust that she unintentionally  ingests or inhales or that contacts her skin).  

∙ Ideal exposure assessments produce a full profile of  each individual's exposures over time

∙ in practice most exposure assessments are limited to  estimating summary values (such as time-averaged  exposure rates).  

 ∙    Many exposure assessments rely on default  

assumptions about media contact rate (such as water and  soil ingestion rates) rather than attempting to estimate  specific exposure factors for every individual or   population of interest. 

o Risk Characterization 

 Final step of risk assessment.  

 Consists of combining the information from the  other three steps in order to estimate the level of  response for the identified health effects @ the  specific level of exposure to the agent( s) of interest in the  defined population.  

 ***Mathematically*** the approach consists of  substituting the specific dose amount into the dose response equation and computing the response  level.  

∙ The risk that is contributed by the exposure itself  is often of more interest than the overall probability of  response so analysts often summarize the result in  terms of…

∙ **the relative risk (πd /π0) 

∙ the additional risk aka, Attributable risk  (πd - π0) 

∙ OR the excess risk 

(πd - π0)  

( 1 - π0) 

πd= Probability of response

d=Dose

π0=estimated probability of response  

without any exposure

∙ **Each of these risk measures adjusts the  estimated probability of response in an exposed individual by the background probability of  response (the response among the unexposed) in a different  manner.

∙ **Example of combined results of risk  

characterization: the attributable risk of kidney cancer  in a frequent consumer of drinking water containing 90 μg/ L of chloroform might be about 0.0026 mg/ kg/ day ×  0.00011 mg/ kg/ day)-1 = 3 × 10-8, or about 3 in 100  million.**

o The Red Book (NRC, 1983) & other reports emphasize  that ***uncertainties associated with risk estimation  should be assessed and discussed as part of the risk  characterization step. 

 Qualitative uncertainties, such as those relating to the carcinogenicity of low exposures to chloroform, were  mentioned in the hazard identification section of this  chapter.

 Substantial uncertainty also exists regarding the  true shape of the dose-response model, particularly  

its reliability at the extremely low dose used for the drinking water example.  

∙ The actual concentration and drinking-water ingestion  rate might not be perfectly known 4 a specific population of interest.

∙ Weight of evidence: suggests that human exposure to an agent or to a group of related agents causes cancer.

o IARC monographs classify agents according to five  categories: 

 Group 1: carcinogenic to humans.  

 Group 2A: probably carcinogenic to humans.  

 Group 2B: possibly carcinogenic to humans.  

 Group 3: not classifiable as to its carcinogenicity to  humans.  

 Group 4: probably not carcinogenic to humans.

∙ Animal experiments: tests often used along with statistical  models to estimate the dose-response relationships for  humans.

∙ De minimis risk: a risk management concept commonly  applied in the United States.  

∙ Chemical Carcinogenesis: Cancer can result from chemical exposure. Cancer  is pathologically defineds as uncontrollable cell growth, growth the reflects  alterations in cell’s genome or gene expression, or both. Chemical induced  carcinogenesis proceeds in stages:  

o Initiation: first, associated w/ irreversible change in cell  genotype or phenotype.  

 @ this time, cell either moves to next stage of process or  

is destroyed typically via programmed cell death called  

Apoptosis.  

 In this stage, chemical carcinogen may act via Genotoxic  

Mechanism & directly damage DNA. Or, may alter signal  

transduction pathways resulting in an altered phenotype.  

Chemicals that alter signal transduction pathways are  

termed Epigenetic.  

o Promotion: 2nd stage. involves factors that facilitate cell growth  & replication (like dietary & hormonal factors).  

 This step is not required for all chemical  

carcinogens & UNLIKE initiation, it is reversible.  

 Example of a promoting agent=the hormone  

Estrogen which activates gene expression pathways in  

target organs like the breast, & thus promotes tumor  

growth.  

o Progression: 3rd stage. Is irreversible & involves  

morphological alterations in the genomic structure &  

growth of altered cells.  

o Metastasis: 4th & final stage. During this stage the affected  cell population spreads from its immediate/initial  

microenvironment 2 invade other tissues & organ systems.  

 Many of known environmental chemical carcinogens must

be bioactivated in order 2 exert damagine effects.  

∙ Example: Benzo[a]pyrene, which must be  

converted 2 its epoxide metabolite in order 2  

damage DNA. Others include metals (arsenic,  

chromium, nickel, etc.), minerals (asbestos),  

aliphatic compounds (formaldehyde & vinyl  

chloride), & aromatic compounds (coke oven  

emissions & naphthylamines).  

 Many enzyme systems can detoxify reactive toxicants b4  

they interact w/ target molecules.  

∙ DNA repair mechanisms can often repair damage  

caused by toxicants. If DNA isn’t repaired, cell may  

undergo programmed cell death b4 the altered DNA

can be replicated.  

∙ Immune System can also seek out & destroy  

transformed cells that have escaped other  

mechanisms of defense.

∙   *RISK MANAGEMENT: involves judging the significance of  risks, comparing risks and costs for different risk  management strategies, discussing these assessments with   stakeholders , & making appropriate decisions or  recommendations. 

o Risk assessment & risk management activities should be  separated to ensure that the best science is used.

o Should be mutually informative w/ Risk Assessment.  ∙ DE MINIMIS RISK: the idea that some risks are so small that  they are acceptable or insignificant from a societal perspective.  o Risk managers and regulatory policies rely on this concept o the value of 1 in 1 million is often used as a threshold  for excess cancer risks;

 Activities that pose risks below this threshold are  considered acceptable under this paradigm.  

 Activities or exposures that cause risks above the  threshold are not necessarily unacceptable under  this paradigm  which is sometimes used to screen out  extremely small risks so that more attention can be paid to  activities that pose larger risks.  

∙ Using the cancer risk estimates in the chloroform  

example, a risk manager might conclude that the risks  

posed by chloroform are societally acceptable under the

principle of de minimis risk.

∙ SAFETY ASSESSMENT: relies on a similar principle as de  minimis risk but b/c procedures that do not directly assess the  magnitude of risk are often employed in safety assessment, it’s  more accurate to say that safety assessment relies on a  philosophy of de minimis exposure.  

o Also referred 2 as regulatory risk assessment or regulatory  toxicology.  

∙ RISK BENEFIT ANALYSIS: Process that determines &  weighs the risks and benefits of a compound’s produced  effects.

o Important 2 examine the risks & benefits in a balance manner.  o Some risks result from activities that are otherwise beneficial.  Example: although chlorine increases cancer risks, it has the  benefit of reducing the risk of waterborne diseases caused by  a variety of microbes.  

 Meaningful 2 compare cumulative risks from all  

disinfection by-products (not just the risks from  

chloroform) 2 the cumulative benefits of the variety of  illnesses prevented by chlorination.

o Sophisticated quantitative techniques, such as calculating quality-adjusted life years, are also available for comparing  more risks and benefits for disparate health outcomes

∙ Difference b/t risk benefit & safety assessment: Differ in  important waysSafety assessment commonly used by regulatory  agencies to select reasonably safe exposure limits or concentration  limits in food, water, air, or other parts of the environment.

o Although often relies on hazard identification and dose response modeling, its aim is to answer the question:  What dose or concentration is safe? rather than to  assess the likelihood of adverse health effects at a  given dose or concentration.

∙ Difference in risk (safety?) assessment logic for  carcinogens and non-carcinogens: 

o Safety assessment for Noncarcinogens: has relied on  the selection of a specifically tested dose that is not  associated with statistically significant increases in  adverse health effects.

 When this no-observed-adverse-effect-level  

(NOAEL) is derived from experiments in laboratory animals, it is typically divided by uncertainty  

factors, sometimes totaling as much as 1,000, in   order to determine a reasonably safe reference   dose. 

 Typically , a factor of 10 is applied to account for  potential differences in susceptibility across  

species (for example, rats versus humans)

 Another factor of 10 is applied for potential  individual differences in human susceptibility

 A third factor of 10 is applied when deriving a  

reference dose for children.

∙ In recent years, safety assessments have  

replaced the NOAEL with a model-based  

estimate of the dose at which the extra risk is 1  

percent, 5 percent, or 10 percent, depending on  

the severity of the outcome.  

o For carcinogens: recent EPA guidance suggests the use of linear interpolation from the lower bound on a  benchmark dose to the origin in order to determine the  lowest dose likely to be associated with a particular de  minimis level of risk. In either case, identification of a safe  dose relies on both dose-response modeling and a risk

management decision regarding the acceptable level of risk  for each health outcome.

• Calculate environmental risk using estimates of exposure  and RfDs or slope factors. 

∙ To calculate RfD’s 1) use LOAEL to calculate  

______________________________________________________________________________

2. Population and Energy

Ch 13 (pp. 417-441) Entire Chapter  

 Key terms & Concepts for Ch 13: 

∙ Explain how each major energy source is used and their relative  percent contribution in the US energy mix: 

∙ Fossil Fuels: 7,921

∙ Solid Biomass: 85.3

∙ Nuclear: 9.1

∙ Hydroelectric: 1.8

∙ Other renewables: 0.8

∙ % with electricity:100

∙ Use per capita: 13,416

∙ North America Energy Use (million metric TOE)1,725 Industry27.2  Transport: 38.9 Agriculture1.1 Service16.3 Residential16.5 

∙ Explain the public health impacts of fossil fuel mining, refining,  transport and consumption:  

∙ Direct & indirect health effects from petroleum production,

transport, and refinement: 

∙ Oil exploration and drilling are associated with several  

occupational hazards, particularly injuries at the well & during  transport by sea & land.  

∙ The drilling industry has higher nonfatal occupational injury  rates than the overall industry average

∙ Occupational fatality rate for the U.S. oil and gas extraction  industry was seven times the national average for

occupational fatalities for the period from 2003 to 2006.

∙ Oil production exposes workers 2 a host of potential  carcinogens.

∙ Exposure 2 crude oil = associated w/ increased risk of  

hematological malignancies (such as acute  

myelogenous leukemia & multiple myeloma in  

petroleum workers).  

∙ In contrastseveral studies have demonstrated no  

significant health effects from working in petroleum  

refineries  

∙ Petroleum transport (particularly internat’l transport of crude  oil in sea-borne tankers is dangerous 2Mishaps w/ tankers or  pipelines can lead 2 spills. Those who cleanup & rely on the  ecosystem services damage by oil spills & those who live near affected area/spill may be affected.  

∙ Health concerns include: injuries, ill-defined  

respiratory & mucous membrane irritation syndromes,  

severe mental health issues, displacement & other  

issues. The demand for oil will affect 4 areas: medical  

supplies & equipment, food production, & energy  

generation, persistent economic downturn w/ associated

social disruption, mental health effects & possible  

armed conflict.  

∙ Significant indirect health effects result from the ways  petroleum is used from dependence on exports.  

∙ Example: some developing countries put gasoline to  

improve combustion efficiency. Lead has significant  

effects on neurological development & removing lead  

from gasoline has lead 2 dramatic declines in blood  

∙ Identify when global oil discoveries peaked and how much oil the  US consumes in a day 

∙ Variety of predictions regarding peak: Some say petroleum peaked  sometime between 1996 & 2006. Others place the global peak b4  2030, others b4 2010, others say it is occurring right now.

∙ May be able 2 determine exact peak by using/employing  formulas originally developed 4 bacterial colony growthcan  possibly predict peak production 4 oil fields.

∙ Oil accounts for 35% of world’s energy consumption

∙ In 2014, US consumed 6.97 billion barrels of petroleum products.

∙ AVERAGE US consumption of: 19.11 million barrels of oil per  day.  

∙ Apply the energy issues discussed in class to the development of  sustainable US energy policy  

∙ Key Concepts:  

∙ There are several energy sources on Earth. The sun is primary  among them, as direct sunlight, as energy for plant growth, and as  stored solar energy in fossil fuels. Other energy sources include  geothermal, hydro, and nuclear.  

∙ A society's energy use varies with its level of socioeconomic  development.

∙ A nation's development is associated with increased energy  use, cleaner energy sources, greater distance between  energy production and end use, and deferment of health  impacts over time.

∙ Each source of energy has a profile of health impacts.

∙ Life cycle analysis— from “harvesting” and transporting raw  materials, to fuel production, to energy transmission and  

consumption, to waste generation and management— clarifies the  full health impacts.  

∙ Major changes in energy patterns may be imminent, driven  by such forces as petroleum depletion and global climate change.  These changes will have important health consequences.  

∙ Energy policy is health policy. Rigorous analysis, using scientific  evidence and tools such as health impact assessments, can help  nations reach the most health-protective energy policies.

∙ Energy: defined as the ability to do work, such as lifting a weight. Activity & civilization depends on ready availability of energy.  

∙ Power: is work done over time. 

∙ Term used In physics.

∙ Coal: a combustible sedimentary rock composed of the fossilized  remains of prehistoric vegetable matter preserved from  biodegradation by water and mud. 

∙ Composed primarily of carbon & hydrogen & small amount of other  elements like sulfur. Primary source for electricity generation  worldwide

∙ Extracted via mining

∙ Produced in pit, underground, strip, and other types of mines

∙ 40% of world electricity production = from coal, 25% of total  primary energy production = from coal.  

∙ Advantages:  

∙ Better than Biomass in terms of health & air pollution: Less  risky 2 health & generates less indoor air pollution than  

Biomass burning.  

∙ Tech improvements are likely 2 result in enhancements such  as carbon combustion.

∙ Rising fuel costs may make it cost effective 2 use coal-to liquid technologies where coal is used as a substrate 2  

generate liquid fuels like diesel & gasoline

∙ Disadvantages:  

∙ Not renewablecoal endowment is finite

∙ Subject to production constraints

∙ Causes indoor air pollution

∙ Tons of health risks

∙ Risk for coal combustion

∙ Technologies that come from coal industry innovation liberate  more CO2 than petroleum extraction & refinement. Would  have 2 be captured & sequestered in order 2 limit  

environmental & health impacts of coal-to-liquid technologies. ∙ Health Risks:  

∙ Very Hazardous Underground mining is associated with:  increased mortality from injuries, nonmalignant  

respiratory disease (black lung, pneumoconiosis).

∙ Regions (such as turkey) have high mortality rates from  asphyxiation after shaft collapses, underground railway  

crashes, & gas poisoning.  

∙ Significant health effects @ point of useindoor air pollution causes respiratory illness, lung cancer, chronic  

obstructive pulmonary disease, premature death,  

weakening of the immune system, compromised lung  function, cancer, arsenic & selenium poisoning,  

fluorosis

∙ Coal combustion @ centralized plants causes: respiratory &  eye irritation, asthma, cardiopulmonary disease,  

cancer, cardiovascular effects such as increased risk  for atherosclerosis, dysrhythmias, deep vein  

thrombosis, & sudden cardiac death.  

∙ Petroleum: fossil fuel that began as prehistoric algae &  zooplankton deposited on lake & ocean floors buried & subjected  2 particular temps & pressure conditions.  

∙ Central role as a fuel, particularly in transportation sector.  

∙ Key ingredient in wide range of synthetic processes (produxion of fertilizers, plastics, resins, textiles, pesticides,  pharma).

∙ 84% converted 2 fuel.

∙ Important role in public health & medicine as transport fuel for  patients, health workers, & supplies, & as a synthetic precursor for a wide range of medical devices & pharmaceuticals.

∙ Crude oil is umped from underground stores under both land and  sea; it is then transported to refineries, where it is distilled into a  variety of fuels & products.  

∙ Advantages:  

∙ Ideal transport fuel

∙ Versatile input 4 a wide array of industrial processes ∙ Dense, light, relatively stable

∙ Abundant

∙ Important role as facilitator for public health & medicine  via transport fuels 4 patients, health workers, & supplies.

∙ Innovation/TechnologyImportant synthetic precursor 4 a  wide range of medical devices & pharma.  

∙ Conventional sources of petroleum are more easily  accessible, can be refined more economically, & serve  as primary source of petroleum.  

∙ No comparably economical, portable, & energy dense  transport fuel  

∙ Transition 2 post peak petroleum era will likely have  health benefits, such as improvements in cardiovascular health due 2 reduced vehicular travel & increased  walking & biking, increased efficiency, less  

consumption of meat, &localization.

∙ Disadvantages:  

∙ Combustion contributes significantly 2 greenhouse gas emissions & thus 2 global warming.  

∙ Produces more CO2 emissions than other fossil fuels & is  responsible 4 majority of cumulative atmospheric CO2 above  preindustrial levels

∙ Nonconventional sources of petroleum are costly to recover ∙ Not renewablelimited supply

∙ Production is depleting sources

∙ Uncertainties in reserve estimates

∙ Differing reporting protocols  

∙ Incentivized skew-ing of total reserve estimates by countries ∙ Peak Petroleum is looming

∙ Health risks:  

∙ Directly: Oil exploration & drilling associated w/ well injuries  & injuries during transport by sea & land. Oil production  exposes workings 2 host of carcinogens, increased risk 4  cancer. Exposure 2 crude oil particularly benzene is  

associated w/: increased risk of hematological  

malignancies such as acute myelogenous leukemia &  multiple myeloma in petroleum workers. ALSO  

Sustains/contributes 2 global warming, which leads 2: heat related illness, exacerbations of climate-sensitive  

cardiovascular & respiratory disease, increased  

incidence of waterborne & foodborne & allergic  

disease, increased mortality from extreme weather &  floods.

∙ Indirectly: Sustains/contributes 2 Climate change, which  may result in population displacement, worsening  

malnutrition, & conflict over scarce resources.

∙ Transition 2 post peak petroleum world likely 2 have big  effects, such as negative impact on: medical supplies &  equipment (including pharmaceuticals, medical transport,  food production, & energy generation.

∙ Could also cause: persistent economic downturn asocial  w/ social disruption, mental health effects, & possibly  armed conflict.

∙ Peak Petroleum: point of maximum production, after which  production inexorably falls. 

∙ Can possibly be determined by using formulas originally developed  4 bacterial colony growthcan possibly predict peak production 4 oil fields.

∙ CURRENT ENERGY PATTERNS: current energy use landscape, has 4  characteristics that date from the industrial revolution:  

1. More developed areas of the world have higher per capita  energy consumption (and higher associated emissions per capita as well).

2. More developed areas rely disproportionately on cleaner forms of energy production that are higher on the energy ladder.

3. More developed regions rely more heavily on electricity, a  more efficient mode of energy production. This translates to  greater economic output per unit of energy input than countries  in the developing world achieve (Grubler, Nakicenovic, and  Jefferson, 1996).  

4. Higher levels of development are associated with increased  capacity and willingness to distribute health impacts both onto  distant populations and to future generations (Holdren and  Smith, 2000).

∙ Biodiesel: fuel/energy manufactured via crops.  

∙ Renewable source of energy.  

∙ Climate Change: a change in global or regional climate patterns  attributed largely to the increased levels of atmospheric carbon  dioxide produced by the use of fossil fuels. 

∙ Particularly refers 2 a change apparent from the mid to late 20th  century onwards.

∙ Life cycle analysis: systematic approach of looking at a product's  complete life cycle, from raw materials to final disposal of the  product.  

∙ It offers a “cradle to grave” look at a product or process ∙ Considers environmental aspects and potential impacts  

∙ Energy ladder: Illustrates the concept that the level of tech  development determines the primary sources of energy that  people employ, the efficiency w/ which they convert energy to  productive work, & the extent to which they limit or control  potentially harmful by-products.

∙ As prosperity increases, societies tend 2 substitute cleaner,  more efficient, & more convenient energy sources for the  less costly but more polluting sources at the ladder’s base.

∙ Captures only 2 dimensions of the relationship

∙ as development increases, so does the physical  

distance b/t energy generation & the end user.  

∙ As development increases, so does the time b/t energy  use & occurrence of health effects on a generational  scale.

∙ Biomass: heterogeneous group of organic materials generated by plants through photosynthesis. 

∙ Includes: wood, corn husks, coconut shells, peat & animal dung.  Used 2 produce liquid biofuels (primarily ethanol & biodiesel).  

∙ Constitutes 7% of world’s primary energy production.  

∙ Advantages:

∙ RenewableReincorporated into organic matter through plant  respiration & photosynthesis

∙ Not significant source of deforestation  

∙ Incorporation of sustainable forestry management & woodlots  can minimize burden of gathering biomass/fuel, & increased  ventilation, chimneys & improved stove design are also used  to combat the disadvantages & their health effects.  

∙ Disadvantages:  

∙ Concern over food price inflation resulting from ethanol  subsidies & crop substitution  

∙ Requires long trips on foot

∙ Exposes women & children (primary gatherers) 2 injuries,  malnutrition, vector borne diseases, sexual violence, & others.

∙ Opportunity cost due to time spent gathering fuel that could  be used productively in other areas, such as education.  

∙ Burning biomass 4 fuel also causes respiratory tract  

infections, lung cancer, & tuberculosis, burn injuries, & other  associated injuries.  

∙ Can devastate local ecosystems where practice intensively &  population density = high.  

∙ Health risks:  

∙ Indoor air pollutionPoor ventilated household combustion in  developing world causes indoor air pollution & causes  

significant health effects.  

∙ Bio Fuels: 2 principal biofuels have different energy & emission  profiles. 

∙ used in different percentage blends.

∙ Advantages:

∙ Data suggests biodiesel has much greater net energy gain  than ethanol.  

∙ Pollutes at a much lower rate than ethanol

∙ Reduces greenhouse emissions by 41% compared to  

petroleum, & compared to ethanol’s 12% reduction.

∙ Significantly ahead of corn ethanol in such terms.  

∙ Blend of 20% biodiesel has net positive effectreduces  emissions of several harmful chemical species, such as  

particulate matter, carbon monoxide & total hydrocarbons.  ∙ Disadvantages:  

∙ Question over biofuels’ (like ethanol) true degree of energy  efficiency when all energy outputs are accounted for

∙ Health risks:  

∙ Not well known & are under active investigation. More work  needed.  

∙ Concern that large-scale conversion from gasoline to E85 wil  lresult in greater ozone production & acetaldehyde emissions  causing net negative health impacts.  

∙ Coke: a residue made from the reductive combustion of  carbonaceous fuel.  

∙ Technology that emerged during industrial revolution in late 1700s.  

∙ Production of coke enabled the production of refined metals &  machine tools.

∙ Coal Gasification: began @ the end of the industrial revolution. Produced coal gas or town gas from coal for use in lighting. 

∙ Coal gas replaced tallow & oil

∙ Coal gas also improved lightingwhich allowed increased  urban security & economic activity.  

∙ Gasoline Powered internal combustion engines &  Electromechanical generators: the 2 inventions that ushered in  modern era in terms of energy usage. 

∙ Led 2 production of motor cars in 1880s & relentless increase in  petroleum-based fuel demand

∙ Enabled centralized production of electrical energy from various  substrates

∙ Electricity was widely & quickly adopted in the developing world.  

∙ Pacala & Socolow’s stabilization wedges: See diagram. When  summed, a sufficient # of wedges could keep atmospheric CO2  levels @ 450 parts per million (PPM), arguably low enough 2 stave off  further dangerous climate change.  

∙ Energy efficiency and conservation

1. Increase vehicle efficiency

2. Reduce use of vehicles.

3. Increase building efficiency.  

4. Increase efficiency of baseload coal plants. Fuel shift  

∙ Fuel Shift

5. Substitute gas for coal for baseload power. Carbon dioxide  (CO2) capture and geological storage  

∙ Carbon Dioxide (CO2) & geological storage

6. Capture CO2 at baseload power plant.  

7. Capture CO2 at H2 plant.  

8. Capture CO2 at coal-to-synfuels plant.  

∙ Nuclear fission  

9. Substitute nuclear power for coal power. Renewable  

electricity and fuels

10. Substitute wind power for coal power.  

11. Substitute solar energy (using photovoltaic cells) for  coal power.

12. Substitute H2 in fuel-cells (using wind energy) for gasoline in cars.

13. Substitute biomass fuel for fossil fuel.

∙ Forests & Agricultural Soils

14. Reduce deforestation & increase planting.

15. Implement conservation tillage.  

∙ CONCEPT OF CLIMATE STABALIZATION WEDGES:  ∙ Fossil Fuels: formed over millions of years as organic material  deposited on the earth’s surface, was buried & subjected 2  pressure & temperature in earth’s crust.  

∙ Fossil Fuels derive their energy from chemical bonds  created during photosynthesis.

∙ Includes: coal, oil, natural gas, or a few less common  

materialsdifferences depend on where organic matter was  deposited & geological forces to which it was subjected.

∙ Oil = most commonly used fuel. Coal also used frequently along  w/ natural gas.  

∙ Very important 2 industrial processes & 2 industries (such as  transportation, health, technology, etc.)  

∙ Natural gas: another fossil fuel. Often found w/ oil deposits.  Prehistoric organic matter that was subject 2 higher  temperatures than adjacent oil. 

∙ Found in coal beds (coal bed methane) & in isolated natural gas  fields.  

∙ Mixture of several gases, primarily methane, also ethane, propane,  butane, pentane & several inorganic gases like CO2, nitrogen,  helium & hydrogen sulfide.

∙ Advantages:

∙ Wide range of uses  

∙ Fewer impurities than other fossil fuels, which means less  pollutinggenerates 30% less CO2 than petroleum & 45% less than coal

∙ Natural gas processing is not associated w/ health risks ∙ Cleaner emissions profile

∙ More efficient combustion

∙ Produce fewer health hazards per joule produced than other  fossil fuels.

∙ Disadvantages:

∙ Difficulties of transport & storage

∙ Volatility & low density are problematic.  

∙ Limited resource

∙ Produces significant amount of CO2 emissions.

∙ Health Risks:

∙ Oil extraction comes w/ significant hazardsparticularly  injuries

∙ Small but significant risk of hydrogen sulfide toxicity  

∙ Extraction=associated w/ cancers

∙ Occupational exposure=small increased risk for bladder  cancer  

∙ Controlled biomass combustion: transformation of wood crop  residues, & animal dung into useful fuel sources.  

∙ Renewable.  

∙ Hydropower: transforms gravitational energy falling in H20  electrical energy. 

∙ Most widely used form of renewable energy in the world (in ’06  hydropower generated 15% of the world’s electricity & 46% of the  electricity from renewable sources).  

∙ Advantages:

∙ Low apparent cost

∙ Up front costs are significant but they are quickly  

recouped from sale of electricity.

∙ Disadvantages:  

∙ Releases significant amounts of methane which is a potent  greenhouse gas.  

∙ Total estimate of global methane emissions may need 2  be adjusted by as much as 20%.

∙ Established costs

∙ Displacement of human settlements

∙ Local ecosystem destruction & damage

16. Health Risks:

a. Increased incidence of malaria & other vector-borne  

diseases  

∙ Nuclear energy: generated thru fission of uranium 235 which  heats h20 to do mechanical work, primarily electricity generation. 

∙ Constituted 6.3% of world’s total energy supply, 15.2% of electricity generation in recent yrs.  

∙ Advantages:  

∙ Does not emit greenhouse gases

∙ Disadvantages:  

∙ Hazardoushigh profile nuclear accidents, like those @ Three  Mile Island & Chernobyl.

∙ Not renewableEarth’s uranium supply = finite.  

∙ Dangerous even w/ safeguardsnuclear waste handling &  transport.  

∙ Health Risks:  

∙ Direct: injuries associated w/ mining, association w/  

nonmalignant pulmonary disease (such as silicosis), Cancers  (lung, lymphoma, leukemia due 2 exposure 2 radioactive  

uranium & radon, Small risk of childhood blood cancers in  surrounding areas, terrorism, armed conflict.  

∙ Indirect: stem primarily from nuclear accidents & potential  exposure 2 radiation from contaminated sites & during  

transport & storagelike Chernobyl.  acute radiation  

sickness, pediatric thyroid cancers, & other cancers.

∙ Other renewable energies: Solar, geothermal, wind, & wave  energy.  

∙ Advantages:  

∙ Lower long-term cost  

∙ Minimal greenhouse gas emission

∙ Disadvantages:  

∙ Poor Aesthetic  

∙ Huge potential for improvement over fossil fuels.  

∙ Health Risks:  

∙ Occupational health concerns related 2 hazardous materials  involved w/ production.  

DISCUSSION QUESTIONS: 

1. List all the different types of energy you use over the course of a  typical day. Create a table that lists each activity and describes the  energy type and source, the alternatives available to you for each  activity, where the energy is produced (at the point of consumption or  more remotely), and the health effects of the energy source. Be sure to consider energy embedded in food as well.

2. Calculate your carbon footprint.  

3. Pick a technical innovation that reduces work and thus improves  energy efficiency, such as a smaller, more fuel-efficient car or a well insulated building with little air circulation. Write a paragraph that  outlines the resulting co-benefits to energy and health and the  potential trade-offs (such as the increased risk of injuries from driving a smaller car or increased exposure to respiratory pathogens in a  building with little ventilation). How might a health impact assessment  determine the ultimate value of the innovation?

4. Externalities signal a form of market failure. List several strategies that could address these market failures, including those that will result in  proper pricing (for greenhouse gas emissions, for instance), and those  that will allow redress for adverse impacts on vulnerable populations.  Which is more effective, proper pricing to minimize externalities or  redress after the fact? Which is more just?

3.Alternative Energy and Air Pollution

Ch 12 (pp. 387-410) Entire Chapter  

 Key terms & Concepts for Ch 12: 

∙ Solar:

∙ Pros: does not create pollution, is renewable energy, solar panels  can be used 4 a long time & require little to no maintenance

∙ Cons: Ineffective in colder regions, cannot be used during the night, not all the light from the sun can be trapped by solar panels, can be  expensive to purchase & install  

∙ Wind 

∙ Pros: Renewable, reduces dependency on foreign countries for oil & gas, doesn’t cause air pollution, has created jobs in the economy.  

∙ Cons: Costly to set up a wind power plant (despite recent  reductions in cost), can only be used in areas which experience high winds which means it can’t be used as a source to extract energy  anywhere on earth, sometimes create noise disturbances, cannot be used near residential areas.  

∙ Geothermal technologies  

∙ Pros: Can be found anywhere on earth, renewable, produces no  pollution, reduces dependence on fossil fuels, results in significant  cost savings as no fuel is required 2 harness energy from beneath  the earth

∙ Cons: Suitable 2 particular regions & cannot be harnessed  everywhere, the earth also releases some harmful gases which may  cause adverse health effects, areas where this energy is harnessed  are prone to earthquakes & volcanoes, and there is a huge  installation cost.  

∙ Nuclear power: 

∙ Pros: emits far fewer greenhouse gases during electricity  generation than coal or other fuel sources, lower Carbon Monoxide  released, low operating costs (relatively), known & developed  technology ready for market, large power generating capacity that  is able 2 meet industrial & city needs (I.E. it is SCALABLE), &  existing and future nuclear waste can be reduced thru waste  recycling & reprocessing  

∙ Cons: can be very dangerous, can cause multitude of  

diseases/illnesses/defects due to radiation, nuclear waste is harmful & is subject to spills/incorrect disposal which could hurt humans,  animals, & destroy the ecosystem, radiation stays in maintenance  materials so they must be disposed of correctly and securely &

aren’t always, high construction costs due 2 coplex radiation  containment systems & procedures, high subsidies needed 4  construction & operation as well as loan guarantees, high known  risks in an accident, unknown potentially harmful risks, long  construction time, target for terrorism, waivers are required 2 limit  liability of companies in the event of an accident (i.e. lack of  culpability/compensation/accountability for workplace injuries,  spills, malfunctions, deaths, illness, etc.), requires large  infrastructure, investment, & coordination, Uranium is not  renewable, it is expensive 2 mine refine & transport, & produces  considerable environmental waste during all of these processes,  less accessibilitymost of the world’s uranium is under land  controlled by tribes/indigenous people who won’t support it being  mined from the earth, the legacy of environmental contamination &  health costs for miners & mines has been catastrophic, the waste  generated lasts 200-500 thousand years, no long-term operating  waste storage sites for this waste in the US, no operating “next  generation” reactors that could reduce waste & reduce safety  concerns, and the Shipping of nuclear waste internationally poses  increased risks/threat to interception by terrorisms/may be conflict  point & used for terror, could significantly increase the risk to  nuclear terrorism.  

∙     3 Ways Water is used in a traditional nuclear plant: 

1.Water is used 2 generate electricity by boiling it &  transforming it into steam which turns a turbine, which turns a generator.

2.Water is used in plant cooling systems which are  needed to cool the steam back to water, so the energy  generating process can continue.

 Once-thru cooling system: withdraws water  

from a water body & circulates it w/in the plant  2 condense the steam from the turbine into  

water through heat absorption.

 Wet Cooling system: circulating water from the  plant moves through the tower & is cooled by  

evaporation.  

3.Water is also used 2 keep the reactor core & used  fuel rods cool (to avoid a potentially catastrophic  failure).

∙ Limiting factors in alternative energy:  

∙ Water Use: H20 is necessary to generate electricity for many  alternative energy sources & it requires a lot of itissues arise when  a plant is built/operates in a place where H20 is scarce or is stressed by competing pressures (such as local farmers’ needs, local  ecosystem needs, local ecosystems that are affected by climate  change & cant’ afford to lose more water). Also, issues disposing of  produced water can be an issue & can destroy the environment &  cause illness, which has also caused conflict & tensions between  energy companies, local residents, & sate & local gov’ts.  

∙ Transmission: issues with delivery of the energy/power to the grid, such as a lack of powerlines, bigger/better energy delivery  infrastructure. Issues w/ energy delivery “congestion”, lack  of/breaking of transmission equipment in the ground, costly  transmission upgrades, higher transmission costs than other  energies & may be subject 2 other discriminatory grid policies,  issues & risks regarding the transmission, lack of investment in new  transmission lines.  

∙ Intermittency: Intermittent renewables are challenging b/c they  disrupt the conventional methods for planning the daily operation of the electric gridtheir power fluctuates over multiple time horizons  which forces the grid operator 2 adjust its day-ahead, hour-ahead, & real-time operating procedures.  

∙ Example: Solar Energy inherently only operational when it is daylight, so grid operator must adjust the day-ahead plan 2  include generators that can quickly adjust their power output  2 compensate 4 the rise & fall in solar power generation.  

∙ Further Issues w/ Intermittency: administration &  operation of energyintermittent renewables mean lapses  in reliability & consistency & efficiency in the delivery of  

energy to meet electric demand. Exacerbated by the energy  grid that has very little storage capacity.  

 ∙     Other:  

∙ Commercialization barriers faced by new tech competing w/  mature tech, price distortions from existing subsidies &  

unequal tax burdens b/t renewables & other energy sources,  failure of the market 2 value the public benefits of  

renewables, market barriers such as inadequate information,  lack of access 2 capital $$, split incentives b/t building owners

& tenants, high transaction costs for making small renewable  energy company purchases  

∙ Apply the energy issues discussed in class to the development of  sustainable US energy policy hydrofracking in NYC for example.  

∙ 6 criteria air pollutants 

∙ Criteria Pollutants: regulatory category including major  pollutants for which the EPA promulgates National Ambient  Air Quality Standards (NAAQS) under the Clean Air Act 2  protect human health & welfare (includes public goods like  agricultural crops, livestock, property, air & ground  transport, even views.)

 ∙     Types:  

∙ Carbon Monoxide

∙ Lead

∙ Nitrogen Dioxide

∙ Ozone

∙ Particulates

∙ Sulfur Oxides

∙ Hazardous Air PollutantsCategory established by the Clean  Air Act Amendments of 1990.  

∙ Includes: volatile organic chemicals, pesticides, herbicides, & radionuclides.

∙ Air pollutants can either be gases or particles.  

∙ Pollutant’s physical form & chemical composition &  characteristics affect its ability to penetrate the  

respiratory system.  

∙ Ambient concentration also determines the exposed  individual’s ventilation rate (# of breaths per minute.)

 ∙     How the Pollutants are emitted:

∙ directly emitted primary pollutant 

∙ Formed in the atmosphere thru physical & chemical  conversion of precursorssecondary pollutant. 

∙ Types of emissions: Natural (Biogenic) or the result of  human activity (Anthropogenic). 

∙ Biogenic example: vegetation, pollens, volcanic gases, &  dust from deserts.  

 ∙     Human health effects: 

∙ Ambient air pollution causes 800,000 premature  deaths per year.  

∙ Impacts/heightens mortality rates

∙ Epidemiological studies investigate the relationship between  air pollutant concentrations and health outcomes under the  real-world conditions of exposure, typically in large  

populations in community settings.

∙ Impacts respiratory system negatively by depositing particles  into parts of the lung via alveoli  

∙ Mortality rate is significantly higher for those who live  in cities w/ the highest levels of air pollution than for  those who live in the least polluted cities.  

∙ Issues with asthma & other respiratory  

illnesses/diseases/effects, such as coughing &  

wheezing.  

∙ Increased risk of hospitalizations

∙ Increased risk of mortality  

 ∙     General corrective actions taken to mitigate the hazard:  

∙ Regulatory: governments enacting legislation and/or federal  agencies 2 improve air quality/protect the environment

∙ Research initiatives: Governments/agencies/organizations  initiating research 2 increase understanding of risks 2 health.

∙ Interventions that are evidence based & built based off of info regarding sources of air pollution & patterns of  population exposure & to associated health risks.  

∙ Interventions that control emissions @ the  source, reduce the volume of emissions,  

increase use of public transportation to  

lower vehicular air pollutants/emission  

controls for automobiles, decrease  

population exposure via information &  

initiatives like the EPA’s Air Quality index which  provides health warnings on high air pollution  

days

∙ Reducing health effects of air pollution via actions @  multiple spatial & institutional levels ranging from  personal decisions made by individuals, to community  & state plans, & multi-government agreements.

∙ Thinning Stratospheric Ozone:  

∙ Cause:  

∙ Ozone is being destroyed by a group of manufactured  

chemicals, containing chlorine and/or bromine. These  

chemicals are called "ozone-depleting substances"  

(ODS).

∙ ODS are very stable, nontoxic and  

environmentally safe in the lower  

atmosphere, which is why they became so  

popular in the first place.

∙ Stability allows them to float up, intact, to  

the stratosphere. Once there, they are

broken apart by the intense ultraviolet  

light, releasing chlorine and bromine.  

∙ Chlorine and bromine demolish ozone  

at an alarming rate by stripping an  

atom from the ozone molecule.  

∙ A single molecule of chlorine can break

apart thousands of molecules of ozone.

∙ ODS have a long lifetime in our  

atmosphere — up to several centuries,  

which means most of the ODS we've  

released over the last 80 years are still  

making their way to the stratosphere, where

they will add to the ozone destruction.

∙ Main ODS are:

∙ chlorofluorocarbons (CFCs)

∙ hydrochlorofluorcarbons (HCFCs)

∙ carbon tetrachloride

∙ methyl chloroform.

∙ Halons (brominated  

fluorocarbons) also play a large  

rolecan destroy up to 10 times as  

much ozone as CFCs can. For this  

reason, halons are the most serious  

ozone-depleting group of chemicals  

emitted.

∙ Controls: 

∙ Development & deployment of Replacement technologies  & chemicals  

∙ Hydrofluorocarbons (HFCs) are being  

developed to replace CFCs and HCFCs, for  

uses such as vehicle air conditioning.

∙ Behavior changes: individuals educating themselves on  protecting themselves from the sun, putting on sunscreen 2  protect their skin, wearing sunglasses/hats to protect eyes &  skin, being mindful of time spent in the sun & limiting time  spent in the sun, getting regular checkups on skin or  

suspicious skin markings, avoiding tanning beds. Also,  

government agencies/organizations/leaders vocalizing  & educating people on the effects of climate change  on the ozone layer & its implications for eye/skin/bodily  healthincreasing awareness

∙ Health Implications: 

∙ Thinning of the ozone has led to increased solar UV-B  radiation (280-315 nm) at the surface of the Earth  

which negatively impacts eye & skin health. Can cause: ∙ Cataract

∙ Pterygium

∙ Ocular melanoma  

∙ Age related macular degeneration

∙ Skin cancer (melanoma & non melanoma)  

∙ Basal cell carcinoma

∙ Squamous cell carcinoma

∙ Suppression of some aspects of immunity  

following UV exposure, which could  

negatively affect immune control of  

infectious diseases & vaccination.

∙ Implications 4 tumor growth

∙ Alteration of the efficiency by which  

pathogenic microorganisms are inactivated  

in the environment.  

∙ Key Concepts:

∙ Air pollution is a major contributor to adverse human health  conditions, from asthma to cardiovascular disease to premature  death.

∙ Air pollution is not just a modern phenomenon; it has been  recognized as a problem for thousands of years.

∙ Air pollution is not a single entity; it consists of distinct,  identifiable components (such as ozone and particulate matter),  each with its own sources, chemistry, and toxic effects.  

∙ Air pollution emissions come from many sources; these can  be natural sources or human activities.  

∙ The ambient concentration of an air pollutant in a particular  location depends on many factors, including emissions sources,  weather, and land patterns.  

∙ Air quality management strategies include controlling  emissions at the source, reducing the volume of emissions,  and decreasing population exposure.

∙ History of air pollution:  

∙ Ambient air pollution:  

∙ Criteria Pollutants:  

∙ Hazardous air pollutants:  

∙ Outdoor Pollutants:  

∙ Particulate Matter:  

∙ Aerodynamic diameter:  

∙ PM10:

∙ PM 2.5/Fine PM:

∙ Ultrafine PM:

∙ Course PM (PM10-2.5):

∙ Total suspended particles (tsp):

∙ Sulfur Dioxide:

∙ Nitrogen Oxides:

∙ Volatile organic compounds (VOCs):  

∙ Tropospheric Ozone:  

∙ Carbon Monoxide:  

∙ Lead:  

∙ Mercury:  

∙ Air Toxics:  

∙ Air Pollution prevention & control:  

∙ Effects of regional air pollution:

DISCUSSION QUESTIONS:

1. What are the primary air pollution problems in your community? What  are the main sources?  

2. How do your everyday activities contribute to air pollution?  

3. How is regional air pollution related to other health and environmental issues?  

4. Air pollution is a complex mixture of multiple contaminants, however  air pollutants are often regulated and studied individually. Why is this  the case? What are the consequences of this separation? How can this  be addressed?  

5. What actions can be taken to lower air pollution emissions? Consider  possibilities at multiple levels: the individual, community, government,  etc.

______________________________________________________________________________ 4. Public Health & Climate Change

 Key terms & Concepts for Ch 10: 

∙ Describe how the Chesapeake Bay is impacted by air emissions:

∙ Explain how mercury moves through the environment, its health  effects and the story of Minamata, Japan  

∙ Explain the connection between energy, food and water withdrawal  from the Ogallala Aquifer:  

∙ CO2 Concentration: the potency/concentration of the major  greenhouse gas. Higher concentrations of greenhouse gases have  contributed 2 global warming via Positive Radiative  

Forcingabsorbing & reemitting infrared radiation toward the lower  atmosphere & earth’s surface.

∙ Present CO2 concentration: 380 PPMV.  

∙ Pre Industrial CO2 concentration: 280 PPMV  

∙ Has risen 35%.  

∙ Explain the greenhouse effect & the influence of short-wave  and long-wave radiation  

∙ Greenhouse Effect: trapping of the sun’s warmth/energy in the planet’s lower atmosphere due 2 greater transparency of the  atmosphere to visible radiation from the sun than to infrared  radiation emitted from the planet’s surface.

∙ Caused by Greenhouse Gases getting trapped.  

∙ Higher concentrations of greenhouse gases contributed 2  global warming/greenhouse effect via Positive Radiative  Forcingabsorbing & reemitting infrared radiation toward  the lower atmosphere & earth’s surface.

∙ Short Wave Radiation: Visible light, shorter wavelength.  Contains a lot of energy. Causes 65% to 90% of melanoma on  skin, which accounts 4 75% of skin cancer deaths. Also can  cause cataracts & eye damage.  

∙ Long Wave Radiation: Infrared light. Contains less energy than Short wave, has longer wavelength than short wave.

∙ SWR & LWR’s role in global warming:  

∙ Solar energy enters our atmosphere as shortwave  

radiation in the form of ultraviolet (UV) rays (the ones that  give us sunburn) and visible light.

∙ The sun emits shortwave radiation because it is extremely  hot and has a lot of energy to give off.  

∙ Once in the Earth’s atmosphere, clouds and the surface  absorb the solar energy.  

∙ The ground heats up and re-emits energy as longwave  radiation in the form of infrared rays. Earth emits longwave radiation because Earth is cooler than the sun and has less  energy available to give off.

∙ Certain greenhouse/atmospheric gases, such as  carbon dioxide, water vapor, and methane, are able  to change the energy balance of the planet by  

absorbing longwave radiation emitted from the  

Earth's surface these gases absorb a majority of the  

outgoing infrared radiation. The more greenhouse gases  present, the more radiation will be absorbed in the  

atmosphere, causing the earth to heat up & atmosphere to  trap increased amounts/concentrations of heat energy.

Abundance of greenhouse gases = an abundance of  trapped heat energy in the atmosphere/earth.  

∙ Characterize the major greenhouse gases and their relative  influence on climate:

∙ Carbon Dioxide: GWP of 1. Remains in the climate system 4  

very long time. CO2 cause increases in atmospheric  

concentrations of CO2 that will last thousands of years.

∙ Methane: influential on climate. GWP of 28 to 36. CH4 emitted  

2day lasts a decade on average. Absorbs more energy than CO2  

but has a shorter lifetime.

∙ Nitrous oxide: GWP 265-298 times that of CO2 for a 100-year  

timescale. N2O emitted today remains in the atmosphere for  

more than 100 years on average.

∙ Chlorofluorocarbons (CFCs), hydrofluorocarbons  

(HFCs), hydrochlorofluorocarbons (HCFCs),  

perfluorocarbons (PFCs), and sulfur hexafluoride  

(SF6): sometimes called high-GWP gases because, for

a given amount of mass, they trap substantially more

heat than CO2. (The GWPs for these gases can be in  

the thousands or tens of thousands.)

∙ Dichlorodifluoromethane CFC-12:  

∙ Chlorodifluoromethane HCFC-22:

∙ Perfluoromethane:

∙ Sulfur hexafluoride:  

∙ Identify the temperature and CO2 concentration cap agreed to  in Copenhagen 2010 by the US and the European Union  

∙ Global Temperature Cap: Limits temperature rise to below 2  degrees Celsius by 2020.

∙ Global CO2 Concentration Cap: 450 PPM. Designed 2 stabilise CO2 concentrations by 2020.  

∙ Public Health & Climate Change: the relationship  

∙ Climate Change causes: a depletion of food & water sources,  heats the earth, traps radiation in the atmosphere, changes  ecosystems, kills populations, causes extreme weather  fluctuations & disasters. It creates new public health issues &  exacerbates existing issues.  

∙ Public Health’s relation 2 climate change: environmental changes  caused by climate change results in: increased incidence of skin  cancer, increased mortality rate amongst skin cancer patient  

populations, increased mortality, injury, & illness rates due to  starvation and/or lack of clean water sources, increased infant  mortality rates, armed conflict for resources, increased injury,  

illness, & mortality rates due to natural disasters, increased  water-borne illness, death, & injury rates due to polluted/dirty  water, results in contaminated food sources (EX: mercury in  fish that is so concentrated that it is poisonous or bad for your  health or baby’s health), illness, injury, & death due to inside & outside air pollutants, increase in incidence of respiratory  illnesses & cancers like lung cancer.  

∙ Key Concepts: 

∙ According to the United Nations Intergovernmental Panel on  Climate Change (IPCC), by 2100 average global temperatures are projected to increase between 1.8 ° C and 4.0 ° C, sea levels will  rise, and hydrologic extremes (floods and droughts) will intensify.

∙ Climate change is likely to have major effects on crop and livestock production, as well as on the viability of  fisheries. The number of people at risk for hunger could double  by midcentury.

∙ Climate change can threaten health more directly  through heat-related morbidity and mortality; flooding  and storms with associated trauma and mental health  concerns; air pollution, especially from ground-level  ozone and potentially from aeroallergens (for example,  pollen and molds); and infectious diseases, particularly  those that are water- or vector-borne.  

∙ Weather-related health risks must be assessed in the  context of concurrent environmental stressors, such as the urban health island effect and land cover-modifying weather  effects on mosquito-borne diseases.  

∙ Risk management of climate change ranges from primary  mitigation of greenhouse gas emissions to a number of  adaptations to a change in climate regime. Both co benefits and unintended consequences of policy changes in  the energy, transportation, agriculture, and other health-relevant sectors must be considered in any comprehensive health  impact assessment of global climate change.

∙ Positive Radiative Forcing:  

∙ Climate Variability:  

∙ Vulnerable Regions:  

∙ Food Production & Malnutrition:  

∙ Fisheries & Ocean Warming and Acidification:  

∙ Heat Waves:

∙ Urban Heat Island:

∙ Albedo:  

∙ Reduced Extreme Cold:  

∙ Natural Disasters:  

∙ Floods:  

∙ Wildfies:  

∙ Sea Level Rise:

∙ Air Pollution:  

∙ Ozone:  

∙ Relationship b/t climate change & air pollution:  

∙ Aero Allergens:  

∙ Allergens & Contact Dermatitis:  

∙ Infections Diseases:  

∙ Water & foodborne diseases:  

∙ Freshwater ecosystems:  

∙ Marine Ecosystems:  

∙ Harmful Algae Blooms (HABs):  

∙ ENSO, el nino southern oscillation:  

∙ Foodborne diseases:  

∙ Effects of weather & climate on vector and rodent borne diseases: ∙ Temp. effects on selected vectors & vector borne pathogens:  ∙ Precipitations effects on selected vectors & vector borne pathogens:  ∙ Vector Borne diseases:  

∙ Mosquito borne diseases:

∙ Tick borne diseases:  

∙ Rodent borne diseases:  

∙ Land use, local climate & infectious disease:

∙ Public Health Response 2 Climate Change:  

∙ Mitigation:

∙ Adaptation:

∙ Stabilization Wedges:  

∙ Vulnerability assessment:

∙ Co-Benefits:

∙ Unintended Consequences:

∙ Climate Change Policy:  

∙ Ethical Considerations:

DISCUSSION QUESTIONS: 

1. Is climate change the major environmental health challenge of the  twenty-first century? Explain the reasoning underlying your answer.  

2. Identify a broad range of current environmental health problems likely  to be exacerbated by climate change. How might existing public health practices be altered to anticipate these effects of climate change?  What other key sectors (beyond health) should be engaged?  

3. What are some of the major driving forces behind both the risks of  climate change and our vulnerabilities to that change? Which scientific  experts would be best able to assemble a comprehensive assessment  of climate change risks? What types of policymakers should be  involved, and at what levels (local, regional, international)?  

4. What are some of the major driving forces behind both the risks of  climate change and our vulnerabilities to that change? Which scientific  experts would be best able to assemble a comprehensive assessment  of climate change risks? What types of policymakers should be  involved, and at what levels (local, regional, international)?

5. What are the potential co-benefits and the potential unintended  consequences of mitigating greenhouse gas emissions?

Ch 10 (pp. 279-317) Entire Chapter  

______________________________________________________________________________ 5. Built Environment

 Key terms & Concepts for Ch 14:

∙ Match a process description to one of the five phases of the  life cycle assessment framework  

∙ Explain the importance of life cycle assessment (LCA) in  alternative energy decision making  

∙ The biofuel debate illustrates the potential for unintended  consequences, especially for vulnerable populations, and the  need for careful analysis of each major strategy taken to address climate change, to achieve what has been called healthy  solutions for climate change

∙ Discuss the links between building efficiency and  environmental/human health  

∙ Explain ways that the built environment impacts health and  fitness  

∙ Discuss take-back effects and the importance of health in  making sustainable choices  

∙ Explain strategies in how public health professionals can play a major role in shifting behavior to abate climate change, reduce energy /water consumption and live a healthier lifestyle:  

∙ Strategies:  

∙ Mitigation: primary prevention. Refers 2 efforts to  stabilize or reduce the production of greenhouse  

gases & possibly sequester those greenhouse gases  that are produced. Can be achieved through policies &  technologies that result in more efficient energy production & reduced energy demand.

∙ Paradigm for mitigation strategies: stabilization  wedges If carbon dioxide emissions have traced an  

upward trajectory for over a century, and if we wish  

to redirect that trend to achieve stable or decreasing

emissions, then we need to employ several  technologies and behavioral changes in the  areas of energy efficiency, reduced  

transportation demand, and so on.

∙ Many of these solutions are technically  

feasible and available at present.  

∙ According to Pacala and Socolow, each of these solutions can be viewed as a wedge, and  

combining wedges is a strategy for stabilizing  

climate. Health professionals have an interest  

not only in implementing these approaches but also in evaluating each wedge to be sure its  

use does not unintentionally threaten public  

health.

∙ More examples: Encourage individuals to: write their senators & congressmen about  

voting & developing ecofriendly legislation,  

bike instead of drive, walk instead of drive,  

innovate & collaborate to invent new green  

technologies, eat less meat, dairy, & eggs to  

reduce methane production, buy & use solar  

panels to reduce nonrenewable energy output.

Use citibike. When have to drive or travel, use public transportation methods.  

Convert to biofuel, hybrid, or electric  

vehicles. Encourage your school to meet  

LEED certification standards.  

∙ Adaptation: efforts 2 reduce the public health  impact of climate change. It is Secondary prevention or preparedness.  

∙ Example: anticipate weather events & prepare  adequately for event to allow emergency  

management authorities and medical facilities to be  impactful and truly reduce injuries, illnesses, deaths  & morbidity. Public health officers should conduct  vulnerability assessments (identify likely events, at risk populations, & opportunities to reduce harm) to  tailor public health programs, health interventions,  rescue/cleanup efforts in the event of a natural  disaster or regional disaster. Utilize public health  surveillance system technologies to detect outbreaks

of infectious diseases in vulnerable areas. Analyze &  improve upon current prevention efforts & rethink  

potential thresholds that could change in the future  due to climate change (i.e. storm runoff volumes,  

frequency of heatwaves).  

∙ Some of the steps to reduce greenhouse gas  

emissions above are Co-Benefits, i.e., they  

yield multiple benefits. For example:

∙ planting trees in cities helps reduce

CO2 levels while also reducing the  

urban island heat effect, reducing  

local energy demand,  

∙ Encourage individuals to:

∙ Go vegetarian/vegan for a few days a week to reduce  harmful emission of methane gases

∙ Avoid overexposure to the sun, wear sunscreen, wear hats  & polarized sunglasses, get regular dermatologist checks of skin markings, moles, &freckles.  

∙ Purchase an electric car, hybrid car, or transform gas tank  into a biofuel car that runs off of biofuels like vegetable oil.  

∙ Purchase only amounts of food that will need, stop  throwing away food & wasting food, decrease waste by  

∙ Decrease carbon footprint by using public transportation,  reducing intake of dairy, egg, & meat products, decrease # of hours you fly per year, practice localization/purchasing  local foods from local farmers, reduce waste, walk more  and drive less, drive with multiple people if possible, spend less time in the shower, turn off your lights when you  aren’t using them, practice excellent recycling rituals,  purchase biodegradable, recyclable & recycled items,  properly dispose of waste.  

∙ Purchase & install solar panels to supplement household  electricity energy needs.  

∙ Offer local community leaders, church leaders,  educators, & local governments/councils evidence  based information & literature on climate chance &

offer resources, such as: paper fact sheets about  

climate change, online carbon footprint calculators, discuss articles & screen/watch videos & documentaries, & host  school speeches & lectures that are interesting &  

informative regarding climate change, & offer small,  

proactive things we can change each day to help save the  environment.  

∙ Key Concepts:  

∙ The design of neighborhoods, towns, and cities can affect  people's health.

∙ Modern public health is historically tied to urban planning and  land use policy.  

∙ Land use and transportation decisions can either support or  undermine routine physical activity, air quality, safety, social  interaction, mental well-being, social equity, and other  

determinants of health.  

∙ Smart Growth principles support sustainable community design  and offer both environmental and human health benefits.  

∙ Health impact assessment (HIA) is a tool that can assist decision  makers in considering the potential impacts of proposed plans,  projects, and policies on the health of populations.  

∙ Emerging research and trends in both community development  and public health are conducive to increasing collaboration  between land use planners and public health professionals.

∙ Built environment:  

∙ Urban Sprawl:  

∙ Components of community design:  

∙ Land use:  

∙ Transportation:  

∙ Travel demand:  

∙ Landscape architecture:

∙ Land conservation:  

∙ Parks and recreation:  

∙ Historic conservation:  

∙ CitiesBirthplace of modern public health:  ∙ Urban planning:  

∙ Land use mix:  

∙ Separation of land uses through zoning:  ∙ Low density development:  

∙ Density:  

∙ Dispersion of activity centers:  

∙ Automobile-oriented transportation systems:  ∙ Disinvestment in central cities:  

∙ Building codes:  

∙ Zoning codes:

∙ Subdivision regulations:  

∙ BMI (body mass index):  

∙ Design for physical activity:  

∙ Parks and greenspace:  

∙ Pollution hot spots:

∙ Vehicle miles traveled:  

∙ Transportation planning:  

∙ Injury risk:  

∙ Moto vehicle injuries:

∙ Pedestrian & bicyclist injuries:  

∙ Active transportation:  

∙ Complete streets:  

∙ Social Capital:  

∙ Smart growth:  

∙ Co-benefit:  

∙ Universal Design:  

∙ Smart Growth Principles:  

∙ New Urbanism:  

∙ Transit oriented development:  

∙ Brownfield redevelopment:  

∙ Transportation demand management:  

∙ Principles of universal design:  

∙ Health impact assessment:  

∙ LEED Neighborhood development program:  

∙ Sustainable development:  

∙ Healthy cities program:  

DISCUSSION QUESTIONS

1. When and why did public health initially become involved with urban  planning?  

2. What kind of roles could a public health professional undertake if hired  to work in a city planning or transportation department? What kind of roles could an urban planner or a transportation planner undertake if  hired to work in a local or state health department?

3. Given unlimited resources, what interventions would you implement to  improve the health of urban populations in wealthy countries? In less  wealthy countries?

4. You have been asked to perform a health impact assessment for a  highway expansion project. What information about the community  and about the project would you request? What kinds of  recommendations might you consider to mitigate the adverse impacts  and promote the healthy aspects of the proposed project?

5. Consider this statement: transportation policy is health policy. Do you  agree or disagree? Justify your answer. 6. You have been asked by local officials to increase the number of children who walk to school in your  community. How would you undertake this project?

Ch 14 (pp. 451-475) Entire Chapter

MID TERM STUDY GUIDE  

1.Risk Assessment and Toxicology

Ch 29 (pp. 1037-1047, 1059) Ch 2 (49-67, 73-75) 

 Ch 29 Sections: Environmental Health Risk Assessment Process,  Risk Management, Summary

 Ch 2 Sections: Intro, Toxicology and Environmental Public Health,  Toxicant Classification, Toxicants in the Body, Regulatory Toxicology,  Summary

 o Key terms & Concepts for Ch 2: 

∙ NOAEL: Value for the highest dose administered for  which no harmful effects are observed.  

o 1 of most important values generated by the evaluation of  dose-response curves yielded during animal testing, where  several values are determined & can serve as basis 4  

regulatory decisions.  

o The NOAL is 1 of the values determined in such studies as  described above.  

o Used by the Environmental Protection Agency in establishing  the reference dose (RfD).

o A selection of a specifically tested dose that is not  associated with statistically significant increases in  adverse health effects.  

o When this no-observed-adverse-effect-level (NOAEL) is  derived from experiments in laboratory animals, it is  

typically divided by uncertainty factors,  

sometimes totaling as much as 1,000, in order to determine a reasonably safe reference dose.  

 Typically, a factor of 10 is applied to account for  

potential differences in susceptibility across species (for  

example, rats versus humans)

 Another factor of 10 is applied for potential individual  

differences in human susceptibility

∙ LOAEL: the lowest observed adverse effect levelthe  lowest concentration/amount of a substance that  causes harmful effects.  

∙   LD50: Lethal dose for 50 Percent. Dose of the chemical  that kills 50% of those exposed to it in a defined time  frame.  

o Low LD50 indicates less of the compound is needed to   cause toxicity, i.e. it is more potent. Expressed in terms  of dose per kilogram of body weight.

∙ Dermal Exposure, Ingestion, Inhalation: Major routes by which humans can be exposed to chemicals. The route of  administration can have significant affect on the toxicity of certain  chemicals.  

o Chlorpyrifos=10x more toxic via oral administration than  dermal application.  

∙   **RfD: an estimate of the daily oral dose of a chemical  that is likely to be w/out appreciable risk 4 an individual when taken over a lifetime. 

o Factors 2 consider when calculating RfD: Uncertainty  factors (when factors are used quantitatively):  ∙ Interspecies uncertainty factor: The 1st 

uncertainty factor (Uf) reflects possible human

animal differences, and introduces a margin of  

safety to account for such interspecies  

differences.  

∙ Intraspecies uncertainty factor: the Second UF

there may be intraspecies differences in the  

response.

∙ Other uncertainty factors: recognition that  

sensitive subpopulations exist.  

o This factor originally thought 2 be addressed

by the intraspecies uncertainty factor, but it  

isn’t.  

 Recent data demonstrates the unique  

susceptibility of children have led to  

the inclusion of an additional safety  

factor for chemicals that may more  

disproportionately children.  

o ***RfD DERIVED AS FOLLOWS***  

 RfD (mg/kg/day) = NOAEL (mg/kg/day)  

UFinter x UFintra x UFother

∙ UFs are typically set @ 10. 

∙ The NOAEL derived from animal studies would be divided by 100 to find the RfD, if no other UFs were deemed to be required/necessary to factor in.  

∙ Slope Factor: used to estimate the risk of harmful  effects (like cancer, disease, etc.) associated with  exposure to a carcinogenic or potentially carcinogenic  substance.

o A slope factor is an upper bound, approximating a 95%  confidence limit, on the increased cancer risk from a lifetime  exposure to an agent by ingestion or inhalation.  

o The estimate is usually expressed in units of proportion of a  population affected per mg of substance/kg body weight-day o Generally reserved for use in the low-dose region of the dose response relationship, that is, for exposures corresponding to  risks less than 1 in 100.

o Slope factors for cancer are also referred to as cancer  potency factors (PF).

∙ Dose response relationship: Most critical aspect of  determining the risk-benefit balance for a given chemical,  used to characterize adverse effects.  

o Must know that the response observed is due to  exposure to the compound.  

o Magnitude of the response should be a function of the  dose administered.

o Should be quantitative method for measuring the  response.  

∙ Dose Response Curve: Part of dose response relationship.  Critical/has important implications 4 risk assessment of toxicity. Critical part of risk assessment.  

 Shape of dose response curve: one can  

determine whether or not a threshold exists 4  the expression of toxicity via evaluation of the  

shape of the dose response curve.  

∙ Threshold concept: built on observation that

4 many chemicals there is a dose below  

which no toxicity is observed.  

o Presence of threshold is well established 4  

many compounds, but GENOTOXIC  

CARCINOGENS (those that directly  

damage DNA) are considered to exhibit a

no-threshold phenomenon: there is no  

dose without risk.  

 Monotonic dose-response curve: typically  

considered in risk assessment. May not be correct for all chemicals.  

∙ For example, vitamins exhibit a U-shaped dose

response curve. Hormesis is often attributed to a  

pattern of low-dose stimulation and high-dose  

inhibition, which produces the characteristic U- or  

J-shaped dose-response curve.  

o At very low levels of consumption, vitamin D

deficiency causes toxic effects such as  

rickets. Once intake rises above the  

deficiency level, a region of homeostasis is  

achieved. However, vitamin D in excess of  

that level can result in kidney damage.  

 Hormesis: Although this U-shaped curve was initially  described 4 radiation effects & nutrients, there is  

emerging evidence that environmental toxicants  

may also exhibit similar dose-response  

relationships. Hormesis is often attributed to a

pattern of low-dose stimulation and high-dose  

inhibition, which produces the characteristic U- or J-shaped dose-response curve

o Biological mechanisms behind hermetic effects  

aren’t currently well established, which brings the  

concept of applying hormesis to the risk  

assessment into question.  

∙ Toxicant Classifications: Chemical class, source of  exposure, & specific organ systems/effects on human  health.

o Examples:  

 Chemical Class: Alcohols, solvents, heavy metals,  oxidants, acids.

∙ May also address physical state whether a  

toxicant exists as a liquid, solid, gas, vapor,  

dust, or fume.  

 Source of Exposure: Industrial wastes, agricultural  chemicals, waterborne toxicants, air pollutants, food  additives.  

∙ This system ignores the biological  

mechanisms that underlie toxicity.

 Organ system affected: Kidney (nephrotoxins),  Liver (hepatotoxins), Heart (cardiotoxins), Nervous  system (neurotoxins), DNA (mutagens,  

carcinogens).  

∙ Looks @ the organ system in which toxic  

effects are most pronounced, I.E. the target  

organ.

∙ FAVORED by most toxicologists when  

working to protect human health one needs  

to consider how a chemical will affect a  

particular physiological function (whether  

blood pressure, respiration, memory, urine  

production, etc) b/c each of these fxns is  

controlled by an organ system Therefore,

organ system classification provides logical  

framework for toxicologists.  

o Example: mercury is known to damage S3

segments of the proximal tubule, S3 brush  

border fxns may slough off into the urine,  

providing a marker for this injury. A  

toxicologist is interested in identifying how  

mercury alters renal fxn might isolate  

proximal tubules in the lab & perform

toxicity tests on these isolated cellular  

sections.  

∙ Endocrine Disruptors: exogenous substances or  mixtures that alter the function of an endocrine system  and cause adverse health effects.  

o Thyroid system, androgenic pathway.

o Six suspected endocrine disrupting chemicals:

Isoflavone, Vinclozolin, Estradiol, DDE, PCB, and PBDE

∙ Toxicology:  

• IDENTIFICATION & CHARACTERIZATION OF TOXIC AGENTS  determined by the following values/tests:  

o Lethal Dose for 50% (LD50) value.  

o Involves exposing laboratory animals 2 compounds &  

determining the dose that killed half the animals. Serves as an  index that allows comparisons among several unrelated  

compounds.  

∙ Weakness:  

o It is a crude method of identification &  

characterization.  

∙ Strengths:  

o The exposure is well defined (unlike the  

exposure in most human situations)

 o the outcome is unambiguous 

 o the measure can be applied across  

different compounds

o Can lead 2 the useful & practical  

 conclusion: if a compound is lethal at very low

doses then human exposures should be  

prevented or strictly controlled. If compound is  

not lethal at very low doses, exposures may be  

less strictly regulated/prevented/controlled.  

o Animal Testing 

o Animals are exposed to a suspected carcinogen at several dose levels. There is also a placebo group. Animals are  observed for defined period of time then sacrificed 2  check 4 evidence of neoplasm.

∙ Example: if a compound causes excess liver cancer in  rats at a relatively low dose, it is prudent to restrict  human exposures. If rodent studies show no adverse  effects at doses orders of magnitude higher than  

humans experience, then a chemical may be approved  to proceed through development.

o Desktop analysis:

o Relies on quantitative structure-activity relationships   ( QSARs); Frequently used by pharma companies in  screening libraries of compounds 4 potential therapeutic  use.

∙ if toxicologist notes that a particular chemical structure  has a particular toxicity, then other chemicals with  

related structures are assessed for the potential to cause similar effects.

∙ Weaknesses:  

o Less definitive: Need 2 extrapolate results to  

human responses, making it Less Definitive  

than animal testing & epidemiological studies.

∙ Strengths:  

o Less expensive  

o More rapid than animal testing  

o In Vitro Testing: 

∙ I nvolves exposure of cell systems (like bacteria   or cultured human cells) 2 a potential toxin. 

Cellular responses such as mutation are observed  & help predict human responses.  

∙ Frequently used by pharma companies in screening  libraries of compounds 4 potential therapeutic use.  ∙ Weaknesses:

o Less definitive: Need 2 extrapolate results to  

human responses, making it Less Definitive  

than animal testing & epidemiological studies.

∙ Strengths:  

o Less expensive  

o More rapid than animal testing  

o QSARs 

 ∙     Used extensively in toxicology 2 ascertain molecular  

mechanisms of action & to identify compounds most  

likely 2 cause potential health effects in living organisms. 

∙ Key function/relied upon function for Desktop  

Analysis.

o Omic Technologies: Genomic, proteomic, & metabolomics tests that provide opportunity 2 examine genes, proteins, &  metabolites on a global scale.  

o DIAGRAM OF test relationships: 

∙ Acute toxicity: exposure 2 high levels of toxicants in  short amount of time/after single dose of a  

substance/multiple doses in a 24-hours, or inhalation  exposure of 4 hours.  

o Example: herbicide paraquat specifically targets the lung via  selective uptake by the diamine/ polyamine transporter. Once in

lung, paraquat readily undergoes oxidation-reduction reactions,  generating free radicals, which can result in lung fibrosis &  ultimately in death b/c of reduced respiratory capacity. Exposure  of humans 2 less than 3 grams of paraquat has been  

demonstrated 2 be lethal.  

∙ Acute Toxicity Test: LD50 test, a multiconcentration or  definitive test(s) consisting of 5 effluent concentrations  designed 2 provide dose-response information expressed as  the percent effluent concentration that is lethal to 50% of test  organisms in a prescribed period of time.

o Tests may be Static OR Flow Through. 

o Static renewal tests: organisms are exposed to a fresh solution of the same concentration of sample every 24 h or other prescribed  interval, either by transferring the test organisms from one test  chamber to another, or by replacing all or a portion of solution in  the test chambers.

 Strengths: Reduced possibility of dissolved oxygen (DO)  depletion from high chemical oxygen demand (COD) and/or  

biological oxygen demand (BOD), or ill effects from metabolic wastes from organisms in the test solutions, Reduced  

possibility of loss of toxicants through volatilization and/or  

adsorption to the exposure vessels, Test organisms that  

rapidly deplete energy reserves are fed when the test  

solutions are renewed, and are maintained in a healthier  

state.

 Weaknesses: Require greater volume of effluent that non renewal tests, generally less sensitive than flow-through  

tests, because the toxic substances may degrade or be  

adsorbed, thereby reducing the apparent toxicity. Also, there  is less chance of detecting slugs of toxic wastes, or other  

temporal variations in waste properties.

o Non renewal tests: organisms are exposed to the same test  solution for the duration of the test.

 Strengths: cheap, cost effective in determining compliance  w/ permit conditions, limited resources required (space,  

manpower, equipment), would permit staff 2 perform many  

more tests in same amount of time, smaller volume of  

effluent required.

 Weaknesses: Dissolved oxygen (DO) depletion may result  from high chemical oxygen demand (COD), biological oxygen  demand (BOD), or metabolic wastes, Possible loss of  

toxicants through volatilization and/or adsorption to the  

exposure vessels, Generally less sensitive than static renewal or flow-through tests, because the toxic substances may  

degrade or be adsorbed, thereby reducing the apparent  

toxicity, Lesser chance of detecting slugs of toxic wastes, or  

other temporal variations in waste properties.

o Flow-through :(1) sample is pumped continuously from the  sampling point directly to the dilutor system; and (2) grab or  

composite samples are collected periodically, placed in a tank  

adjacent to the test laboratory, and pumped continuously from the  tank to the dilutor system. The flow-through method employing  continuous sampling is the preferred method for on-site tests.  

Because of the large volume (often 400 L/day) of effluent normally  required for flow-through tests, it is generally considered too costly  and impractical to conduct these tests off-site at a central  

laboratory.  

 Strengths: Provide a more representative evaluation of the  acute toxicity of the source, especially if sample is pumped  

continuously directly from the source and its toxicity varies  

with time, DO concentrations are more easily maintained in  

the test chambers, A higher loading factor (biomass) may be  

used, The possibility of loss of toxicant due to volatilization,  

adsorption, degradation, and uptake is reduced.

 Weaknesses: Large volumes of sample and dilution water  

are required,Test equipment is more complex and expensive,  

and requires more maintenance and attention, More space is  

required to conduct tests, b/c of the resources required, it  

would be very difficult to perform multiple or overlapping  

sequential tests.

∙ Chronic toxicity: exposure to low levels of toxicants for  long periods of time.

o Example: development of emphysema or developing lung  cancer following years of cigarette smoking.  

 In this situation, the compounds contained in cigarette  smoke don’t cause an immediate acute toxic outcome, but  years of exposure 2 compounds in cig smoke may  

overwhelm the protective defenses of the body & result in  damage 2 the lung.  

∙ Chronic Toxicity Test: Animal Testing. 

• Chemical absorption, distribution, metabolism and  excretion: the sequence of steps that determine a bodily response after  exposure 2 a XENOBIOTIC (a chemical foreign to the body).  ∙ ABSORPTION: 

o Once someone has come in contact w/ toxic compound, the  compound may gain access 2 the body.  

o Compound must actually traverse a biological barrier (not  enough 4 compound 2 just come in contact w/ skin, be inhaled  into the lungs or enter intestinal track).

o Each of these pathways/entrance ways exhibit  

characteristics that affect absorption:  

o GI track: designed for nutrient absorption. Large  

surface area w/ numerous transport mechanism. Many

toxicants can take advantage of this system to enter the  body.  

o Lungs: toxicants can be absorbed thru pulmonary  

alveolithe alveoli are fxnal units of the lung & are sites  of gas exchange b/t air & the blood supply. Allow  

diffusion of most water-soluble compounds. Water

soluable compounds dissolve mucous lining of the  

airways & may be absorbed from there. Lipid-soluable  (fat soluable) gases can also cross into bloodstream via  alveoli. Large particles & aerosol droplets of a toxicant  can be deposited in the upper part of the lungs where  cilia attempt 2 excrete them. Smaller particles &  

aerosols penetrate more deeply, reaching alveoli, where  absorption is very efficient.  

o Skin: Many occupational exposures occur via this route.  Intact skin offers an effective barrier against water

soluble toxicants, but fat-soluble toxicants can readily  penetrate the skin & enter bloodstream.  

∙ DISTRIBUTION: 

o Once in bloodstream, toxicant can be distributed  

throughout body.

o If toxicant=Lipid soluble, it’s often carried thru the aqueous  environment of the bloodstream in association w/ blood proteins  such as albumin.  

 Toxicants generally follow the laws of diffusionthey  move from areas of high concentration 2 areas of low  

concentration.  

o Chemicals absorbed thru intestines are shunted 2 the liver thru  portal vein in the First Pass Process & may undergo  

metabolism promptly. Limited # of chemicals may be excreted  unchanged into bile or by the kidneys into urine.  

∙ METABOLISM:  

o Once in the body, most toxicants undergo Metabolic  Conversion, aka BIOTRANSFORMATION 

 A process mediated by enzymes. Majority of  

biotransformation rxns occur in liver, which is rich in  

metabolic enzymes.  

 Nearly all cells in body have some capacity for  

metabolizing xenobiotics.

 Generally, metabolic transformations lead 2 produx  that are more polar & less fat soluble.

 B.T.’s sometimes yield increasingly toxic products ∙ Example: oxidation of methanol to formaldehyde  

and formic acid (Methanol is a a relatively nontoxic

compound in its native form, formaldehyde & formic  

acid are compounds that are quite toxic 2 the optic  

nerve & can cause blindness).  

o The METABOLIC PRODUCT yielded is thus more soluble in  urine which facilitates excretion.  

 Example: benzene is oxidized to phenol & glutathione  combines w/ halogenated aromatics 2 form nontoxic &  

more polar mercapturic acid metabolites.

 o Key terms & Concepts for Ch 29: ∙ Risk assessment: Process of identifying & evaluating  adverse events that could occur in defined scenarios.  o Attempts 2 answer 3 questions: What Can Happen? How  likely is it to happen? What are the consequences if it does  happen?  

o Consists of hazard identification, dose-response  assessment, exposure assessment, and risk  

characterization.

o It is a rapidly evolving, interdisciplinary endeavor that  encompasses many philosophies and techniques.  

o Is the synthesis of existing scientific information often  aimed at addressing specific regulatory or policy issues. A mixture of science and judgement. Not a “science”, relies heavily on science based info but does not generate new empirical  evidence on health effects like toxicology of epi do.  

∙ Environmental health setting Risk Assessment: A  Quantitative framework for evaluating & combining evidence  from toxicology, epidemiology, & other disciplines, w/ the goal of  providing a basis 4 decision making.  

o Formally defined by the Red Book in 1983. It is common  practice.

∙ USES DATA from human and animal studies are combined with  assumptions and mathematical models to quantify the risk of  various exposures & 2 guide decision making about those  exposures. 

o It’s a process that involves hazard identification, hazard  characterization or dose-response assessment,  exposure assessment, and risk characterization. 

o Focuses on health impacts that might result from  exposure 2 a particular agent or from working in, living in, or  visiting a particular environment.  

o Used 2 help determine acceptable limits 4  

concentrations of pollutants in air, water, soil, & biota  & in emissions from vehicles & industry.

o Susceptible 2 criticism b/ c it is an attempt either 2 estimate  an unmeasured past or present, OR 2 predict an unknown future, or both.

 When used as basis 4 environmental health regulations or  other important decisions, even small changes in risk  

estimates can have large econ consequences.

 Example of risk assessors in this context: looks  

@/analyzes the health risks of…

o drinking water w/ chemical & microbial  

contaminants.

o eating fish contaminated with mercury or  

polychlorinated biphenyls (PCBs).

o breathing particulate matter and other airborne  

contaminants.

o being exposed to natural and man-made sources of  

ionizing radiation.

∙ **4 STEPS OF RISK ASSESSMENT:** A conceptual  framework 4 enviro health risk assessment. Formalized in  NRC report. Divides risk assessment into 4 elements: Outlined  in the The Red Book.

o Hazard Identification: 

 The process of identifying & selecting environmental  agent(s) & health effect(s) 4 assessment.

 Process includes causal inference for particular health  outcomes based on the strength of the toxicological  and epidemiological evidence for causation.

∙ Sometimes the scope of inquiry is limited to a single  agent and single health effect from the outset, leading to a  fairly straightforward hazard identification process. Other times  

∙ Sometimes the scope of inquiry is very broad typically  leading to the selection of key agents and their most important  health effects for risk assessment purposes.

o Dose Response Assessment 

 Attempts 2 describe the quantitative relationship  b/t exposure & disease.  

∙ In some cases direct evidence of the level of response @ the  dose of interest is available, & a mathematical dose-response  model is unnecessary. This is RARE.  

 Most Dose Response Assessments frequently rely on  mathematical models in order 2 estimate responses 4  exposure that fall b/t experimental dose groups or 4  

observational data 4 which doses are typically continuous w/  few or no repetitions.

o Mathematical models may also be used to adjust  effect estimates 4 differences in species, gender,  race & other factors that may confound the  

observed dose-response relationship, or may be used  2 directly incorporate toxicological mechanisms that affect the shape of the dose response curve.  

 ***Linearized Multistage Model:*** Example of  well known dose-response model for cancer. o Assumes every molecule of exposure adds more  risk of cancer. 

o At low risks, this model predicts a nearly linear  

relationship between the dose (d) and the  

probability of response (πd): 

πd ≍ π0 + β1d 

(π0 is the estimated probability of response 

without any exposure & β1 is the effect of the dose.) 

 Threshold Models : example of another well-known  dose response model.

o Assumes nobody exposed @ a level below a  

critical threshold dose will develop cancer as a  

result of exposure.  

 Maximum Likelihood Estimation: Method used in risk  assessments that assumes equivalence on a mg/ kg/  day basis.  

o Although other methods are sometimes used to  

extrapolate results from one species to another, many  risk assessments use this method.  

o Used 2 determine that β1 = 0.00011 (mg/ kg/  day)-1 

 This provides the best fit to the rat data for the  

multistage model.

o This multistage model predicts that every mg/  kg/ day of chloroform exposure contributes an additional lifetime cancer risk of  

approximately 0.011 percent.  

o Exposure Assessment 

 Includes the estimation or measurement of the  magnitude, duration, and timing of human  

exposures to the agent of concern.

∙ Requires explicit definition of the exposed population  and the routes by which it might be exposed to the  agent.  

∙ Often quite difficult to conduct due 2 inherent difficulties in  measuring complex, time-varying behavior (such as the  frequency and amounts of water consumed by an individual or  the amounts & origins of soil and dust that she unintentionally  ingests or inhales or that contacts her skin).  

∙ Ideal exposure assessments produce a full profile of  each individual's exposures over time

∙ in practice most exposure assessments are limited to  estimating summary values (such as time-averaged  exposure rates).  

 ∙    Many exposure assessments rely on default  

assumptions about media contact rate (such as water and  soil ingestion rates) rather than attempting to estimate  specific exposure factors for every individual or   population of interest. 

o Risk Characterization 

 Final step of risk assessment.  

 Consists of combining the information from the  other three steps in order to estimate the level of  response for the identified health effects @ the  specific level of exposure to the agent( s) of interest in the  defined population.  

 ***Mathematically*** the approach consists of  substituting the specific dose amount into the dose response equation and computing the response  level.  

∙ The risk that is contributed by the exposure itself  is often of more interest than the overall probability of  response so analysts often summarize the result in  terms of…

∙ **the relative risk (πd /π0) 

∙ the additional risk aka, Attributable risk  (πd - π0) 

∙ OR the excess risk 

(πd - π0)  

( 1 - π0) 

πd= Probability of response

d=Dose

π0=estimated probability of response  

without any exposure

∙ **Each of these risk measures adjusts the  estimated probability of response in an exposed individual by the background probability of  response (the response among the unexposed) in a different  manner.

∙ **Example of combined results of risk  

characterization: the attributable risk of kidney cancer  in a frequent consumer of drinking water containing 90 μg/ L of chloroform might be about 0.0026 mg/ kg/ day ×  0.00011 mg/ kg/ day)-1 = 3 × 10-8, or about 3 in 100  million.**

o The Red Book (NRC, 1983) & other reports emphasize  that ***uncertainties associated with risk estimation  should be assessed and discussed as part of the risk  characterization step. 

 Qualitative uncertainties, such as those relating to the carcinogenicity of low exposures to chloroform, were  mentioned in the hazard identification section of this  chapter.

 Substantial uncertainty also exists regarding the  true shape of the dose-response model, particularly  

its reliability at the extremely low dose used for the drinking water example.  

∙ The actual concentration and drinking-water ingestion  rate might not be perfectly known 4 a specific population of interest.

∙ Weight of evidence: suggests that human exposure to an agent or to a group of related agents causes cancer.

o IARC monographs classify agents according to five  categories: 

 Group 1: carcinogenic to humans.  

 Group 2A: probably carcinogenic to humans.  

 Group 2B: possibly carcinogenic to humans.  

 Group 3: not classifiable as to its carcinogenicity to  humans.  

 Group 4: probably not carcinogenic to humans.

∙ Animal experiments: tests often used along with statistical  models to estimate the dose-response relationships for  humans.

∙ De minimis risk: a risk management concept commonly  applied in the United States.  

∙ Chemical Carcinogenesis: Cancer can result from chemical exposure. Cancer  is pathologically defineds as uncontrollable cell growth, growth the reflects  alterations in cell’s genome or gene expression, or both. Chemical induced  carcinogenesis proceeds in stages:  

o Initiation: first, associated w/ irreversible change in cell  genotype or phenotype.  

 @ this time, cell either moves to next stage of process or  

is destroyed typically via programmed cell death called  

Apoptosis.  

 In this stage, chemical carcinogen may act via Genotoxic  

Mechanism & directly damage DNA. Or, may alter signal  

transduction pathways resulting in an altered phenotype.  

Chemicals that alter signal transduction pathways are  

termed Epigenetic.  

o Promotion: 2nd stage. involves factors that facilitate cell growth  & replication (like dietary & hormonal factors).  

 This step is not required for all chemical  

carcinogens & UNLIKE initiation, it is reversible.  

 Example of a promoting agent=the hormone  

Estrogen which activates gene expression pathways in  

target organs like the breast, & thus promotes tumor  

growth.  

o Progression: 3rd stage. Is irreversible & involves  

morphological alterations in the genomic structure &  

growth of altered cells.  

o Metastasis: 4th & final stage. During this stage the affected  cell population spreads from its immediate/initial  

microenvironment 2 invade other tissues & organ systems.  

 Many of known environmental chemical carcinogens must

be bioactivated in order 2 exert damagine effects.  

∙ Example: Benzo[a]pyrene, which must be  

converted 2 its epoxide metabolite in order 2  

damage DNA. Others include metals (arsenic,  

chromium, nickel, etc.), minerals (asbestos),  

aliphatic compounds (formaldehyde & vinyl  

chloride), & aromatic compounds (coke oven  

emissions & naphthylamines).  

 Many enzyme systems can detoxify reactive toxicants b4  

they interact w/ target molecules.  

∙ DNA repair mechanisms can often repair damage  

caused by toxicants. If DNA isn’t repaired, cell may  

undergo programmed cell death b4 the altered DNA

can be replicated.  

∙ Immune System can also seek out & destroy  

transformed cells that have escaped other  

mechanisms of defense.

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