Environmental Science 301, Fundamentals of Industrial Hygiene
Fall 2003
Lecture notes outline I

(Everyone knows that these rough outlines are not meant to be complete
nor are they meant to be a substitute for attending the lectures.)

How industrial hygiene differs from environmental management

Environmental management concerns

• Community human health

• Vegetation and wildlife

• Chemical byproducts into surface water, community air, land disposal

• Resource conservation

• Species habitat

Industrial hygiene concerns

• Worker safety

• Worker health, acute and chronic

Health v. safety

Acute v. chronic exposure

Long term actual exposure v. short term possible (accidental usually) exposure

Evolution of workplace protection: safety measures, then health (chronic effect) protection.
Occupational hazards were seen as part of one's job in the past.

What we mean by “occupational hazards”

Ease of cause-effect determination for acute, difficult for chronic effects.

Environmental management – Industrial hygiene overlap (MSU undergraduate courses, FYI)

• Occupational health (Ensc 301, Ensc 490)

• Air quality (Ensc 420, Ensc 425)

• Epidemiology (Ensc 440)

• Toxicology for setting standards (Ensc 442)

• Risk assessment (Ensc 435)

See the syllabus for some of these courses.

Chronic exposure health standards attempt to avoid disease, while safety standards attempt to lower the probability of accidents and/or lessen the severity of an accident's harmful effects.

Acute v. chronic adverse effects

Acute and chronic exposures, effects.
For acute, exposure-effect relationship is clear.
For chronic exposure-effect relationship is often not clear.

Safety = acceptable risk

Anticipation/Recognition = knowledge, experience
Evaluation = measurements
Control = lower exposures or possibilities of exposures

Probabilities and consequences

Recognition, Evaluation, Control, how probability and consequence applies to each.
For recognition and evaluation, could estimate/determine the likelihood of an adverse effect. For control, could lower the probability and/or consequence.

For accidents (safety), lower the probability of an accident and lower the potential severity of the consequence of the accident.

Toxicity versus hazard, examples. Toxicity an inherent property of a chemical, while hazard is situational. Also, chemicals may be more toxic under certain situations, e.g. carbon tetrachloride is more toxic to the liver if ethyl alcohol is consumed.

Threshold Limit Values, Permissible Exposure Limits written to protect against acute, chronic effects.

Chronic effects are avoided by setting an 8-hour time weighted average concentration for workplace exposure 40 hours per week for a working lifetime. Note the importance of the averaging time. For an 8-hour average the following is computed to be 5 ppm.

If the exposure to 20 ppm for one hour causes an adverse effect then the chemical will also be assigned a short term exposure limit, e.g., 10 ppm for one hour, to protect against the potential acute effect AND the chronic effect.

The importance of averaging time for workplace air standards. Examples of 8-hour average and 15-minute average (within the data set from which the 8-hour average is calculated), as example in class.

Start Tuesday, September 2, 2003
Routes of exposure: ingestion, inhalation, skin contact/absorption.

Toxicology
Dose-response relationship.
Dose-response curve. Dose on x axis, Response on y axis.
Generally, increasing dose, increasing response. Keep in mind: which response?

Dose-response.
Dose (rate)
Units for dose rate can be mass per time (grams/day, e.g.); also mass per unit body weight per time (grams/kilogram-day, e.g.)

Dose rate example: 3 mg carbon tetrachloride per m3 of air times 8 m3 air/workday = 24 mg carbon tetrachloride per day. Can add absorption factor (value between 0 and 1) and also fraction delivered to the target organ (value between 0 and 1) to get a better estimate of dose. In most cases, these two are given values of 1 (100%) because data are not available or because this assumption produces a more conservative (higher) estimate for the dose rate.

Variations in response. Some workers will experience the endpoint at a much lower dose than normal. For some chemicals (not generally) some workers will be susceptible or hypersusceptible (this term is more often used for an allergic response).

Allowable workplace concentration based on 8 hours/day, 5 days/week, working lifetime (30 or so years).

Response is scored using an endpoint.

Dose-response curve is fit to the several (usually 3-4) dose-response data points.

Endpoint: the physical, chemical, behavioral, or physiological change used as an indicator of response in an experiment. Chosen by the experimenter. If different endpoints are used, different dose-response curves will result. Apply to standard setting. See below for a list of possible adverse effects, all of which could be used as endpoints.

Examples of responses that could be used as the measure of an adverse effect (endpoint) in a dose - response study:

• Death

• Change in blood presssure

• Change in heart rate

• Tissue pathology

• Pain

• Dizziness

• Tumor formation

• Infertility

• Irritation to skin, eyes, nose

• Change in organ function

Questions for the incomplete list above:

• Is the response objectively measureable?

• Is it reversible?

• Is it always adverse?

• How useful is it for setting a workplace standard?

Characteristics for susceptible groups :

• Genetic makeup

• Health status

• Nutritional status

• Tobacco, alcohol, drug (OTC, prescription, illegal) use

• Age

First four applicable to workplace, age not because very young, very old assumed to be absent.

Using thresholds, susceptible groups in setting workplace standards.

USEPA requirement to protect entire community all of the time; OSHA protects for 40 hours per week, and excludes young, old, ill. Sets standard to protect about 95% of workers. I.e., excludes some hypersusceptibles from protection.

Threshold dose definition, example

Start Thursday, September 4^th
The first response (change of any kind) that occurs after exposure to a chemical (or physical or biological) agent is an adaptive response . This could be an increase in blood pressure or breathing rate to compensate for the effect the chemical is having, e.g. If the chemical is absorbed in the blood, biochemical reactions will also begin, especially in the liver. Liver enzymes will catalyze oxidation, reduction, hydrolysis, or synthesis reactions that change the absorbed chemical to another form. In most cases these reactions will change the chemical to a less toxic and more water soluble species. In some cases the chemical is (temporarily) "activated" to a more toxic form in the liver and then is changed to a less toxic compound. Many carcinogens (agents that increase the risk of tumor formation in exposed groups) are activated by body metabolism.

If the chemical is not water soluble (the opposite of water soluble is fat soluble, meaning that it dissolves in, will be stored in, fat tissue), the biochemicals reactions in the liver will change it to a more water soluble form. This means that the chemical will be more readily excreted from the body.

Enzymes are proteins, and proteins are made from amino acids, which are coded for by DNA. . Therefore a worker's abililty to metabolize certain chemicals will depend on his genetic inheritance. This is chemical specific, meaning that a worker might have enzymes that detoxify 100 chemical types but lack the ability to metabolize the 101st. One is not generally deficient in the ability to metabolize absorbed chemicals.

LD50 definition, interpretation, units.
LC50 definition, interpretation, units. More appropriate for workplace use; not as many studies, however.

Units for dose rate can be mass per time (grams/day, e.g.); also mass per unit body weight per time (grams/kilogram-day, e.g.)

Uncertainty factors when using toxicity data to set workplace standards (and community health standards).

Types of hazards: chemical, physical, biological, ergonomic. Examples of each. Most important is chemical, then physical for most workplaces, but in a microbiology laboratory studying the plague organism the most important would be biological obviously.

Doses and dose rates are readily expressed for chemicals and most physical hazards but not for biological and ergonomic exposures.

Start in the table below on Tuesday, September 9, 2003

Sources of toxicity (dose-response) data, advantages and disadvantages.

Know definitions and aspects of the various sources of information.

No threshold chemicals : carcinogens, mutagens
Cancer theory: mutagen, loss of growth control.
No threshold assumption by USEPA and OSHA.

Ames test, screening for mutagens.
Why liver enzymes are added to the petri dish.

FYI Agency for Toxic Substances and Disease Registry Cancer Policy Framework.

FYI See Environmental Health & Safety Online for OSHA standards and much more.

For health-based standards for exposure to carcinogens, lower lifetime risk of cancer from the exposure. Here we are following the no threshold assumption used for carcinogens by the federal regulatory agencies: OSHA, USEPA, and others.

Lifetime risk of cancer from exposure to a particular carcinogen equals an agency (EPA )-assigned risk factor times the dose rate of the carcinogen.

Example:

Risk factor is 1 x 10^-5 per day/mg (yes, the units are inversed).
Dose rate is the assumed constant concentration, in say, 5 mg of the chemical per cubic meter of air breathed times 20 m3 of air breathed per day, or 100 mg/day

So 1 x 10^-5 day/mg times 100 mg/day = 1 x 10^-3 = one in a thousand lifetime risk of cancer from a constant lifetime exposure to the chemical.

Note this is an incremental risk, so if the overall cancer risk in the US is 0.23, then this exposure increases one's risk to 0.231, on average (Note).

For health-based standards for exposure to carcinogens, lower lifetime risk of cancer from the exposure. Here we are following the no threshold assumption used for carcinogens by the federal regulatory agencies: OSHA, USEPA, and others.

Lifetime risk of cancer from exposure to a particular carcinogen equals an agency (EPA )-assigned risk factor times the dose rate of the carcinogen.

Routes of exposure
Inhalation and skin
Skin designation in workplace standards.

Inhalation

Gases and vapors

Possible adverse effects:

1. irritation on contact.

Deposition/absorption most strongly dependent on solubility in water. Examples, see table in text. Irritation in upper respiratory tract if readily soluble in water.

2. Absorption to blood

Systemic effect

Target organ adverse effect

Start in the table below on Thursday, September 11, 2003

Particulate matter (aerosols)
Possible adverse effects:

1. irritation on contact.

2. Absorption to blood

Systemic effect

Target organ adverse effect

3. Fibrosis

Respiratory tract anatomy: upper respiratory tract, bronchi, bronchioles, alveoli, deposition areas for variously-sized particulate (>10, 5-10, <5 micrometers particle diameter).

Size-selective nature of respiratory system
Use size-selective air samplers to check for particles less than a certain size.

X axis: particle diameter, microns
Y axis: percent of particles captured

Mucociliary escalator
Pulmonary macrophages

Skin (and eye) exposure, possibilities

1. No adverse effect

2. Local irritation

3. Local sensitization

4. Absorption to blood

5. Local irritation and absorption to blood

Types of toxic agents/effects

Primary, secondary irritants

Primary, main effect local irritation
Secondary, main effect absorption to blood; can be local and absorb to blood together

Meaning of Skin designation in the regulations

Asphyxiants, two types

Simple

How, examples. Trouble if oxygen content is less than 18 percent by volume.
Confined space standard,   FYI Scroll down this list of OSHA standards for more information.

Chemical

        Preventing oxygen uptake from the atmosphere
        Preventing oxygen use at the cellular level

    a. Chemical asphyxiant that prevents oxygen uptake from the air: carbon monoxide.
        Source of CO is incomplete combustion of a carbon fuel. Examples.
        Hemoglobin, carboxyhemoglobin, dose level = percent carboxyhemoglobin (COHb)
        Normal 0.5% COHb; this level comes from normal metabolism
        If the air contains less than around 100 ppm CO, it takes about 6-8 hours before reaching equilibrium

        At 12 ppm, increased frequency of angina attacks and decreased exercise performance in angina patients , the susceptible group

        USEPA 8 hour community air standard 9 ppm, below the threshold of 12 ppm.
        OSHA 8 hour workplace standard 50 ppm (recently proposed 35 ppm, but not in effect)

Why USEPA standards stricter than OSHA (review)

Start here on Tuesday, September 16, 2003

    b. Chemical asphyxiant by preventing oxygen use: hydrogen cyanide. Impairs cytochrome oxidase enzyme, shutting down oxidative metabolism.
      FYI  Discussion of an antidote for overexposure to cyanide.

Neurotoxic agents
1. Ethanol, organic solvents
CNS depression, narcosis, anesthesia

2. Metals
   Adverse effects on enzymes, nerve damage. Lead, mercury examples.

3. Pesticides (organophosphates family)

Interference with nerve impulse transmission by acetylcholinesterase inhibitors. (The link calls them cholinesterase inhibitors, which is the same thing). The inhibition of acetylcholinesterase, the enzyme that breaks down acetylcholine, causes overstimulation.

Carcinogens, mutagens, teratogens

Link between mutagen and carcinogen

Consequences of a mutation

• The cell dies

• The cell's function is impaired

• DNA repair (the mutation is restored to the previous genetic configuration). FYI only; we didn't cover this.

• Apoptosis (programmed cell death, resulting in the elimination of mutated cells). FYI only; we didn't cover this.

• Tumor growth

Congenital birth defects v. teratogenic effects

Teratogenic effects: the case of thalidomide.
The first-trimester problem.

FYI Fetal Protection in the Workplace

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Environmental Science 301 syllabus page
www.faculty.mcneese.edu/es301notes1F03.htm
Last modified: Tuesday, September 16, 2003
Contact:  Dr. Bruce Wyman