Environmental and Occupational Medicine: An Introduction

Emory University - Rollins School of Public Health
Atlanta, Georgia

Instructor(s): Frumkin, Howard
Subject area: Health / Medicine
Department: Public Health
Level: Undergraduate Medical
Number of participants: 90
Duration of exercise: 90 minutes
Cost/equipment needed: None
Learning objective: Provide Information
Teaching style: Passive Learning

Please note that the copyright for this course project is retained by the instructor.



This lecture is presented to first year medical students at Emory University as part of their Patient/Doctor Course. The lecture provides a broad overview of environmental and occupational medicine beginning with a discussion of exactly what the field is, why it is relevant, and the role of physicians in this field. A discussion of environmental exposures, health effects and how to think about the possible links between the two is included. The most common work-related diseases and injuries are reviewed and students are given guidelines form taking an occupational history. Preventive strategies and resources in occupational safety and health are discussed. Several examples of environmental and occupational hazards are discussed in detail including latex sensitivity, lead toxicity, hazardous waste sites, environmental estrogens, air pollution, and global climate change.


The Patient/Doctor Course
February 26, 1997

I. INTRODUCTION

A. Some scenarios you might encounter:

1. You're an obstetrician. One of your patients, a pregnant woman who works as a laboratory technician, asks if she should change her job or stop working because of the chemicals to which she and her fetus are exposed.

2. You're an orthopedic surgeon. One of your patients, a middle-aged man, tells you that that he is totally disabled from chronic back pain, which he attributes to many years of lifting heavy objects as a warehouse worker.

3. You're a cardiologist. A long-distance truck driver asks you how soon after his recent myocardial infarction he'll be able to return to work and what kinds of tasks he'll be able to perform.

4. You're a surgeon. A former asbestos worker with lung cancer asks you if he can submit a claim for workers' compensation for his disease.

5. As an oncologist, you observe an unusual cluster of bladder cancer cases among middle-aged women in a small town.

6. You're a family practitioner. One of your patients, the vice-president of a small tool and die company, asks you to advise his company regarding prevention of occupational disease among his employees.

7. As a pediatrician, you diagnose lead poisoning in a young child, and wonder about the source of the lead. Could it be the dust brought home on the workclothes of the father, who works in a battery plant? Could it be lead paint in the child's home or day-care center? Could other children also be in danger of exposure?

8. As an internist, you are visited by three women who work for a plastics company. They all complain of headaches and severe rashes on their hands and arms. From the history they give, it seems that the problem is work-related.

9. As a family practitioner, you provide medical backup to the elementary schools in your town. Several teachers remark to you that more and more children every year seem to have asthma, and that the teachers are becoming experts in the use of inhalers. They ask you if asthma is really on the rise, and if so why.

B. Definition of environmental and occupational exposures

C. Why bother thinking about these exposures?

1. Patient care: your patients will ask you questions, and need your assistance, with health problems related to exposures.

2. Preventive medicine: this field offers wonderful opportunities to prevent injury and illness among your patients.

3. Public health: some of the major health issues we face as a society relate to environmental and occupational exposures.

D. The field of Occupational and Environmental Medicine

1. A specialty with its own residency training and Board certification.

2. OEM specialists work in academic centers, industry, managed care and HMO settings, consulting firms, and government agencies.


II. HOW TO THINK ABOUT THE HEALTH EFFECTS OF ENVIRONMENTAL EXPOSURES

A. Think about the EXPOSURE

1. What is it?

2. How much is there?

3. What is the pathway to people?

B. Think about the HEALTH EFFECT

1. What is it?

2. How much of it is occurring?

C. Are the EXPOSURE and the HEALTH EFFECT linked?

D. What should the physician do?

1. Diagnosis and treatment

2. Advice to your patients and the community

3. Prevention


III. LEADING WORK-RELATED DISEASES AND INJURIES

A. Occupational lung diseases

1. Asbestosis
a. Asbestos: a naturally occurring Mg silicate
b. Population at risk: 7-13 million
c. Selikoff: 10-20% of shipyard and asbestos workers will die of asbestos-related diseases
d. Effects:
1) pleural thickening
2) pulmonary fibrosis
3) lung cancer
4) mesothelioma
e. Synergy with cigarettes

2. Silicosis
a. Ancient disease: Hippocrates wrote of respiratory illnesses of masons, stonecutters, quarrymen
b. Silica is silicon dioxide; free crystalline silica causes silicosis
c. Silicotic nodules, PMF, superimposed infection, especially TB, atypical mycobacteria
d. 60K currently exposed workers will contract some degree of silicosis

3. CWP (Coal Worker's Pneumoconiosis)
a. "Black Lung"
b. About 5% prevalence among coal miners
c. Nodules, obstructive changes, PMF

4. Byssinosis
a. "Brown lung," "Monday morning asthma"
b. Acute and chronic airways disease
c. Affects workers with dusts of cotton, flax, hemp
d. Picking, blending, carding, spinning, weaving
e. 35K retired and current textile workers have significant disability

5. Occupational asthma
a. May be immunologic or nonimmunologic
b. Grain dusts, flour, metals, inorganic chemicals, isocyanates, enzymes, fungi

6. Lung cancer
a. Arsenic, asbestos, chloroethers, chromates, ionizing radiation, nickel, PAH's
b. Clinically just like other lung cancers, i.e. smoking-related cases

B. Musculoskeletal injuries

1. Major examples
a. Low back injuries
b. Repetitive motion-associated trauma: carpal tunnel syndrome (CTS), tendonitis
c. Vibration-associated injuries: whole-body vibration vs. segmental vibration

2. Important because of preventability through job redesign, principally through the use of ergonomic principles.

C. Occupational cancer

1. Examples:
.
ICD-9ConditionIndustry/OccupationAgent
151Stomach CancerCoal minersCoal dust
155Liver hemangiosarcomaVinyl chloride productionVinyl chloride
160Nasal cancerWoodworkers, cabinetmakers
Boot & shoe producers
Radium workers
Nickel smelting & refining
Wood dust
Unknown
Radium
Nickel
161Laryngeal cancerAsbestos workersAsbestos
158, 63Mesothelioma of pleura, peritoneumAsbestos workersAsbestos
170Bone cancerRadium workersRadium
187Scrotum cancerLathe & metal workers
Coke oven workers, petroleum refiners, tar distillers
Cutting oils
Soots, tars, tar distillates
188Bladder cancerRubber and dye workersBenzidine, beta-naphthylamine, & derivatives
189Renal cancerCoke oven workersCoke oven emissions
204Leukemia, lymphocyticRubber industry
Radiologists
Unknown
Radiation
205Leukemia, myelocyticMany
Radiologists
Benzene
Radiation
207ErythroleukemiaManyBenzene

.
2. Occupational cancer can be challenging for both the clinician and the epidemiologist because:
a. it occurs years after exposure (the principle of latency)
b. people can be exposed to multiple carcinogens on the job
c. people can be exposed to carcinogens in the general environment and through lifestyle (e.g. smoking)
d. many occupational cancers are clinically identical to nonoccupational cancers
e. clusters are difficult to study

D. Major trauma

1. NIOSH estimates 10 million/yr, 3 million severe, between 5,000 and 10,000 fatal

2. Mortality rates highest in mining, agriculture, and construction. 34% overall are MVA's.

3. Examples include amputations, fractures, eye loss, and lacerations.

E. Cardiovascular disease:
The American Heart Association lists six environmental factors with potential impact on cardiovascular disease: water hardness, trace elements, occupational inhalants, CO, noise and radiofrequency, physical and psychosocial stress. Of these, three are relevant in the occupational setting:

1. Chemical exposures
a. Carbon monoxide (CO): asphyxia
b. Carbon disulfide (CS2): hypertension, atherosclerosis
c. Halogenated hydrocarbons: sudden death, probably due to arrhythmias
d. Nitroglycerin and nitrates: rebound vasospasm

2. Noise: HTN

3. Psychosocial stress

F. Disorders of reproduction

1. Multiple adverse outcomes possible:
a. Maternal factors: irregular menses, decreased fertility, increased miscarriage rates.
b. Paternal factors: sperm abnormalities, decreased fertility.
c. Fetal factors: birth defects, developmental abnormalities, subsequent cancers.

2. Examples of known reproductive toxins:
a. Lead: Increased miscarriage rates among exposed pregnant women, semen abnormalities among exposed men, impaired neuropsychological development among offspring.
b. Methylmercury: Teratogenesis.
c. Dibromochloropropane: Male sterility.
d. Persistent organic compounds such as DDT, dioxins, and PCBs: Endocrine disruption.

G. Neurotoxic disorders

1. Peripheral neuropathy: Pb, Hg, CS2, n-hexane

2. Toxic encephalitis: DMAPN, pesticides

3. Psychosis: CS2, Mn

4. Extreme personality changes

5. Parkinsonism: Mn

H. Psychologic disorders

1. Neuroses

2. Personality disorders

3. Alcoholism

4. Drug dependency

I. Noise-induced hearing loss

1. Very preventable, both with early screening and with primary prevention.

2. Insidious onset, conversation loss later.

3. 10 million US workers affected.

J. Dermatologic conditions

1. Contact dermatitis

2. Chloracne: cutting oils, PCB's, dioxin

3. Heat and chemical burns

4. Abrasions

K. Infectious diseases: Mostly of interest with respect to agricultural workers, animal handlers, and health care workers.


IV. GETTING THE INFORMATION YOU NEED

A. Taking an occupational history

1. The important questions to ask
a. A description of all jobs held
b. The exposures on the job
c. The timing of the patient's symptoms
d. Symptoms or illnesses among coworkers
e. Non-work exposures and other factors

2. When to take an occupational history
a. Respiratory disease
b. Skin disease
c. Neuropsychiatric disease including dementia
d. Hearing loss
e. Back and joint symptoms
f. Cancer
g. Exacerbation of coronary artery disease
h. Liver disease
i. Illnesses of unknown cause

3. Be humble! You might not understand everything your patient tells you, but don't be afraid to ask

B. How to get further information about what you hear:

1. Getting the generic names of chemicals:
a. The Material Safety Data Sheet
b. Contact the manufacturer
c. The Poison Control Center (589-4400 in Atlanta)
d. The National Institute for Occupational Safety and Health (NIOSH)
e. Reference books (e.g. Clinical Toxicology of Commercial Products)

2. Researching the effects of chemicals:
a. Reference books (e.g. Medical Toxicology by Ellenhorn and Barceloux, Hazardous Materials Toxicology by Sullivan and Krieger)
b. Computer searches: Medline, Toxline, Toxnet, and other data bases, both on-line and on CD-ROM.
c. Call the local occupational medicine specialist.


V. PREVENTIVE STRATEGIES IN OCCUPATIONAL SAFETY AND HEALTH

A. Substitution of hazardous exposure with less hazardous exposure, e.g. substitute toluene for benzene

B. Engineering changes, e.g. automatic hopper loading with vinyl chloride instead of hand-loading

C. Equipment redesign, e.g. change in height of work station

D. Job redesign, e.g. have two workers, not one worker, unload heavy textile roll

E. Personnel policies, e.g. worker rotation

F. Personal protective equipment, e.g. respirators

G. Worker selection: note serious risk of discrimination, nonabatement of hazards


VI. SOME SPECIFIC SITUATIONS

A. Latex sensitivity: an occupational hazard of health care workers

B. Lead toxicity: an ancient hazard still with us

C. A hazardous waste site in Georgia: the challenges of assessing unmeasured exposures

D. Environmental estrogens: endocrine disruption by the environment?

E. Air pollution: Is the EPA a health agency?

F. Global warming: The big, big picture.


Latex sensitivity: an occupational hazard of health care workers

(An article is included here: Robbins, Jim. "Rubber Gloves: Peril for Some," The New York Times Health Section, (January 29, 1997))

I. WHAT IS LATEX?

A. Start with rubber

B. Additives and accelerators include thiurams, carbamates, and derivatives of thiourea, benzothiazole, and amines.

C. Exposure can occur through rubber gloves, condoms, diaphragms, rubber orthodontic devices, catheters, balloons, the rubber handle of a squash racket, and children's toys.

II. THE DEVELOPMENT OF AN "EPIDEMIC"

A. Contact dermatitis to rubber first reported in 1933.

B. Latex allergy reports became common in the 1980s, and have continued to increase. Why?
1. Better recognition and diagnosis by physicians.
2. More use of gloves.
3. Changes in glove manufacturing.

III. WHO IS AT RISK?
.
Prevalence of latex sensitivity in various groups
Category Prevalence
Spina bifida patients 18-68%
Atopic health care workers 24%
Health care workers 7-10%
General population 1-5%

.
IV. CLINICAL MANIFESTATIONS

A. Contact dermatitis (type IV delayed hypersensitivity)

B. Urticarial skin lesions

C. Rhinoconjunctivitis and asthma

D. Anaphylaxis (type I IgE-mediated immediate hypersensitivity)

E. Cross-reactivity with banana, avocado, kiwi, chestnut

V. APPROACHES TO PREVENTION

A. Go latex-free!

LATEX REFERENCES:

Latex Hypersensitivity Committee. Latex allergy -- an emerging healthcare problem. Ann Allergy, Asthma, & Immunol 1995; 75: 19-21.

Hunt LW, Fransway AF, Reed CE, et al. An epidemic of occupational allergy to latex involving health care workers. J Occup Environ Med 1995; 37: 1204-09.

Sussman GL, Beezhold DH. Allergy to latex rubber. Ann Internal Med 1995; 122(1): 43-6.

Slater JE. Latex allergy. J Allergy Clin Immunol 1994; 94: 139-49.

Granady LC, Slater JE. The history and diagnosis of latex allergy. Immunol and Allergy Clin North America 1995; 15: 21-29.


Lead toxicity: an ancient hazard still with us

(A local article on lead found in the soil of school grounds is included)

I. THE EXPOSURE

A. Lead is a heavy metal. It is found naturally with other metals such as copper, and when mined it is used in a wide range of applications: batteries, bullets, printing, paint (formerly), gasoline (formerly), and others.

B. Adults can be exposed at work (smelters, battery plants, welding, etc.) or through recreational activities (stained glass, firing ranges, lead sinkers). Children can be exposed through eating paint, playing on contaminated soil, or exposure to their parents' work clothes.

C. Routes of absorption include ingestion and inhalation.

D. The amount of lead a person has absorbed is reflected by the blood lead level, measured in mcg/dL. The CDC's level of concern is 10 mcg/dL, OSHA's permissible level for workers is 40-50 mcg/dL, and levels above 70 or 80 mcg/dL cause acute toxicity.

II. THE HEALTH EFFECTS

A. Neurologic system

B. Blood

C. Renal toxicity

D. Gastrointestinal symptoms

E. Reproductive toxicity

Further reading:
CDC. Preventing Lead Poisoning in Young Children. Atlanta: Centers for Disease Control, 1991.
Cullen MR, Robins JM, Eskanazi B. Adult inorganic lead intoxication: presentation of 31 new cases and a review of recent advances in the literature. Medicine 1983; 62: 221-47.

Or read the lead chapters in any of the major environmental and occupational health textbooks:
Sullivan and Krieger, Hazardous Materials Toxicology: Clinical Principles of Environmental Health (Baltimore: Williams and Wilkins, 1992).
Rosenstock and Cullen. Textbook of Clinical Occupational and Environmental Medicine (Philadelphia: Saunders, 1994).
Rom, Environmental and Occupational Medicine (Second Edition) (Boston: Little, Brown, 1992).


A hazardous waste site in Georgia: the challenges of assessing unmeasured exposures

(A local article about and illegal hazardous storage site is included here)

I. THE EXPOSURES

A. Over the years huge amounts of hazardous wastes have been generated by industry and private citizens. The U.S. continues to produce approximately 275 million tons of hazardous waste annually, just over one ton per person.

B. Although these wastes can be treated, most have been dumped or left behind. The EPA currently lists approximately 40,000 uncontrolled hazardous waste sites, of which approximately 1,500 are "Superfund" sites eligible for cleanup with federal funds.

C. Of these sites approximately 48% are abandoned waste storage/treatment/recycling sites, 33% are abandoned manufacturing facilities, 4% are government facilities (military bases, weapons complexes), 4% are mines, and 11% fall into other categories.

D. A wide range of toxic materials are found in hazardous waste sites:
.
CategoryExamples
Metalslead, arsenic, mercury
VOCstrichloroethylene, toluene, benzene, chloroform, tetrachloroethylene, 1,1,1-trichloroethane, methylene chloride, ethylbenzene, xylene, vinyl chloride, carbon tetrachloride
Halogenated pesticides and related compoundsDDT, PCBs
PAHsbenzo(a)pyrene
Radionuclides
Biological wastes


E. These materials can reach people through a variety of routes:

INSERT FIGURE 56.1 FROM SULLIVAN AND KRIEGER P 619

II. THE HEALTH EFFECTS

A. Concern and alarm in the community

B. Acute toxicity

C. Reproductive toxicity

D. Immunotoxicity

E. Skin rashes

F. Cancer

G. Neurotoxicity

Further reading:
Andrews JS, Frumkin H, Johnson BL, et al. Hazardous Waste and Human Health: International Congress on the Health Effects of Hazardous Waste. Princeton: Princeton Scientific Publishing, 1994.
National Research Council. Environmental Epidemiology: Public Health and Hazardous Wastes. (Washington: National Academy Press, 1991).
Griffith J, Duncan R, Riggan W, Pellom A. Cancer mortality in U.S. counties with hazardous waste sites and ground water pollution. Arch Environ Health 1989; 44: 69-74.
Geschwind S, Stolwijk J, Bracken M, et al. Risk of congenital malformations associated with proximity to hazardous waste sites. Am J Epidemiol 1992; 135: 1197-1207.
Ozonoff D, Colten ME, Cupples A, et al. Health problems reported by residents of a neighborhood contaminated by a hazardous waste facility. Am J Ind Med 1987; 11: 581-97.


Environmental estrogens: endocrine disruption by the environment?

I. THE THEORY: certain classes of organic chemicals, such as dioxins, PCBs, and chlorinated pesticides, can bind with estrogen receptors and exert estrogenic effects.

II. OBSERVATIONS FROM WILDLIFE BIOLOGY:

A. Rachel Carson, in Silent Spring (1962) described disrupted reproductive function in birds (abnormal nesting behavior, thinned eggshells) following DDT exposure.

B. More recent evidence, e.g. alligators in Lake Apopka, FL.
An experiment with alligator eggs incubated at a warm temperature
Incubation medium Male hatchlings Female hatchlings Intersex hatchlings
Water 100%
Estradio l20% 80%
DDE 40% 20% 40%


III. OBSERVATIONS FROM HUMAN BIOLOGY

A. We have good evidence that persistent organic chemicals (POPs) are widely distributed in human tissues, even in remote populations.

B. Early evidence that estrogenic chemicals can threaten human health: DES.

C. Several major trends could be hormonally mediated:
1. Declining sperm counts (controversial!)
2. Increasing endometriosis
3. Increasing infertility
4. Increasing breast cancer
5. Increasing testicular cancer

IV. OPPOSING EVIDENCE:

A. Most POPs are very weak estrogens

B. Some POPs are estrogens, and some are anti-estrogens; this should balance out their effects


REFERENCES ON ENDOCRINE DISRUPTERS:
Stone S. Environmental estrogens stir debate. Science 1994; 265: 308-10.

Hileman B. Environmental estrogens linked to reproductive abnormalities, cancer. Chem Engin News 1994; January: 19-23.

Colborn T. Environmental estrogens: health implications for humans and wildlife. Environ Health Persp 1995; 103 Suppl 7: 135-6.

Davis DL, Bradlow HL. Can environmental estrogens cause breast cancer? Scientific American 1995; 273(4): 167-72.


Air pollution: Is the EPA a health agency?

(An article on the proposal to tighten air standards is included here)

A 36-year-old woman presents to her family practitioner in Atlanta concerned about her asthma. She explains that she had asthma for a few years in childhood, but this resolved spontaneously. Eight years ago she moved to Mexico City for two years, where she worked as a journalist. Her asthma returned and became fairly severe. After returning to the U.S., she lived in Phoenix, and had no further problems. However, she moved to Atlanta last year, and has had episodes of wheezing, especially during the summer. She is also concerned because her four-year-old son seems to have asthma. She wonders whether Atlanta's atmosphere may be contributing to their problem, and what advice you would give her.

I. THE EXPOSURE: "criteria" pollutants that the EPA must regulate, as required by the 1970 Clean Air Act :

A. Ozone: a "secondary pollutant" not emitted directly but formed by the reaction of hydrocarbons and oxides of nitrogen (NOx) in the presence of sunlight. Common where motor vehicles are common, since they release both constituents. A respiratory irritant that impairs lung function and causes and/or aggravates several kinds of lung disease.

B. Carbon monoxide: A byproduct of incomplete combustion from cars, generators, etc. Usually doesn't accumulate except in closed spaces. Binds with hemoglobin, causes cellular asphyxia.

C. Sulfur dioxide: A byproduct of burning sulfur-containing fossil fuels, mostly at power plants and other industrial facilities. A principal cause of acid rain. Found together with particulates, hence the term "acid aerosols." Soluble in water, so it forms sulfurous and sulfuric acid on contact with mucous membranes. This causes mucous membrane irritation and impaired mucociliary clearance, and exacerbates asthma.

D. Particulates: Dust, soot, smoke, and certain chemicals such as oxides of silicon and iron. Sources include motor vehicles, factories, power plants, wood burning. The smaller particles bypass the respiratory defenses and reach the lower airways. Higher particulate levels correlate with more respiratory symptoms and higher mortality.

E. NOx: Nitrogen oxide (NO) and nitrogen dioxide (NO2) are produced by high-temperature combustion in car engines, energy plants, and factories, from oxygen and nitrogen naturally in the air. Also produced by microbial action, volcanoes. Combines with water to form nitric and nitrous acids. Toxic to airways but less so than ozone.

F. Lead: See above. Much less of a problem as an air pollutant since it was removed from gasoline in the mid-1970s.

G. Hydrocarbons: These are volatile organic compounds (VOCs) from gasoline, industrial production, and the use of solvents.

Estimated U.S. population at risk in air pollution nonattainment communities
Population subgroupPollutant(s)Number Proportion of the subgroup that is at risk
Preadolescent children 14)PM SOx, ozone, NOx 31.5 million63%
Elderly 65)PM SOx, ozone 18.8 million 60%
Asthmatic children 18)PM SOx, ozone, NOx2.3 million61%
Adult asthmaticsPM SOx, ozone, NOx4.3 million65%
Persons with COPDPM SOx, ozone, NOx8.8 million64%
Persons with CHDCOCO3.5 million33%
Pregnant womenCO Pb1.6 million38%
Children 5)Pb74, 0003%3%


Source: Neher and Koenig, 1994

II. THE HEALTH EFFECTS

A. Acute, high-dose exposures as in Meuse River Valley, Belgium (1930), Donora, Pennsylvania (1948), London (1952): thousands of sick people (cough, shortness of breath, headaches, vomiting, burning eyes, running noses) and many excess deaths, mostly among the elderly or those with underlying heart or lung disease.

B. Chronic, lower-level exposures: Irritation of eyes, nose, throat by sulfur oxides, acid aerosols.

C. Asthma: Increased pollution levels (both particulates/acid aerosols and ozone) are associated with asthma exacerbations. This is notable since asthma prevalence, hospitalization rates, and mortality are all increasing.

D. Acute respiratory infections: In both children and adults, infections such as bronchitis and pneumonia are associated with higher levels of several pollutants, including SO2, NO2, and ozone.

E. Chronic obstructive pulmonary disease: Although smoking is the major cause of COPD, air pollutants (especially SO2 and particulates) can probably also cause it and can clearly exacerbate it.

F. Mortality: In large cities with variations in air pollution levels, mortality increases one or two per cent on polluted days, and declines one or two per cent on especially clean days. The major factor seems to be particulates.

Health impact of various air pollutants
PM+++++Respiratory symptoms and acute illness
SOx++trace-Exacerbates asthma
NOx+trace-_Bronchospasm in persons without asthma
CO--_-Increased mortality
ozone+++_-Implicated in carcinogenesis


Source: Neher and Koenig, 1994

III. APPROACHES TO PREVENTION

A. Activity advisories

B. Pollution prevention

Further reading:
Rusznak C, Devalia JL, Davies RJ. The impact of pollution on allergic disease. Allergy 1994; 49 (Suppl 18): 21-7.
Barnes PJ. Air pollution and asthma. Postgrad Med J 1994; 70: 319-25.
Neher JO, Koenig JQ. Health effects of outdoor air pollution. Am Fam Physician 1994; 49: 1397-404, 1407-08.
Gong H. Health effects of air pollution: a review of clinical studies. Clin Chest Med 1992; 13: 201-14.
Bates DV. Adverse health impacts of air pollution -- continuing problems. Scand J Work Env Health 1995; 21: 405-11.


Global warming: the big, big picture

I. ROOT CAUSES

A. Population growth: The world currently has 5.7 billion people, and is projected to have about 10 billion by 2050.

B. Increasing energy use: Mostly from fossil fuels, and increasing rapidly, especially in eastern Europe and China.

II. TWO RELATED PROCESSES THAT RESULT:

A. Thinning of the ozone layer

The stratosphere (20-50 km up) normally contains ozone that absorbs incident ultraviolet radiation. But chlorofluorocarbons, a family of refrigerants and aerosols, rise into the stratosphere where they undergo the following reactions:
CFC + UV radiation Cl

Cl + O3 ClO + O2

ClO + O Cl + O2


The Cl atoms are recycled, and continue attacking other ozone molecules. The thinning of the ozone layer was recognized in 1985 by the British Meteorological Survey in Antarctica, and at international meetings in 1987 and 1988, phaseout of CFCs was planned by 1999. However, the long half-life of CFCs means that current effects on the ozone layer will persist for about a century even if all production stops immediately.

B. Global warming

The greenhouse effect refers to the heat-retaining properties of the gas layer that surrounds the earth (or of the windshield in your car). Ultraviolet radiation comes from the sun, and is ordinarily reflected back from surfaces as radiant or infrared energy. The greenhouse gases retain that reflected energy. We have been increasing the amount of greenhouse gases for about 100 years.
GREENHOUSE GASES AND WHERE THEY COME FROM
Atmospheric Concentrations
Gas Source Pre-Industrial 1990 Change
Water vapor
CO2 Combustion 280 ppm 353 ppm 1.8 ppm/yr
CH4 Combustion peat, rice cultivation, cow flatus 800 ppb 1720 ppb 15 ppb/yr
N2O Combustion 288 ppb 310 ppb 0.8 ppb/yr
CFCs Industrial production 0300-500 ppt 10-17 ppt/yr
Ozone Automobiles


Atmospheric science is imprecise but it appears the average global temperature has increased by 0.3 to 0.6 degrees Celsius over the last century. Current estimates are that we will see a global temperature increase of 1 to 5 degrees in the next 50 to 100 years, probably in the lower end of that range. The greatest temperature increase would be in temperate zones, and the smallest increases at the equator and poles.

III. DIRECT AND INDIRECT EFFECTS ON HUMAN HEALTH

A. From increased exposure to UV-B radiation:

1. Impaired growth of some plants (including food plants such as maize) and phytoplankton (an important component of aquatic food chains and an important fixer of atmospheric CO2).

2. Suppressed immune function.

3. Skin damage: sunburn, loss of skin elasticity, "premature aging."

4. Cancer: All skin cancers (melanomas, basal cell carcinomas, squamous cell carcinomas), lip cancer.

5. Cataracts.

B. From global warming:

1. Changed weather: more violent disturbances?

2. Changes in vegetation and food supplies: loss of some crops.

3. Further atmospheric changes: thawing of the permafrost, increased methane, causing more warming.

4. Rising sea level as polar ice caps melt: Currently estimated to reach 0.5 meters over 50 years. Loss of coastal cities and low-lying areas such as Bangladesh, Mauritius, Florida; disruption of fishing grounds; relocation of large populations.

5. Loss of drinking water supplies with salination of fresh water tables.

6. Direct effects of heat: heat exhaustion and heat stroke.

7. Infectious diseases: vector-borne diseases (malaria, eastern equine encephalitis, western equine encephalitis, St. Louis encephalitis), water-borne diseases (cholera).

8. Frightening but plausible scenarios include disruption of food supplies and famine; mass migrations; social unrest; epidemics.


IV. AN IMAGINARY LOOK 100 YEARS INTO THE FUTURE: GEORGIA'S HEALTH IN 2096

Skin cancer is now Georgia's leading cancer, in both incidence and mortality. It finally surpassed lung cancer in about 2050, due to constantly increasing exposure to UV-B radiation caused by thinning of the ozone layer. The second leading cause of cancer mortality is liver cancer, although this may decrease soon. Experts attribute the pandemic of liver cancer that began in the 2040's to the chronic drought in grain-producing regions of the midwest U.S. that began a decade earlier. Because of the drought, grain from those areas became extensively contaminated by aflatoxin. But there were worldwide food shortages, and there was no choice but to consume that grain, so the FDA lifted its aflatoxin restrictions and released contaminated grain for use. However, in the last decade northern Canada and northern Russia have become the world's major suppliers of grain, and new distribution systems are in place, so it is hoped that Georgians -- indeed, all Americans -- will have uncontaminated grain to eat. Oncologists and dermatologists remain busy.

Of course, many of our health problems arise from the refugee crises of the last few decades. By 2040 the global temperature had risen an average of five degrees Fahrenheit. With melting of the polar ice caps, ocean levels had risen about one foot. Large areas of Florida and the Georgia coast became uninhabitable, both because of flooding and because of salination of the fresh water table. At the same time, the state's population had increased by 25 per cent over 1990 levels, placing great pressure on all of Georgia's fresh water. With the rising oceans, available fresh water supplies were simply overwhelmed. Truly, water is the "fluid of the 21st century," with far more social and strategic importance than oil ever had 100 years ago. It is estimated that between 2040 and 2065, 4 million people migrated into Georgia from Florida, and 3 million Georgians, mostly from coastal and southern parts of the state, became internal refugees. The metropolitan Atlanta population reached 8 million by 2060.

This helps explain the steady increase in violence as a cause of death. Violence, which 100 years ago was a leading cause of death only for selected age-sex-race groups, is now a leading cause of death for all races and both sexes, beginning at age 15. The growth of neighborhood trauma centers in the 2050's and 60's helped somewhat, but wound infections have continued to defy our efforts to treat them. It is hoped that the new 24th-generation cephalosporins will provide effective treatment for some time. Trauma surgeons remain busy, and the 18 residencies in Atlanta are expected to produce enough surgeons to meet demand through the end of the century.

Infectious disease also poses great challenges. As the global temperature continued to rise in the first few decades of the century, tropical diseases invaded Florida, and reached Georgia soon thereafter. According to the Division of Tropical Diseases at the Georgia Department of Public Health, the three leading infectious diseases in the state are now malaria, dengue fever, and yellow fever. Northern areas of the state have been relatively spared, but tuberculosis remains a serious problem in the large refugee camps in Dalton, Rome, and Gainesville. The cholera epidemics that have occurred approximately once each decade seem to be aggravated by the shortage of fresh water, which compromises sanitary practices. Bubonic plague and Lyme disease were major problems in the middle years of the century after crop failures and food scarcity displaced rodent populations from south Georgia into more populated parts of the state. However, effective rodent control campaigns in the 2060's helped control these diseases.

The heat itself is a significant cause of morbidity and mortality. Waycross now has 120 days each year with temperatures over 100 degrees, and Atlanta has 85. The mortality rate from heat stroke continues to rise slowly, especially among the elderly.

The bright spots are in the cardiovascular and respiratory diseases. Ischemic heart disease has continued to decline since the 1980's and is now rare. Experts attribute this to several factors: the virtual disappearance of smoking after 2040 when warming and water shortages caused the U.S. tobacco crop to fail, widespread caloric deprivation due to food shortages, and the general shift away from meat and dairy products due to the unavailability of grazing land. Similarly, the prevalence of asthma peaked at about 35% in 2040, and seems not to be increasing further.

Further reading:
Leaf A. Potential health effects of global climatic and environmental changes. New Eng J Med 1989; 321: 1577-83.
Longstreth J. Anticipated public health consequences of global climate change. Environ Health Persp 1991; 96: 139-44.
Last JM. Global change, ozone depletion, greenhouse warming, and public health. Ann Rev Pub Health 1993; 14: 115-36.
McMichael AJ. Planetary Overload: Global Environmental Change and the Health of the Human Species (Cambridge: Cambridge University Press, 1993).
Chivian E, McCally M, Hu H, Haines A, Eds. Critical Condition: Human Health and the Environment (Cambridge MA: MIT Press, 1993).
Health and Climate Change, a series of articles in The Lancet from October to December, 1993, and published as a monograph in 1994 (London: The Lancet, 1994).


SOURCES OF INFORMATION

A. Texts:

LaDou, Occupational Medicine (Norwalk CT: Lange, 1990). (PAPERBACK)
Levy and Wegman, Occupational Health, Third Edition (Boston: Little, Brown, 1994) (PAPERBACK)
McCunney, A Practical Approach to Occupational and Environmental Medicine (Boston: Little, Brown, 1994) (PAPERBACK)
Rosenstock and Cullen, Textbook of Clinical Occupational and Environmental Medicine (Philadelphia: Saunders, 1994)
Rom, Environmental and Occupational Medicine. Second Edition (Boston: Little, Brown, 1992)
Zenz, Occupational Medicine: Principles and Practical Applications, Third Edition (Chicago: Year Book Medical Publishers, 1994)
International Labour Organization, Encyclopedia of Occupational Health and Safety (Fourth Edition, Geneva, 1995)

B. Journals:

American Journal of Industrial Medicine
Occupational and Environmental Medicine
Scandinavian Journal of Work, Environment and Health
Journal of Occupational and Environmental Medicine
International Journal of Environmental and Occupational Health





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